Oxidative Stress Essay

Oxidative Stress Essay
During physical activity, the body undergoes many changes in the muscles, lungs, heart, and bones.
The heart rate increases as the activity level increases, this happens to supply more oxygenated
blood to the muscles. When there is an increase in training it decreases the resting heart rate, and the
blood pressure decreases due to blood vessel formation (Larson et al. 2012). An individual who may
use this to supplement their physical activity would be someone most likely trying to avoid disease.
For instance, in stage 1 hypertension, unhealthy, or has an obese gene. Sustained high blood
pressure can result in hypertension which is a precursor to the development of cardiac and/or renal
hypertrophy (Duarte et al. 2001). Seen in prior animal studies and in Edwards et al. (2007) the
patient must be at a specific range (over 120/80 mm Hg) in order for quercetin supplementation to
show effects.
Also in Askari et al. (2012), they found that Vitamin C was needed for quercetin supplementation to
decrease oxidative stress. When one exercises excessively there is an increase in oxygen
consumption which can lead to oxidative stress ... Show more content on Helpwriting.net ...
The change in blood pressure can be rapid in these activities, and the heart is required to pump faster
causing strain on the blood vessels. The main reason as to why they would take quercetin
supplements is possibly they have a family history of hypertension and want to take all preventive
measures that are available. I recommend that if the individual has talked to a physician and taking
quercetin has no adverse effects on their health, then it would be of no harm to test it out for 3
months and see if there is any difference. I, however, would not recommend this for a healthy
individual to reduce blood pressure since no studies have confirmed
... Get more on HelpWriting.net ...

Urate Pro-Oxidant Summary
The pro–oxidant effects of urate could be the link between hyperuricemia and inflammatory disease,
yet the mechanism is poorly understood. In humans urate builds up in our serum from dietary
purine. Urate is an antioxidant of reactive oxygen species, yet, high serum urate (hyperuricemia) is
associated with gout, metabolic syndrome and cardiovascular disease. The link between
hyperuricemia and inflammatory disease is oxidative stress. Urate acts as a pro–oxidant by
generating reactive oxygen species and promoting the oxidation of LDL. Urate's switch from
antioxidant to pro–oxidant could be concentration dependent, ergo the 'dose makes the poison'.
Novel oxidant urate Hydroperoxide could be responsible for the pro–oxidant effects of urate by

Protandim Research Paper
Protandim and It's Effects The corporation LifeVantage has made a scientific break through. They
may have possibly found a "crack" in the aging process of mammals. Through a dietary supplement,
taking one tiny, yellow pill once a day may help slow down the effects of oxidative stress on
mammal's cells. They call this wonderful little miracle Protandim, looking through studies
Protandim is proving its miracle like effects. Protandim has had positive effects, including but not
limited to slowing the aging process, increasing all mammal's health, and preventing disease.
Oxidative stress can be closely compared to "rusting" of mammal's cells. Free radicals are unstable
molecules that ravage or "oxidize" cells throughout the body in a process ... Show more content on
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"Western blot analysis of p53 and Bax in mitochondrial fraction (left) and examination of apoptosis
(right) in mouse skin epidermal tissues. Succinate dehydrogenase subunit B (SDHB) served as the
loading control. The levels of p53/Bax were normalized to that of SDHB. Statistical analysis was
performed using one–way ANOVA (for multiple group comparison) followed by Newman–Keuls
post–test. Ctrl, basal diet; Veh, vehicle control (DMSO); Pro, Protandim. *, p The product
Protandim has been tested and trialed various times by many different species and in many different
out looks. This product has been tried for plenty of diseases and conditions and seems to continue to
shock people with its versatility. Protandim is something people should be taking on a daily basis
and the studies and articles cited have proved that. Protandim has had positive effects, including but
not limited to slowing the aging process, increasing all mammal's health, and preventing disease.
The research discovered has proven to be very pleasing and

Oxidative Stress Theory Of Aging
1. Introduction
As we know age is the greatest risk for cognitive decline which may lead to most of the
neurodegenerative diseases (Floyd&Hensley 2002) such as Alzheimer's disease, ALS, Parkinson
disease and others. Aging involves a lot of changes include physical, biology, chemistry and also
psychology (Riddle&Glisky 2007). With an increase aging population, the cognitive impairments
have become a major concern in sociology burden as well as economically. Cognitive impairment
such as spatial discrimination (Gage et al. 1984; Geinisman et al. 2004; Moffat&Resnick 2002),
working memory (Frick et al. 1995) and executive function (Zelazo et al. 2004) have been observed
deteriorate during aging. However, the exact mechanisms that contribute to age–associated cognitive
decline are still debatable.
The age–related cognitive decline are shown to involved in oxidative molecular ... Show more
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Damage to proteins and lipids as well as DNA has been shown to increase during aging in numerous
organisms comprise of Caenorhabditis elegans, Drosophila melanogaster, mice, rat and humans.
(Golden et al. 2002; Hamilton et al. 2001; Sohal et al. 1993; Stadtman 2001; Yan&Sohal 1998).
Reduction in antioxidant defense system or significant increment in oxidative stress has resulted in
poor lifespan (Ishii et al. 1998; Melov et al. 1999; Moskovitz et al. 2001). With a growing body of
evidences towards the oxidative stress theory, an exact relationship between accumulation of
reactive species or oxidative stress theory and aging process especially cognitive deterioration has
not yet been establish and strongly proven. Therefore, understanding the mechanisms of cognitive
decline is likely to be important in developing effectiveness intervention for a better

Antimicrobial And Antioxidant Activities Of Leaves
The present study was carried out to evaluate the antimicrobial and antioxidant activities of leaves
of Elephantopus scaber by using different solvent (ethyl alcohol ,acetone and aqueous). The leaves
extract from Elephantopus scaber using different solvents to extract were evaluated for antioxidant
activity by using DPPH method using a different concentrations (1, 10, 20, 30, 40, 60, 80, 100)
μg/ml. The results of this method was compared with ascorbic acid as standard. The IC50 value of
standard (ascorbic acid) was found to be 20 mg/ml. This study showed the strongest DPPH radical–
scavenging activity of (52.54±0.81)% inhibition at concentration of 40 mg/ml, and IC50 value was
30 mg/ml was found the scavenging activity of (44.92±0.26)% for ethyl alcohol extract. Acetone
extract of leaves was found at of concentration 60 mg/ml scavenging activity of 53.26±0.34%. The
IC50 value of aqueous extract of leaves was (60)μg/ml with percentage inhibition of (54.28±0.28)%
followed by (44.57±0.53)% at concentration 40 mg/ml. Introduction
Elephantopus scaber L. (Elephant's foot) is an important medicinal plant which is distributed
worldwide in all tropical regions [1]. The whole plant (root, leaf and bark) is used medicinally,
because of the presence of sesquiterpene lactones, deoxyelephantopin,isodeoxyelephantopin,
scabertopin, stigmasterol,epifriedelinol, lupeol and stigmasterol throughout the whole plant [2][3].
As per the traditional system of medicine, it is reported that the

Chemistry Of Cancer Essay
Emma Salvo
Honors Chemistry
October 18, 2017
Rough Draft: The Chemistry of Cancer
Introduction According to the National Institutes of Health, in 2016 more than 595,000 people died
from cancer, and the US is projected to spend more than $150 billion in the treatment of cancer by
2020 ("Cancer Statistics"). Many of us know a friend or loved one who was killed by a form of
cancer, and we may know someone fighting the disease right at this very moment. For this project, I
wanted to look at the chemical reasons for why cancer forms, how it grows in the human body, and
what can be done to stop it. While scientists are still learning about cancer and its effects, there is a
lot of scientific evidence that points to free radicals as one of the ... Show more content on
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The result is what we call a free radical cascade, an enormous chain reaction of free radicals that
quickly wreaks havoc on living tissue" (Howard). Because of the constant loss of one electron, the
organic molecules affected by the free radical are being oxidized. This has caused scientists to refer
to the process as "oxidative stress" (Nimse and Pal).
However, in other cases, enormous molecules can be created as the oxygen molecule takes an
electron from a nearby hydrocarbon. It glues itself to the original molecule and leaves the end of that
original molecule one electron short. For example, the following reaction shows what happens when
an organic peroxide comes into contact with ethylene. Asterisks show an unpaired electron.
R–O–O–R → R–O* + *O–R
R–O* + H2C=CH2→ RO–CH2–CH2*
RO–CH2–CH2* + H2C=CH2 → RO–CH2–CH2–CH2–CH2*
(Atteya)
As the reactions show, the unpaired electron chops the double bond between the carbon atoms in
ethylene, turning it into longer and longer free radicals.
Free Radicals and Cancer
Free radicals can cause cancerous tumors when they form longer and longer free radicals in one

location (Atteya), causing the proteins and other compounds the body naturally produced to become
transformed into larger and more complicated organic compounds that the body doesn't know what
to do with. Dr. Atteya refers to this as "localized" cancer.
However, free radicals

Essay on Alzheimer's: A Look into the Disease
AD: A Look into the Disease
Background problem Despite being known for over one hundred years the cause of Alzheimer's
disease (AD) is still not completely understood. This terminal disease affects about 800,000 people
in the UK and is expected to greatly increase in number of cases in the coming years. AD has proven
to be an elusive disease to understand; yet it is more important than ever to continue researching AD
in attempt to find a cure for the many people and family members that this disease affects.
Purpose
Since 1907, when Alois Alzheimer characterized AD, many hypotheses and theories have been
developed. However, there has been little progress toward understanding the pathophysiology that
could lead to a cure. ... Show more content on Helpwriting.net ...
Language problems develop where the patient will have difficulty naming simple objects or
maintaining conversation. A person may also wander as the disease develops. The patient will be in
a previously familiar area, but feel completely lost and not know how to get back home. Reasoning
skills including ability to make decisions and judgments are affected. Eventually the disease
progresses to the brainstem affecting vital functions eventually resulting in death. One hypothesis on
the etiology of AD is the Amyloid Cascade Hypothesis. The Amyloid Cascade Hypothesis is based
on the defining characteristics of AD being amyloid plaques and neurofibrillary tangles in the brain.
This hypothesis basically proposes accumulation of amyloid–beta is the first pathological event that
leads to the neurofibrillary tangles and eventually AD. This hypothesis is not universally accepted
because there is no mechanism that proves that amyloid–beta accumulation causes neurofibrillary
tangles. The reason the amyloid–beta cannot be definitively linked to the formation of
neurofibrillary tangles is the lack of evidence to prove whether amyloid–beta is harmful or not.
Recent theories suggest that oligomers of amyloid proteins are the cause of AD. Some other theories
that may lead to or cause AD include: oxidative stress, mitochondrial dysfunction,
Prion/transmission,

Oxidative Stress On Athletes
There is a general idea that moderate and regular physical training may enhance the immune
function and more often decrease the risk of immune related illness. Numerous studies have shown
the correlation between exercise and immunity responses on athletes. It is broadly clear that the
practices of good a nutrition intake endures more beneficial results and improve performance on
athletes. Although most of the nutrients we consume through our foods everyday may not be enough
to receive the entire healthy nutrient's needed. Soccer is a sport that requires athletes to use their
energy vigorously and at the end of each match the energy is decreased. At this point free radicals
can be produce through intensive exercise training such as soccer. These ... Show more content on
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One study examine how nutrient intake influences female soccer players, immune responses,
oxidative stress, and muscle damage. The study focused in the consumption of macronutrients and
micronutrient intake. Findings on the study showed a significant correlation on nutrient intake in
decreasing oxidative stress, muscle damage, and immune responses on these athletes. These findings
suggest that antioxidants are essential for the body to recover and prevent any injuries. Although it is
well known that vitamin deficiencies can create difficulties in training and recovery, the role of
antioxidant supplementation in a well nourished athlete is controversial. The experimental studies
are often conflicting and conclusions are difficult to reach. Nevertheless, most of the data suggest
that increased intake of vitamin E is protective against exercise induced oxidative damage (Gravina
et al. 2012). It is hypothesized that vitamin E is also involved in the recovery process following
exercise. Currently, the amount of vitamin E needed to produce these effects is unknown. The diet
may supply enough vitamin E in most athletes, but some may require supplementation. Exercise has
shown an effect on lymphocyte response and the total blood cell counts (Sureda et al. 2005). This
concludes that exercise increases the production of free radicals, therefore nutrition

The Negative Effects Of Oxidative Stress
Kozakowska et al., (2015) findings show that it is possible for exercises to support special
adaptations as regards to the group and vigor of the physical activity engaged. Based on their
findings, they hypothesize that the adaptations occur to protect the muscles from disproportionate
ROS generation, hence, enhancing the motor activities (Kozakowska et al., 2015). Their findings
show that light exercises and warm–up regimens reduced erythrocyte MDA and raised erythrocyte
SOD performance in patients with MD who engaged in regular light workouts. This study is
corroborated by the study done by Al–Naama et al., (2015) whose findings were that low–intensity
exercises was adequate to improve MDA levels and carbonyl protein – which is ... Show more
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Some studies suggest that the apoptotic activities cause sequential death of cells through
biochemical processes that change the traits of the cells. Some of the changes occur through DNA
mutation, swelling of the cell plasma membrane, and the impairment of the mRNA (Rowland &
Pedley, 2010). Research in apoptosis has divulged new findings suggesting that the process
irrepressible once it begins making it one of the most highly controlled process of the cell
functioning (Gießing, 2005). Another study on the role of apoptotic activity divulges that this
activity may be started by one of two pathways, namely the intrinsic and extrinsic pathway (Elmore,
2007). When MD patients engage in high–intensity exercises cause a decrease in the production of
ROS that makes cells in the intrinsic pathway to self–engage and kill themselves as they are
sensitive to the stress on the cells. The death that occurs in the cells in the extrinsic pathway is
thought to be due to the activation of the caspases that cause the death of cells and enzymes that
debase protein functions. In the case of extrinsic pathway cell death, it assumed that both pathways
prompt the death of cells (Elmore, 2007). A research conducted by Rahimov and Kunkel (2013)
explored the role of high–intensity exercise on the myofiber membrane in MD. Their study found
adverse effects in terms of the weakening of the myofiber membrane. The possible cause for this as
they

Urate's Pro-Oxidant Effects
Urate's pro–oxidant effects could link hyperuricemia and inflammatory disease, yet the mechanism
is obscure. For humans, dietary purine is broken down and released as urate. Urate builds up in
human serum because we lack the enzyme Uricase to promote its excretion. In healthy doses urate
acts as an antioxidant and scavenges reactive oxygen species. Yet, high serum urate (hyperuricemia)
is associated with gout, metabolic syndrome and cardiovascular disease, the link being oxidative
stress. Urate promotes oxidative stress by generating reactive oxygen species or promoting
biomolecule oxidation. Concentration affects urate's antioxidant or pro–oxidant activity, ergo the
'dose makes the poison'.
Novel oxidant urate hydroperoxide could aggravate

The Effect Of Oxidative Stress On Diabetic Individuals
antioxidant enzyme status. With this information one could hypothesize that the aspartame may have
had a catalytic effect when mixed with methotrexate, and in turn MTX amplified the effects since it
has been shown to cause oxidative stress when administered in higher doses. Diabetic individuals
are mentioned by scientist, Iyyaswamy and Rathinasamy, a number of times throughout the
documentation of their study. The significance of diabetics to the study are not mentioned and
readers of the article are left to wonder why in the introduction it is mentioned that the consumption
of aspartame in diabetic individuals is on the rise. The writers reference diabetics again, in the
conclusion, stressing the importance of creating awareness among those that consume aspartame
and of the significant health risk that result from aspartame consumption. As one reads it is easy to
pick up on the beliefs the scientist hold in regards to the importance of diabetics and their aspartame
use. The obvious importance of these beliefs certainly could have been supported better throughout
the text. It was confirmed by the study that oxidative stress is a byproduct of aspartame
consumption. A diabetic's cells are already affected by oxidative stress (Asmat Ullah, 2015, p. 4). A
healthy balance is needed between free radicles and the antioxidants that neutralize them for the
body to function properly on the cellular level. The balance of diabetics is affected more
aggressively then healthy individuals

Oxidative Stress Case Study
Oxidative stress significantly contributes to IR–associated cellular toxicity and utilization of
antioxidants can mitigate such toxicity which induced by IR [34]. In our study, it was observed that
the IR exposure revealed a marked nephrotoxicity that was evidenced by a significant elevation in
serum levels of urea and creatinine which reflects a marked impairment of the kidney function. Such
results were reported by the previous studies [35], which documented that serum levels of urea and
creatinine are good markers of nephrons functional capacity. However, the serum level of creatinine
is a more indicative than the urea concentration in the first phases of kidney disease, while the level
of urea begins to increase only after the ... Show more content on Helpwriting.net ...
Similar data have been reported previously by Elkady and Ibrahim [36] and Kutanis et al. [40].
Meanwhile, pretreatment of HMB prior to IR exposure increased the antioxidant levels and
decreased the levels of MDA when compared with IR–exposed rats. These results showed that HMB
attenuated IR–induced lipid peroxidation and that was compatible with the study of Rao et al. [22]
who suggested that the decrease in MDA concentration could be due to the ability of HMB to
scavenge secondary reactive radicals or to prevent the formation of superoxide or hydrogen
peroxide in response to IR exposure. It was stated that HMB is a potent ONOO_ scavenger that can
protect the cells against peroxy nitrite–induced diseases [41]. Along these lines, the reaction
between O2·– and NO may be diminished by the activity of HMB, whereas the enzyme–catalyzed
reaction by SOD would debilitate in this manner thus, the SOD can be maintained. It was reported
that HMB can reduce hydroxyl radical and presumably repress the formation of H2O2 in the
reaction chain, which may at last prompt the maintaining of intracellular GSH levels [18, 42, 43].
Antioxidant, activity of HMB in our investigation, may be ascribed to the phenolic nature of HMB
which could have prompted free radicals scavenging [18]. However, the

The Effects Of Caffeine On Oxidative Stress
In the present study, the MDA level was measured as an index of lipid peroxidation in order to
observe the effect of caffeine on the oxidative stress induced by AlCl3 in cortex, hippocampus and
striatum brain areas. Brain tissues are more vulnerable to oxidative stress other than tissues for many
reasons such as high oxygen consumption (more than 20% of the total inspired oxygen), the
presence of abundant amount of polyunsaturated fatty acids which are susceptible to free radicals
attack, low antioxidant levels, high iron content in addition to the non–regenerative nature of
neurons (Nehru and Anand, 2005; Kim et al., 2015). All these reasons may explain why brain is
more susceptible to aluminum toxicity than other organs. In the present ... Show more content on
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The present results showed that daily protection with caffeine attenuated the increase in MDA levels
in AlCl3–intoxicated rats. Supporting the present finding, previous studies have revealed the
antioxidant potential of caffeine against lipid peroxidation in various animal models of neurologic
diseases, including Alzheimer's disease (Prasanthi et al., 2010), epilepsy (Souza et al., 2013) and
Parkinson's disease (Khadrawy et al., 2017). It has been demonstrated that caffeine has the ability to
scavenge reactive oxygen species (Devasagayam et al., 1996) and modulated the brain antioxidant
system through increasing the content of GSH and activities of antioxidant enzymes like glutathione
reductase and superoxide dismutase (Abreu et al., 2011). Generally, the antioxidant capacity of
caffeine was similar to that of the established biological antioxidant GSH and significantly higher
than ascorbic acid (Devasagayam et al., 1996). Accordingly, this may explain the ability of caffeine
to attenuate lipid peroxidation induced by AlCl3 in the current study via direct scavenging of
reactive oxygen species or by increasing GSH content and antioxidant enzymes activities.
The present data revealed that daily oral administration of AlCl3 resulted in a significant increase in
NO levels in the cortex, hippocampus and striatum. NO is the smallest signalling molecule within

The Rat Model Of Depression
In the present study, the rat model of depression was induced by the daily i.p. injection of reserpine
for 15 days. This was followed by monitoring the motor activity to check the development of the rat
model of depression. Then the depressed rats were treated with cannabis extract to study its effect on
this model.
After 15 days of daily reserpine injection, a significant decrease in motor activity was recorded as
assessed by the open field test (OFT). Together with the hunched back appearance that was observed
after 15 days, these behavioral changes indicate the development of rat model of depression which
was maintained by the daily i.p. injection for another 15 days.
After 30 days of daily reserpine injections, the significant changes in the OFT parameters and
hunched back appearance persisted and were similar to those observed after 15 days of reserpine
treatment. In addition to the motor deficits, the present depletion in cortical and hippocampal
monoamine levels induced by reserpine confirms the development of the rat model of depression,
since the central depletion in 5–HT, NE and/or DA have been postulated as the main cause for the
pathogenesis of depression (Schechter et al., 2005)
Our results were consistent with the study of Antkiewicz–Michaluk et al. (2014) who found a
distinct depressive–like behavior in the forced swimming test, motor impairment, and reduced levels
of dopamine, noreepinephrine, and serotonin in the brain after treatment with a low dose of

Oxidative Stress Response
Oxidative stress response during infection Candida albicans inside phagocytes After internalization
of C. albicans in phagocytes, it has been observed that the target fungal pathogen like any other
microbial pathogen follows the path from phagosomes to phagolysosomes and gets fumigated and
killed. During infection, Candida species are exposed to higher levels of reactive oxygen species
(ROS), reactive nitrogen species (RNS) and antimicrobial peptides, low pH and reactive chloride
species (HOCl) inside macrophages and neutrophils, and survival through these harsh conditions is
essential for establishing disease and virulence. C. albicans evolved systems to directly scavenge the
ROS produced by host cells and establish systemic infection. C. ... Show more content on
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The increased sensitivity to oxidative stress and growth defect in minimal medium of S. cerevisiae
gsh1 mutant cells displays the importance of GSH in fungal cell survival (Grant et al., 1996). The
killing or growth defect by oxidants, disulfiram, hypochlorite (HOCl), and heavy metals is also
rescued by using exogenous GSH in medium (Kwolek–Mirek et al., 2011; Kwolek–Mirek et al.,
2012; Thorsen et al., 2009). Consequently, the deletion mutant of GCS1 (homologue of S. cerevisiae
GSH1) have imapaired tolerance to ROS, decreased killing by phagocytes, and diminished virulence
in systemic candidiasis mouse model (Yadav et al., 2011). Moreover, the other enzymes in GSH
system glutathione reductase (Glr1) of C. albicans have been shown to have reduced resistance to
hydrogen peroxide and play a major role during infection in host (Tillmann et al., 2015).
Morphogenesis of Candida under the control of oxidative stress response The killing of
phagocytosis after the infection by activating apoptosis, necrosis and recently discovered
phenomenon known as pyroptosis has been attributed to the ability of C. albicans to undergo
morphogenesis from budding yeast to filamentous fungal cells. This change in form provides it with
tools to escape

Free Radicals And Oxidative Stress
Nowadays, oxidative stress is the major risk factor for several health complications. Free radicals
are the normal byproduct of cellular metabolism that leads to oxidative stress, resulting in damage to
nucleic acids, lipids and proteins, and is an underlying cause of various diseases in the human
system, including cancer, cardiovascular diseases, inflammatory conditions, diabetic complications,
Alzheimer's disease and ageing [4–8].
Free radicals promote tumor growth by activating certain signal transduction pathways that induce
the transcription of c–fos, c–jun and c–myc, the proto–oncogenes that stimulate tumor development
[1, 2]. Excessive free radicals produced during cellular metabolism can attack the deoxyribose DNA
backbone and bases, which causes mutation and in turn leads to cancer. ... Show more content on
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A dynamic balance between free radicals and antioxidants is necessary for proper physiological
function [4]. Natural antioxidants may be incompetent in promoting complete protection from free
radicals. Various synthetic antioxidants such as butylated hydxoxyanisole, butylated
hydxoxytoluene, propyl gallate, tertiary butyl hydroquinone play a key role in scavenging of free
radicals, and some of them have been shown to possess potent scavenging ability than the natural
antioxidants

The Effect Of Dl- 2 On Antioxidant Capacity And Its...
Effects of DL– 2–hydroxy–4(methylthio)butanoic acid supplementation on antioxidant capacity and
its related gene expression in lung and liver of broilers exposed to low temperature
J.P. Wang, G.L. Yang, K.Y. Zhang, X.M. Ding, S.P. Bai, Q.F. Zeng*
Institute of Animal Nutrition, Key Laboratory for Animal Disease–Resistance Nutrition of China
Ministry of Education, Sichuan Agricultural University, Chengdu, Sichuan, China, 611130
*Corresponding author：Prof. Qiufeng, Zeng
Tel (Fax): 86–28–86290922; Email: zqf@sicau.edu.cn
Abstract
DL–2–hydroxy–4(methylthio)butanoic acid (DL–HMTBA) exhibits a higher antioxidant capability
in vitro as compared to DL–methionine, but the mechanism is not known. A total of 400 8–d–old
broilers were allotted to a 2 [Low (14–16℃) or control temperature] × 2 (0.17% or 0.51% DL–
HMTBA) factorial arrangement to investigate effects of DL–HMTBA on the gene expression
related to oxidative stress in low temperature. The hepatic glutathione (GSH), superoxide dismutase
(SOD) and glutathione peroxidase (GSH–Px) activities were decreased, while protein carbonyl and
malodndialdehyde content in lung were increased in low temperature (P10–fold decrease in CβS
protein levels. Therefore, it indicated that DL–HMTBA supplementation may increase MAT–1A and
CβS gene expression, to enhance Met trans–sulfuration to GSH, then to increase antioxidant
capacity of broilers exposed to low ambient temperature (39). Further work is needed to determine
whether the

Investigating The Protective Effects Of Pre- And Post...
Abstract: The pre– and post– treatments effects of Habak, one of Mentha longifolia subspecies, as
one of the famous folk medicine was studied in mouse bone–marrow cells in contrary to the
mutagenicity of cyclophosphamide (CP). Male Balb/C mice were pre– and post–treated orally with
aqueous extract of Habak at variable concentrations (250, 500 and 1000 mg/kg b.wt) for 24h and
48h respectively. Mice were injected intraperitoneally with CP for 24h pre– and post–treatment with
Habak. Assessment of cell viability of animals treated with Habak aqueous extract and/or CP was
performed using trypan blue exclusion assay. Investigating the protective effects of pre– and post–
treatments with Habak aqueous extract on genotoxicity of CP were evaluated with chromosome
aberrations and DNA damage using the comet assay. Cell viability of mice bone–marrow cells was
activated with the low and medium concentrations of Habak, however, the highest concentration
induced cytotoxicity significantly. When animals treated with Habak prior to CP, the chromosome
aberrations were reserved highly significant in comparison with animals injected with CP. Also,
Habak reduced the chromosome abnormalities induced by CP when mice pre–treated with CP. The
efficacy of Habak was recorded when it reduced DNA damage induced by pre– and post–treatment
with CP as assessed with percentage of DNA damage, tail length and tail moment ratio. In
conclusion, the whole aqueous extract of Habak has the ability to reduce the

Oxidative Stress Research Paper
Oxidative stress and strokes
In the pathogenesis of acute ischemic stroke low molecular antioxidants are absorbed in the reaction
with free radicals generated during oxidative stress. The endogenous catalytic system comprises a
number of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase.
Among these, the first line of defense is the catalase, which decomposes hydrogen peroxide, since
its accumulation can lead to the formation of free radicals (12, 13).
Oxidative stress culminates due to the imbalance between pro–oxidants and antioxidants and
consecutive excessive production of reactive oxygen species. Reactive oxygen species are biphasic,
taking part in normal physiological processes, but are also involved in a number of disease
processes, which mediate damage to cell structures, including lipid membranes, proteins and DNA.
Cerebral circulatory system is the main objective of oxidative stress, because it plays a critical role
in the pathogenesis of ischemic brain damage as a result of a cerebrovascular attack. Superoxide, the
main reactive oxygen species, and its derivatives cause vasodilatation by opening potassium
channels, as well as deterioration of vascular reactivity. However, reactive oxygen species are
involved in normal physiological processes, including cell signaling, ... Show more content on
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In post–ischemic brains oxidative stress triggers the activation of microglia and astrocytes (20),
leading to sharp increases in the levels of inflammatory mediators such as cytokines, chemokines
and matrix metalloproteases (21), and causing a loss of integrity of the endothelial cells in the brain,
as manifestated by the upregulation of cell adhesion molecules and neurotrophic infiltration (22).
This is likely to provoke a consecutive secondary inflammation and glial immune response,
resulting in permanent damage to the brain cells

Stress And Oxidative Stress
4. Discussion The present study indicated that increase activation ROS, p–JNK, p–ERK, p–p38
levels in CA group as compared to sham group at 72h of reperfusion. Compared to CA group, only
treatment with inhibitor of p38 induced ROS increased, survival rate and NDS reduced and
hippocampal injury while treatment with JNK inhibitor or ERK inhibitor reduced markedly ROS,
increased survival rate and NDS and didn't lead hippocampal cell injury. The results indicated that
activation JNK and ERK may be involved in neuronal cell death while activation of p38 may be
involved in neuroprotection in rat subjected to CA/CPR. The brain is one of the most of organ
exhibiting high oxygen consumption and robust production of ROS [15]. In the normal ... Show
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Upon an oxidative stress, thioredoxin becomes oxidized and disassociates from ASK–1, leading to
activation of JNK and p38 pathways through oligomerization of ASK–1 [20]. Several reports
provide evidence that JNK activation as pro–apoptotic kinases in response to cerebral ischemia
reperfusion [21, 22]. JNK can induce phosphorylation of Bax, cytochrome C and activation
caspase–3 [21, 23, 24]. Moreover, increase JNK promote neuronal death by reducing the anti–
apoptotic function of Bcl–2 in transient brain–ischemia/reperfusion [25]. Indeed， treatment with
JNK inhibition increase survival rate and NDS in SP group. By contrast, the up–regulation JNK may
be related CA1 hippocampal cell death in SKF group. The activation of p38 is a key determinant of
cell survival through modulation of ROS. P38 can regulate antioxidative synthesis by enhancing
mTOR/p70S6K signaling lead to module consequence of the ROS content in the cells. By contrast,
cells lacking p38 induces ROS accumulation, which leads to cell death [26]. Thus, p38 has been
known as diverse functions beyond the control of cell death and survival in the nervous system [27].
Recently, research indicated that p38α controls self–renewal and fate decision of neurosphere–
forming cells in adult hippocampus [28]. Indeed our results indicated that absent of p38 may be
related to accumulation ROS lead to hippocampal

Stress And Oxidative Stress
Aerobic organisms need molecular oxygen (O2) for respiration or oxidation of nutrients to obtain
energy. There are some reactive by–products of cellular respiration, derived from molecular oxygen,
that are generated continuously in cells grown aerobically, such as hydrogen peroxide (H2O2)
superoxide anion radical (O2–), and the highly reactive hydroxyl radicals (OH).These reactive
oxygen species (ROS) are essential for various functions such as homeostasis and cell signaling but
an imbalance in favor of reactive oxygen species results in oxidative stress (OS) (Kashmiri et
al.,2014). Oxidative stress (OS) result in interference in the functioning of biological systems that
maintain levels of environmentally produced reactive oxygen species (ROS), by readily detecting
and detoxifying them (Lucana et al., 2012). Living organisms have adopted mechanisms to protect
themselves against oxidative stress, by producing enzymes such as catalase and superoxide
dismutase, small proteins like thioredoxin and glutaredoxin, and molecules such as glutathione (
Cabiscol et al.,1999). Metallo–enzymes such as superoxide dismutases are the primary antioxidant
enzymes that protect cells from oxidative damage of superoxide radicals, by catalyzing dismutation
of superoxide (O2–) to hydrogen peroxide and oxygen. Superoxide dismutases, as name suggests
dismutes superoxide. Dismutation reaction is that in which two equal but opposite reactions occur
on two separate molecules. SOD takes two

The Role Of Oxidative Stress On A Free Radicals
The role of oxidative stress is the imbalance of detoxified free radicals. When the body fails to
detoxify free radicals, the free radicals take an electron from another molecule. As a result, the
molecule is no longer stable. An unstable molecule can lead to damage within the cell and cause the
cell to function improperly. Therefore, preventing oxidative stress is very important for the cell to
maintain its proper function. If the cell does not function properly, an increase in antioxidants can
help to repair the cell. Antioxidants are produced by the cell but increasing antioxidants for example
in ones diet can reduce the amount of free radicals in the body that cause harm and as a result lead to
oxidative stress in the body. Oxidative stress is an imbalance between the manifestation of reactive
oxygen species and the bodies' ability to detoxify the reactive intermediates, the free radicals, or to
repair the damage resulting from the free radicals. Free radicals are uncharged molecules that have
unpaired electrons. Free radicals floating in the cell are dangerous because free radical will take and
or steal electrons from other molecules in the cell. When a molecule does not have the correct
amount of electrons that specific molecule cannot function properly. When one molecule does not
function correctly is can cause other cells to function improperly and cause damage to the cell and
other parts. Free radicals in the body can interacts with different cell components such

Antioxidant and Anti-Inflammatory Properties of Lunasin
Antioxidant and Anti–inflammatory Properties of Lunasin:
Experimental, clinical and epidemiological studies have revealed that chronic inflammation is
involved in the development of approximately 15–20% of malignancies worldwide52, being clearly
associated with increased risk of cancer and cancer progression53. It is believed that persistent
inflammatory cells recruitment, repeated generation of reactive oxygen species (ROS), pro–
inflammatory mediators and continued proliferation of genomically unstable cells contribute to
neoplasic transformation which ultimately result in tumor invasion and metastasis54. Determination
of anti–inflammatory and/or antioxidative properties has been proposed as a good indicator for
screening any anticancerous agents55,56. Oxidative stress and inflammation are two of the most
critical factors implicated in carcinogenesis and other degenerative disorders such as colon cancer
and inflammatory bowel diseases respectively. Hernandez–Ledesma and co–worker investigated
how lunasin, affect these factors. Lunasin inhibits linoleic acid oxidation and acts as 2, 20–azino–bis
(3–ethylbenzothiazoline–6–sulfonic acid) (ABTS) diammonium salt radical scavenger. Furthermore,
using Lipopolysaccharides (LPS) stimulated RAW 264.7 macrophages, lunasin reduced the
production of ROS by LPS induced macrophages in a significant dose–dependent manner. Lunasin
also inhibited the release of pro–inflammatory cytokines (tumor necrosis factor–a [TNF–a] and
interleukine–6

Taking a Look at Oxidative Stress
Oxidative stress is one of the most important stimuli that initiates CCl4 mediated liver damage.
Lipid peroxidation as result of oxidative stress is well known to be involved in the liver injury (Lin
et al., 2012). There are a number of studies that has reported the alkynated halogen CCl4 to be
widely used as a hepatotoxin to induce liver toxicity in experimental animal models (Weber et al.,
2003). Analysis of histopathology revealed that intragastric administration of CCl4 causes damage
to the hepatic architecture, as CCl4 is metabolized in the cytochrome P450 mixed oxygenase system
found in the endoplasmic reticulum of liver cells and extra hepatic tissues (Fang et al., 2008).
CYP2E1 is a major cytochorme found to be involved in carbon–chlorine bond reductive cleavage
and biotransformation of CCl4 to trichloromethyl radical (CCl3). These cytochrome systems
catalyze many reactions involved in drug metabolism and synthesis of cholesterol and other lipid
metabolites both in endogenous substrates, such as ethanol and acetone as well as exogenous
substrates which includes carbon tetrachloride (Tang et al., 2013). In the presence of oxygen, CCl3
generates the highly reactive metabolites such as trichloromethyl peroxy (CCl3OO) free radicals
which covalently bind to the cellular macromolecules, lipids and polyunsaturated fatty acids in the
cellular membrane. Trichloromethyl peroxy (CCl3OO) free radicals react with suitable substrates to
complete its electron pair. CCl3OO is

Symptoms And Symptoms Of Epilepsy
Epilepsy is a chronic neurological issue described by repeated unconstrained seizures, it is often
accompanied by behavioral changes and cognitive deficient. Many patients with epilepsy suffer
from psychiatric disorders as depression, anxiety, psychotic disorders and personality changes.
Behavioral changes and cognitive deficient associated with seizures may be caused by underlying
structural lesions. The effects of seizures and epileptic foci which discharge impulses affect brain
function. Indeed, inflammation &learning, memory deficiencies and anxiety like behaviors are
joined by durable changes in the forebrain expression of glutamate receptor. The idea that
inflammation may incite interminable tissue brokenness applies to epilepsy, as well as to a few CNS
issue. Experimental studies and clinical setting highlight the likelihood of association of
inflammatory processes in epileptogenesis of seizures and establishment of a chronic epileptic
focus. Studies have revealed increasing in production of specific inflammatory mediators such as
(IL1β, NF–κB IL6 and TNF–α) associated with up–regulation of their receptors in the chronic
epileptic cerebrum.
Nuclear factor kappa b (NF–κB) and tumor necrosis factor–α (TNF–α) induce oxidative stress and
apoptosis in many cell types also cytokines and inflammatory mediators may participate to cause
excitotoxic and apoptotic neuronal death.
The part of oxidative stress in epilepsy is additionally bolstered by studies which suggest that

Cyp2e1 Week 1 Research Paper
ThUNCORRECTED PROOF
A R T I C L E I N F O
Article history:
Received 3 March 2016
Received in revised form 21 April 2016
Accepted 22 April 2016
Available online xxx
Keywords:
Furan
Rat testis
Oxidative stress
Histopathology
Caspase–3
CYP2E1
A B S T R A C T
Furan is produced in a wide variety of heat–treated foods via thermal degradation. Furan
contamination is found to be relatively high in processed baby foods, cereal products, fruits juices,
and canned vegetables. Several studies have demonstrated that furan is a potent hepatotoxin and
hepatocarcinogen in rodents. However, few studies have investigated the toxic effects of furan in the
testis. In addition, the exact mechanism(s) by which furan exerts toxicity in the testis has not been
fully ... Show more content on Helpwriting.net ...
Food Addit. Contam. Part A Chem. Anal. Control Expo.
Risk Assess. 30, 654–659.
Selmanoglu, G., Karacaoglu, E., Kilic, A., Kockaya, E.A., Akay, M.T., 2012. Toxicity of food
contaminant furan on liver and kidney of growing male rats. Environ. Toxicol.
27, 613–622.
Shayakhmetova, G.M., Bondarenko, L.B., Kovalenko, V.M., Ruschak, V.V., 2013.
CYP2E1 testis expression and alcohol–mediated changes of rat spermatogenesis indices and type I
collagen. Arch. Hig. Rada Toksikol. 64, 51–60.
Shayakhmetova, G.M., Bondarenko, L.B., Voronina, A.K., Anisimova, S.I.,
Matvienko, A.V., Kovalenko, V.M., 2015. Induction of CYP2E1 in testes of isoniazid– treated rats
as possible cause of testicular disorders. Toxicol.
Lett. 234, 59–66.
Srinivasan, K., 2014. Antioxidant potential of spices and their active constituents. Crit.
Rev. Food Sci. Nutr. 54, 352–372.

Taubert, D., Glockner, R., Muller, D., Schomig, E., 2006. The garlic ingredient diallyl sulfide
inhibits cytochrome P450 2E1 dependent bioactivation of acrylamide to glycidamide. Toxicol. Lett.
164, 1–5.
Terrell, A.N., Huynh, M., Grill, A.E., Kovi, R.C., O'Sullivan, M.G., Guttenplan, J.B.,
Ho, Y.Y., Peterson, L.A., 2014. Mutagenicity of furan in female Big Blue

Oxidative Stress Lab Report
Biochemistry of Free Radicals and Oxidative Stress
The research was done by Sabry M. El–Bahr at the Department of Biochemistry, Faculty of
Veterinary Medicine, P.O. Box 22758, Alexandria University, Egypt. The overall purpose of this
experiment was to study the causes of oxidative stress that is caused by free radical. It is known that
the free radicals and the Reactive Oxygen Species (ROS) are used interchangeably. ROS can
damage DNA, biomembrane lipids, proteins and other macromolecules. The primary source of ROS
is the leakage of electron from the respiratory chain during the reduction of molecular oxygen to
water generating superoxide anion. The classification of ROS includes oxygen centered radicals and
oxygen centered non– radicals. Moreover, ... Show more content on Helpwriting.net ...
The system can take care of those reactive oxygen species, some of them are enzymes, including
glutathione peroxidase, catalase and superoxide dismutase which are the most major antioxidant
enzymes that are capable to minimize oxidative stress in the organelles, and some are non–enzyme
antioxidants such as glutathione, selenium, vitamin C and E. Oxidative stress is when the balance is
in favor of oxidase, so when the antioxidants systems in the cell cannot keep up, something gets out
of whack and things start to come oxidized. This can happen in a lot of ways, we have endogenous
sources of ROS; things that are happening in the cell like aerobic cellular respiration where the ROS
are being produced as a result of some byproduct or some cellular process that supposed to be
occurring like electron transport in cellular respiration or breaking down fatty acid and peroxisome.
In this study, scientist found that there are levels of free radicals reactivity of the compounds that are
being produced in the cell; some with least reactivity such as H2O2, and some are highly reactive
such as OH. The free radicals can affect the cell negatively. One of the element that generates free
radicals and causes oxidative stress is cadmium. It increases lipid peroxidation and/or changes
intracellular glutathione levels. However, investigators found that some plants such as curcumin is a
natural drug that works

Oxidative Stress
Module ten discussed oxidative stress, and the causes, as well as consequences of liver disorders.
Oxidative stress occurs when there is an abnormal balance between nonspecific oxidation reactions,
and the body's ability to counteract them. A nonspecific oxidation reaction refers to one that
involves free radicals reacting in a disorderly fashion with other molecules. Free radicals are highly
reactive molecules that can cause cellular damage, targeting that of carbohydrates, lipids, proteins
and nucleic acids. Free radicals within the body can lead to fragmentation of proteins causing them
to have an abnormal function, oxidize polysaturated lipids at their double bond causing disruption in
the membrane function, and cause mutations in DNA. Antioxidants react directly with free radicals
in the body to render them inactive. Some antioxidant ... Show more content on Helpwriting.net ...
Glutathione and uric acid are antioxidants that are made by the cells. Glutathione performs most of
its antioxidant activity within the cell, while uric acid does most of its antioxidant activity in the
blood plasma. The antioxidants, which can be obtained from the diet, include vitamin C, vitamin E,
carotenoids and selenium. The liver disorders discussed were that of a fatty liver and alcoholic liver
disease. A fatty liver is a disorder that is characterized by the accumulation of triglycerides within
liver cells, causing the liver to enlarge up to three times its normal size. The accumulation of
triglycerides in the liver will cause the liver to have a yellow appearance. A fatty liver can be caused
several ways, such as obesity, protein energy malnutrition, metabolic disorders, and chronic alcohol
consumption. The treatment for a fatty liver depends on the cause for the fatty liver. For example, if
a fatty liver is caused by chronic alcohol consumption, then the patient would need to stop
consuming alcohol in order to reverse the damage.

Oxidative stress promotion: Disturbance of the...
Oxidative stress promotion: Disturbance of the prooxidant–antioxidant balance in favour of the
former is termed as oxidative stress (Aly et al. 2010; Uchendu et al. 2012). The outcome of this
multistep process is tissue damage which builds a path from the onset of tissue damage through
diseases to finally apoptosis (Agrawal and Sharma 2010). Damage induced by oxidative stress
occurs through the production of reactive oxygen species (ROS) which includes oxygen derived free
radicals such as superoxide anion, hydroxyl radical and non radical derivatives as hydrogen
peroxide (Tebourbi et al. 2011; Verma et al. 2007). ROS induces alterations and damage to
macromolecules like lipids and proteins, most common phenomena being lipid peroxidation ...
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Pyrethroids also interfere with Ca balance. They inhibit both Ca–ATPase and Ca–MgATPase. This
results in impact on neurotransmitter release and inhibition of Ca uptake (Coats 1990).
Xenobiotics may enhance the sensitization to allergens because of their modulating effect on T–
cells. Neoantigen formation, metabolism of xenobiotics into reactive–haptenic metabolites,
induction of costimulatory enzymes and sensitization of T–cells can give rise to autoimmunity and
allergies (Reichrtova et al. 1999).
Health Impacts of pesticide exposure:
Human exposure whether directly or through diet may result in acute and delayed health effects.
Food contaminated with toxic pesticides is associated with severe effects on human health (Kaushik
et al. 2009, Forget 1991; Amoguis et al. 2010; Androutsopoulos et al. 2012). WHO estimates show
that over 500,000 people died from self poisoning in South East Asia and Western Pacific during
2000 alone (WHO 2001; Litchfield 2005). In developing countries, the estimated annual incidence
rate in agricultural workers was found to be 18.2 per 100 000 full–time workers and 7.4 per million
school children (Bolognesi and Merlo 2011). In India, poisoning due to pesticides was first reported
in 1958 in Kerela where over more than 100 people died after consuming parathion contaminated
wheat flour (Karunakaran 1958) and the proportion has been quite

Investigating The Protective Effect Of Spermine Against...
Abstract
The current study was conducted to investigate the protective effect of spermine against toxicity of
lead and /or gamma irradiation in male rats. Eight groups of rats were used in this study (control,
irradiated group (6 GY), lead (40 mg/kg b.wt.), spermine (10 mg/kg b.wt), lead plus irradiation,
irradiation plus spermine, lead plus spermine, irradiation plus lead co–treated with spermine) for
consecutive 14 days. Complete blood count (CBC) and blood glucose–6–P–dehydrogenase (G6PD)
were measured in blood. Moreover, malondialdhyde (MDA), glutathione (GSH), metallothionin
(MT) levels and catalase (CAT) activity were investigated in liver, kidney and brain. G6PD
significantly decreased post exposure to lead and /or gamma irradiation. Hepatic, renal and brain
MDA, GSH, MT and CAT were significantly increased in lead intoxicated group, while GSH, CAT
and MT were significantly decreased in gamma–irradiated group. Spermine administration
alleviated changes in CBC, G6PD, MDA, GSH, CAT and MT to normal control levels, but with
significant increase in G6PD activity and platelets count. In conclusion, spermine acts as antioxidant
and plays a prophylactic role against intoxication with lead and/or gamma irradiation exposure.
Keywords: Rat, lead, gamma irradiation, spermine, antioxidant.
Introduction
Exposure to lead is inescapable as it occurs through many routes including contaminated air, water,
soil, food, and consumer products. The safe threshold for lead exposure has

Antioxidants And The Human Body
Numerous scientific studies show that the people whose food intake is rich in antioxidants and who
also take antioxidant supplements, have better chances to live longer, healthier and happier lives.
Antioxidants are a family of vitamins, minerals, and other nutrients that may prevent or delay some
types of cell damage. Thus, they might be beneficial in preventing diseases and contribute to the
length and quality of human life. Hundreds of antioxidants are produced in the human body, but
some necessary antioxidants must be obtained from the outer sources. But do they work separately
in our bodies? Or antioxidants in our bodies can incorporate with each other in order to improve
human lives. Some studies about antioxidants come up with a ... Show more content on
Helpwriting.net ...
The special power of this network antioxidants is that they have an ability to regenerate one another
after they played their roles in body functions. For example, if one of the antioxidants changes
because of oxidation process after it fought the body enemy particle, the other network antioxidant
can help the first one and turn it back into an antioxidants that are ready to fight again. The five
antioxidants that form the network are Lipoic acid, Vitamin E, Vitain C, Coenzyme Q10, and
Glutathione. Even though these antioxidants work perfectly together, each has his unique functions
in the human body alone. For example, Lipoic acid is the most powerful antioxidant in the
antioxidant network, because it can regenerate three out of four other network members their change
during oxidation processes. It can be used effectively to treat diabetes and significantly protect
bodies against stroke.
The natural level of vitamin E in our bodies is very low, so it must be obtained from outer sources.
Vitamin E protects lipoproteins from oxidation, which is the first step toward formation of
atherosclerosis and heart diseases. It also reduces the risk of prostate cancer and fights against of
progression of Alzheimer's disease. Our bodies don't produce Vitamin C, which is believed to be
essential for our immune system. Numerous studies prove that Coenzyme Q10 is a very effective to
threat diseases associated with the human heart, such as high blood pressure, congestive heart

Obesity And Oxidative Stress
The study of oxidative stress and obesity has stimulated several attempts in recent times to define
the contribution of the individual components of the metabolic syndrome to oxidative stress as it is
in metabolic syndrome patients. Although there have been recent attempts to do so, studies have
revealed the role of obesity as a critical and core component in the development of metabolic
syndrome. Essentially, obesity plays an integral role in amplifying oxidative stress. It has been
proven that patients who are obese show oxidative stress–induced decreased vasodilatory response
to acetylcholine. This response inversely relates to body mass index, waste to hip ratio, fasting
insulin and insulin resistance [70]. This situation remains to be

Lead Poisoning Research Paper
Heavy metal poisoning is nothing new. It has been known for centuries that some heavy metal
compounds are quite toxic to people. A particularly infamous and widely known heavy metal is lead.
Lead has been a particular useful element in early human history. It saw many uses from making
jewelry to the height of its use in the ancient world as Roman plumbing. Most people would shudder
at the thought of drinking water from lead pipes with all the hysteria associated with lead; however,
lead pipes or more commonly lead solder are still around today though mainly in outdated water
lines that have been grandfathered. Oddly enough, the Romans were actually aware of the toxic
properties of lead. Lead workers were even described as being notoriously ... Show more content on
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It rather is becoming a problem due to pollution. A recent and highly publicized lead poisoning case
was that of Flint, Michigan's water supply. Lead poisoning in the U.S. is generally caused by
contaminated water. Lead in the public water supply is generally due to absorption from lead pipes
or solder. Absorption of lead into water has been found proportional to the temperature of the water.
Unsurprisingly, the warmer the water, the higher the lead concentration; however, the change in lead
concentration compared to the temperature shift is quite surprising. Ơ Between 10 and 23 degrees
Celsius, it has been shown that a 1 degree shift in temperature can change the dissolved lead
concentration by 5 percent. Δ Another factor which impacts the amount of dissolved lead in tap
water is water

Uranium Exposure
Uranium Exposure and Oxidative Stress
There are many ways for cancer to get in the body, like exposure to uranium and oxidative stress.
[8]. When the mechanisms of the body loose the protein Glutathione it leads to making oxygen free
radical neutral. Two of the most important proteins in the body are glutathione (GSH) and
superoxide dismutase (SOD). Glutathione (GSH) works as an antioxidant [9]. Also, glutathione
(GSH) has an important job that removes toxic metals out of the body because glutathione (GSH)
has a sulphydryl group. This group strongly binds with toxic metals, effectively [3]. When uranium
enters the body, it will reduce glutathione (GSH). When there is a reduction of glutathione (GSH), it
leads to an increase of the ... Show more content on Helpwriting.net ...
Superoxide dismutase has a job of repairing the damage to the cells that the reactive oxygen species
causes. When glutathione decreases in the body, it leads to the increase of reactive oxygen species
and damages the DNA in the body. Also, glutathione (GSH) and superoxide dismutase (SOD) help
the brain to clean and remove the toxicity bypass easily into the brain tissues. Glutathione combines
to toxic metals from the brain and tissues, and then removes it by a pathway through the bile to the
feces, and out of the body. When the amount of glutathione falls, because of exposure to toxic
metals, it leads to loads of toxicity in the kidney. Then, because these toxic metals are very large and
destroy the renal tubule cells, it leads to less excretion and an acid shift of the blood. When
glutathione fails to remove the toxicity of metals from the body, it causes more damage to the
kidney, and the increase of toxicity will increase reactive oxygen species levels. Then, this leads to
the risk of cancer and immune linked illnesses. Porphyria in the urine can show us that the kidneys
have failed to work. In addition, because glutathione has a function that works as an antioxidant and
neutralizes free radicals, this helps

Low Oxalate Diet
What Is a Low Oxalate Diet (And How Can It Heal Your Strange Symptoms?)
Have you found yourself struggling with strange symptoms your doctor can't seem to find a cause
for? Are you beginning to agree with him that the problem might be in your head?
If so, you're not alone. Millions of people are living with hidden autoimmune conditions, allergies,
and food sensitivities that make them miserable but often don't show up on standard medical tests.
By now, I'm sure you've heard of celiac disease, lactose intolerance, and peanut allergies.
But, did you know that there are other food sensitivities just being brought into the mainstream?
Ones you may have not even heard of yet?
These include, but are certainly not limited to, histamine sensitivity, ... Show more content on
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According to research http://kidneystones.uchicago.edu/how–to–eat–a–low–oxalate–diet/
, diets that are low in calcium can raise urine oxalate levels. This is because proper calcium levels
can inhibit intestinal oxalate absorption.
A randomized controlled trial (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1455427/) studied
men with hypercalciuria (elevated calcium in the urine) and placed them on one of two diets to
check which would be the most effective in the prevention of kidney stones (a common symptom of
oxalate sensitivity).
One group followed a diet low in calcium and oxalate. The other followed a diet higher in calcium
with restricted intake of oxalate, protein, and salt.
At the five–year mark, the latter group had a 51 percent lower rate of stone recurrence than those
following a low–calcium diet.
Talk with your doctor about testing you for calcium deficiency and/or hypercalciuria if you're
experiencing symptoms of oxalate sensitivity before following the low oxalate diet.
It could make all the difference in your health.

What Causes Oxalate

Effects Of Rooibos Tea
Rooibos tea is a highly consumed hot beverage by many worldwide for its sweet flavor and great
aroma. The tea is prepared from a South African endemic plant Aspalathin linearis. The escalation of
Rooibos consumption over the years paralleled the rise of consumer concerns of the importance of
food and beverages in prevention of health threats and diseases (Joubert et al., 2013). The study by
Steenkamp and co–workers (2004) demonstrated high radical scavenging ability of superoxide and
hydroxyl of Rooibos extract that superseded that of other commercially available South African
herbal teas which are honey bush tea and roselle scientifically called (cyclopia intermedia)and
(Hibiscus Sabdariffa L.) that are commercially available.
Rooibos tea ... Show more content on Helpwriting.net ...
It brings–about the conversion of the decapeptide Angiotensin I to the potent vasoconstrictor
Angiotensin II causing increases in the blood pressure by narrowing the blood vessels (Zhao and
Xu., 2008). Blood vessels narrow because the Bradykinin which causes the blood vessels to dilate is
being degraded by the ACE in Kenin–Kallikrein System consisting of proteins that form part in
inflammation (Hemming., Selkoe.,

Rat Model Of Depression : Induced By Daily I.p
In the present study, rat model of depression was induced by daily i.p. injection of reserpine for 15
days. This was followed by monitoring the motor activity to check the development of rat model of
depression. Then the depressed rats were treated with cannabis extract to study its effect on this
model. After 15 days of daily reserpine injection a significant decrease in the motor activity was
recorded as assessed by the open field test (OFT). Together with the hunch back appearance that was
observed after 15 days, these behavioral changes indicate the development of rat model of
depression which was maintained by daily i.p. injection for another 15 days. After 30 days of daily
reserpine injections the significant changes in the OFT parameters and hunch back appearance
persisted and were similar to that have been observed after 15 days of resrpine treatment. In addition
to the motor deficits, the present depletion in the cortical and hippocampal monoamine levels
induced by reserpine confirms the development of rat model of depression. Since, the central
deficiencies in serotonin, norepinphrine and/or dopamine have been postulated as the main cause for
the pathogenesis of depression (Schechter et al., 2005) Our results were consistent with the study of
Antkiewicz–Michaluk et al., (2014) who found that the treatment with a low dose of reserpine
induced a distinct depressive–like behavior in the FST, motor impairment, and additionally a
significant decrease in the level of

Selenium: Oxidative Stress In The Body
Brianne Atkins Selenium is an essential trace element found in the body that works in conjunction
with other vitamins to support the powerful detoxification process. When combined with Vitamin E,
Selenium can help prevent oxidative stress from occurring in the body which is crucial in the
prevention of many diseases such as heart disease and cancer. According to Dr. Mandal (2015),
"Oxidative stress is essentially an imbalance between the production of free radicals and the ability
of the body to counteract or detoxify their harmful effects through neutralization by antioxidants."
Selenium goes to work in the body as a powerful antioxidant, and it is required for the production of
Glutathione, which is a key antioxidant in our bodies. Antioxidants are important in keeping the
body healthy by fighting off the free radicals that our cells are exposed to on a daily basis. ... Show
more content on Helpwriting.net ...
Selenium deficiencies have been linked to various illnesses such as depression, a weakened immune
system, and infertility in both men and women. The most selenium rich foods to incorporate into
your daily diet are brazil nuts, seafood such as yellowfin tuna and sardines, grass fed beef, eggs,
spinach, and sunflower seeds. Selenium is not only found in foods though, it can be found in soil as
well. According to Dr. Axe (2016), there have been selenium deficiencies linked to certain regions in
China where the soil has been shown to have very low levels. The RDA for selenium is 55 mcg/day
and the Daily Value is 70 mcg (Axe,

Effects Of Renal Intoxication
Renal injury due to KBrO3 intoxication could be evaluated by assessment of serum urea, creatinine,
and uric acid, which were used as early indicators of renal dysfunction [39].The significant increase
in serum urea, creatinine and uric acid in the KBrO3 –treated rats indicate the development of renal
dysfunction and reduced glomerular filtration rate. The increase in uric acid level also may be due to
degradation of purines and pyrimidines which strongly related to the significant increase in xanthine
oxidase activity resulted in overproduction of uric acid. The increase in xanthine oxidase activity
does not only catalyze the formation of uric acid but also generate ROS. Therefore, the elevated
xanthine oxidase activity could explain the ... Show more content on Helpwriting.net ...
Pro–inflammatory cytokines, including tumor necrosis factor α (TNF–α) and IL–6, are thought to
act as a central factor in the pathophysiology of chronic kidney disorders [43]. Oxidative stress is
also involved in the inflammatory response. ROS can induce inflammatory processes by activation
of transcription factors, which induce secretion of pro–inflammatory cytokines, including TNF–α
and IL–6 [44]. In this study, results illustrated that KBrO3 induced an inflammatory reaction
indicated by increasing renal TNF–α and IL–6 levels . However, treatment with taurine and /or
vanillin prior KBrO3 administration suppressed the overproduction of TNF–α and IL–6 in renal
tissue provided a protective effect against kidney pathological changes. Interestingly, the observed
results show that pretreatment of rats with vanillin also caused the apparent reduction in levels of
proinflammatory cytokines such as interleukin (IL)–1β, IL–6, and tumor necrosis factor–alpha . This
is in accordance with the previous results obtained [45] reported that pre–treatment with vanillin
resulted in a normalization

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