Antioxidant And Anti-Inflammatory Properties Of Lunasin

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
... Get more on HelpWriting.net ...

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 Helpwriting.net ...
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

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 Helpwriting.net ...
"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

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 О± (TNF–О±) 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–О± and IL–6 [44]. In this study, results illustrated that
KBrO3 induced an inflammatory reaction indicated by increasing renal TNF–О± and IL–6 levels . However, treatment with taurine and /or vanillin
prior KBrO3 administration suppressed the overproduction of TNF–О± 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)–1ОІ, 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

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
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 (GieГџing, 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

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 authorпјљProf. 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 (14–16в„ѓ) or control temperature] Г— 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 CОІS protein levels. Therefore, it indicated that
DL–HMTBA supplementation may increase MAT–1A and CОІS 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

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 Helpwriting.net ...
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

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

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

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 (IL1ОІ, NF–ОєB IL6 and TNF–О±) associated with up–regulation of their receptors in the chronic epileptic cerebrum.
Nuclear factor kappa b (NF–ОєB) and tumor necrosis factor–О± (TNF–О±) 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

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 Helpwriting.net ...
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

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 more content on Helpwriting.net ...
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]. IndeedпјЊ 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. P38пЃЎ can regulate antioxidative synthesis by enhancing mTOR
/p70S6K signaling lead to module consequence of the ROS content in the cells. By contrast, cells lacking p38пЃЎ 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 p38О± 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

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 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 Helpwriting.net ...
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

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

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 withgout, 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

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 alsopsychology
(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 content on Helpwriting.net ...
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

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 inhibitscytochrome 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

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) Ојg/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 (52.54В±0.81)% inhibition at concentration of 40 mg/ml, and IC50 value was 30 mg/ml was found the scavenging
activity of (44.92В±0.26)% for ethyl alcohol extract. Acetone extract of leaves was found at of concentration 60 mg/ml scavenging activity of
53.26В±0.34%. The IC50 value of aqueous extract of leaves was (60)Ојg/ml with percentage inhibition of (54.28В±0.28)% followed by
(44.57В±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

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 ... Show more content on Helpwriting.net ...
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

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,

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

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

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

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

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.,

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 Helpwriting.net ...
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 в†’ R–O* + *O–R
R–O* + H2C=CH2в†’ RO–CH2–CH2*
RO–CH2–CH2* + H2C=CH2 в†’ 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

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
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

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

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 Helpwriting.net ...
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. Ж 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. О” Another factor which
impacts the amount of dissolved lead in tap water is water

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 O2В·– 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

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,

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

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

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

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 Helpwriting.net ...
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

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

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

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