This document discusses reactive oxygen species (ROS) and antioxidants in biology and medicine. It defines key terms and explores the origins and effects of different ROS like superoxide, nitric oxide, and hydroxyl radicals. It also examines the mechanisms of tissue damage caused by ROS and the roles of antioxidant defense systems in preventing damage. Biomarkers of oxidative stress and lipid, DNA, and protein damage are reviewed. Evidence suggests ROS contribute to periodontal tissue destruction in periodontitis through lipid peroxidation and oxidative damage.
in this presentation, the light is focused on discussing the Reactive oxygen species, oxidative stress, how it forms, how it affects the body and what are the diseases that correlate with oxidative stress.
nevertheless, how it can be balanced by the antioxidants and what is their role in oxidative stress.
in this presentation, the light is focused on discussing the Reactive oxygen species, oxidative stress, how it forms, how it affects the body and what are the diseases that correlate with oxidative stress.
nevertheless, how it can be balanced by the antioxidants and what is their role in oxidative stress.
During favorable conditions, the level of reactive spices in the cell is limited to what is required for normal cellular activities. They act as important components of signaling pathways. Plants control some important processes such as defense, hormonal signaling and development by using them as signaling molecules. And An equilibrium is steblished between antioxidant system and ros formation. But when plant feels an external stress like, drought,cold, salt etc. the level of reactive specease increases above the basal level a situation that we call oxidative stress. These reactive molecules during oxidative stress, they react with biomolecules like as carbohydrates, unsaturated lipids, proteins, nucleic acids. Proteins are the most abundant cellular targets of the oxidative species, more than DNA and lipids, making up 68% of the oxidized molecules in the cell. Ros reacts with proteins which results in protein modification called redox PTMs.
Just regarded to those who trying to learn somethings.. . thanks to those who read this slide... Just pray for me , for my parents and for my teachers...
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
During favorable conditions, the level of reactive spices in the cell is limited to what is required for normal cellular activities. They act as important components of signaling pathways. Plants control some important processes such as defense, hormonal signaling and development by using them as signaling molecules. And An equilibrium is steblished between antioxidant system and ros formation. But when plant feels an external stress like, drought,cold, salt etc. the level of reactive specease increases above the basal level a situation that we call oxidative stress. These reactive molecules during oxidative stress, they react with biomolecules like as carbohydrates, unsaturated lipids, proteins, nucleic acids. Proteins are the most abundant cellular targets of the oxidative species, more than DNA and lipids, making up 68% of the oxidized molecules in the cell. Ros reacts with proteins which results in protein modification called redox PTMs.
Just regarded to those who trying to learn somethings.. . thanks to those who read this slide... Just pray for me , for my parents and for my teachers...
Oxidative Stress in Aging and Human Diseases - Exploring the MechanismsQIAGEN
Many modern diseases, including cancer, cardiovascular disease, diabetes, liver disease, arthritis and neurodegenerative disease are related to aging, and aging is closely linked to oxidative stress. Intensive research is being conducted to understand the antioxidant defense mechanism, the mechanisms of aging itself, as well as their roles in human diseases. This slidedeck provides an update on how oxidative stress is linked to aging and how inflammation leads to aging through DNA damage, telomere dysfunction, cellular senescence and oxidative stress. Recent progress on the health benefits of antioxidants and examination of their potential mechanisms in the prevention and treatment of chronic diseases are also covered. Various assay technologies to tackle the complex signaling pathways in this process will be introduced. Learn how you can apply these advanced tools to your research!
role of free radicals in human diseases. Inside the human cells, there is an effective antioxidant defence system to counter damaging actions of reactive oxygen species. ... Direct damage to structural proteins and DNA inside the cells may result in loss of cell architecture and lack of its ability to restore.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Surgical Site Infections, pathophysiology, and prevention.pptx
Reactive oxygen species
1.
2. Introduction
Definitions
Reactive oxygen and antioxidant species in biology and medicine
Atomic and molecular oxygen – basic principles
Origin and formation of ROS and oxygen radicals
Superoxide and nitric oxide
Hydrogen peroxide
The hydroxyl radical
Mechanisms of tissue damage
Protein damage
Lipid peroxidation
DNA damage
Antioxidant defense systems
Classification of antioxidants
Ascorbic acid (vitamin C)
α-Tocopherol (vitamin E)
Carotenoids
Co-enzyme Q10
Uric acid
Polyphenols
Glutathione
3. • Pathophysiology of periodontal destruction caused by ROS
• Measuring ROS and oxidative stress/ damage in biological samples
Biomarkers of lipid peroxidation
Biomarkers of DNA damage
Biomarkers of protein damage
• Evidence for the presence and role of ROS in periodontal tissue damage
• Conclusion
4. Introduction
The majority of periodontal tissue destruction is caused by an
inappropriate host response to those microorganisms and their
products.
More specifically, a loss of homeostatic balance between
• Proteolytic enzymes & their inhibitors
• Reactive oxygen species (ROS) and the antioxidant
defense systems
• pro inflammatory and anti inflammatory cytokines
5. ROS are produced in animals and humans under various physiological and
pathological conditions
They act in phagosomes as agents toxic to micro-organisms, fungi, parasites,
and neoplasmic cells
While most ROS have extremely short life they can cause substantial
damage to tissue and cellular components, e.g., cellular phospholipid,
nucleic acid, protein, carbohydrate, and enzymes
6. Definitions
Free radicals Any species capable of independent
existence that contain one or more
unpaired electrons.
Antioxidants Those substances which when present at
low concentrations, compared to those of
an oxidizable substrate, will significantly
delay or inhibit oxidation of that substrate
by radical. Halliwell B, Gutteridge JM 1992
Halliwell B.,1991
7. Oxidative stress A disturbance in the pro-oxidant–
antioxidant balance in favor of the former,
leading to potential damage., Sies H 1991
Redox potential Is a measure (in volts) of the affinity of a
substance for electrons, relative to
hydrogen. Ower PC, Ciantar M et al 1997
17. Superoxide establishes a pro-inflammatory state in a variety of ways, such as
triggering nuclear factor-kB transcription of pro-inflammatory cytokines
18. Nitric oxide formation
Nitric oxide is synthesized from L-arginine by a family of enzymes called
nitric oxide synthases.
There are three forms:
• type 1 nitric oxide synthase – brain enzyme (bNOS);
• type 2 nitric oxide synthase – inducible enzyme (iNOS),
found in macrophages;
• type 3 nitric oxide synthase – endothelial cell enzyme
(eNOS).
Endothelial cell nitric oxide synthase causes smooth muscle relaxation within
blood vessels
19. Macrophage-derived inducible nitric oxide synthase is of interest when
released simultaneously with superoxide it forms the reactive nitrogen
species peroxynitrite anion
NO. + O2- = ONOO-
While peroxynitrite is not a true radical it is now believed to be responsible for
many of the cytotoxic effects
20. Activities include
• Lipid peroxidation;
• Glutathione depletion by oxidation;
• Nitrotyrosine formation which may inhibit superoxide dismutase
activity
• DNA damage by nitrosilation, deamination and oxidation;
• High concentrations cause rapid cellular necrosis
• Low concentrations cause apoptosis
21. Hydrogen peroxide
• Hydrogen peroxide is a weak ROS, the potential of which to cause
tissue damage is limited to its interaction with transition metal ions
undergo “Fenton reaction” in the presence of Fe2+or Cu2+ ions, forming the
most potent of all oxygen radicals, the hydroxyl radical (•OH).
Fe+2 + H2O2 ----------> Fe+3 + °OH + -OH
The dismutation of hydrogen peroxide also gives rise to the ROS called
singlet oxygen ( 'O2 )
Removal of singlet oxygen is achieved by carotenoid pigments, which
will absorb the energy of singlet oxygen and release heat
22. • Increase adhesion molecule expression
• Cause cell proliferation
• Induce apoptosis
• Modulate platelet aggregation.
• Unless concentrations exceed 50μM the cytotoxicity of hydrogen
peroxide is limited and its biological significance is more as a cell
signaling molecule.
23. The principal enzymes charged with removal of hydrogen peroxide are the
antioxidant enzymes catalase, which predominantly acts intracellularly
Glutathione peroxidase, which operates within mitochondria and
extracellularly, thioredoxin-linked peroxidases.
Hydrogen peroxide is also ingested at high concentrations in tea and coffee
and is thought to diffuse into oral mucosal cells
It is also produced by oral bacteria and salivary hydrogen peroxide is used
by the salivary peroxidase system to oxidize thiocyanate into antimicrobial
products.
24. Hydroxyl radical
The hydroxyl (•OH) radical and the related perhydroxyl radical (HO2-) are
the most potent species known to cause damage and destruction to an
array of cellular and tissue components. Specifically, damage may affect
cellular and extracellular targets.
Cellular targets
• lipids
• carbohydrates
• protein damage
• DNA– damage
• oxidation of anti-proteases
• low molecular weight species
Extracellular targets
Extracellular matrix component like collagens and structural proteins
31. The preventative antioxidants function by enzymatic removal of superoxide
and hydrogen peroxide or by sequestration of divalent metal ions, preventing
Fenton reactions and subsequent hydroxyl radical formation
Lactoferrin is probably more important than transferrin within the periodontal
tissues, given the dominance of the neutrophil infiltrate and the recognition of
high levels of lactoferrin within gingival crevicular fluid.
The chain-breaking antioxidants are the most important within extracellular
fluids
Low molecular weight species donate electrons before becoming oxidized,
requiring subsequent reduction or replacement to maintain the body’s
antioxidant capacity
32. The lipid soluble antioxidants (a-tocopherol and the carotenoids) act at the
cell membrane level and protect against lipid peroxidation, whereas the
water-soluble scavengers are more important within the extracellular tissue
fluids.
However, several antioxidants have dual and sometimes triple actions.
ascorbateEg:
The efficacy of an antioxidant depends upon:
• its location (intra- vs. extracellular or cell membrane bound);
• the nature of the ROS-challenge;
• other antioxidant species important in co-operative
interactions.
• other environmental conditions (e.g. pH, oxygen tension).
34. General functions of anti oxidants
• Scavenging water-soluble peroxyl radicals;
• Scavenging superoxide and perhydroxyl radicals;
• Prevention of damage mediated by hydroxyl radicals on uric acid;
• Scavenger of hypochlorous acid;
• Decreases heme breakdown and subsequent Fe2+ Release thereby
preventing Fenton reactions;
• Scavenger of singlet oxygen and hydroxyl radicals;
• Re-forms a-tocopherol from its radical;
• Protects against ROS-release from cigarette smoke.
35. Ascorbic acid (vitamin C)
Vitamin C is an essential nutrient and plasma levels are approximately 30–
60μM but reduced in smokers
Gingival crevicular fluid levels are reported to be three-fold higher than
plasma levels
Vitamin C is an essential nutrient with a recommended daily intake of 40–60
mg
36. Ascorbate is converted by radical attack to the ascorbyl radical, which then
breaks down to dehydroascorbate
Dehydroascorbate can be converted back to ascorbate directly by reduced
GSH or by the NAD-semi-dehydroascorbate reductase enzyme system, which
also utilizes GSH.
These systems are intracellular and thus ascorbate within the extracellular
fluids is rapidly depleted (oxidized) in conditions of oxidative stress unless
adequate GSH levels are present
37. α-Tocopherol (vitamin E)
Vitamin E is generally regarded as the most important and effective lipid-
soluble antioxidant in vivo, vital to maintaining cell membrane integrity
against lipid peroxidation
Its antioxidant behavior is the result of a single phenolic OH group, which
when oxidized gives rise to the vitamin E (tocopheryl) radical
Reduced form of co-enzyme Q10 (ubiquinol) in the lipid environment and
ascorbic acid in the aqueous phase will reconstruct vitamin E.
38. Carotenoids
Carotenoids are tetraterpines with over 600 variants., some are.
• lycopene;
• a-carotene;
• b-carotene;
• lutein;
• cryptoxanthine;
• retinol (vitamin A1);
• dehydroretinol (vitamin A2)
Derived only from the diet (green vegetables, tomatoes, fruits), lycopene
predominates in plasma
Like many other extracellular antioxidants, b carotene levels and intake
are reduced in smokers, whereas others such as lycopene appear
unaffected by smoking
β-carotene is efficient at scavenging singlet oxygen (1O2) and other
carotenoid antioxidant activities include the scavenging of peroxyl radicals
39. Co-enzyme Q10 exists in an oxidized form (ubiquinone or CoQ) and a reduced
form (ubiquinol or CoQH2), both of which possess antioxidant activity
Co-enzyme Q10
co-enzyme Q10 deficiency has been demonstrated in the gingival tissues of
periodontitis subjects
Hansen IL, Iwamoto Y, Kishi T, Folkers K, Thompson LE.
Bioenergetics in clinical medicine. IX. Gingival and leucocytic deficiencies of
coenzyme Q10 in patients with periodontal disease.Res Commun Chem Pathol
Pharmacol1976:14: 729–738
Exact mechanism is not known
40. Uric acid
Normally uric acid is oxidized to allantoin enzymatically or by hydroxyl radicals
but the enzymatic route does not occur in humans, therefore allantoin
formation is used as a marker of urate oxidation by ROS (measured as
allantoin:urate ratio)
Polyphenols
Battino et al. proposed that the polyphenolic flavenoids are absorbed following
dietary intake of, in particular, vegetables, red wine, and tea are helpful in
inflammatory diseases.
No current data regarding exact mechanism.
41. Glutathione (GSH)
Glutathione is a non-essential tri-peptide. it can be synthesized within the
cell; however, its constituent amino acids are “essential” and obtained
through the diet.
It is essential to the glutathione peroxidase antioxidant enzyme system,
which removes hydrogen peroxide by converting two GSH molecules to
one GSSG molecule and water
Is one of the most vital intracellular antioxidant scavengers
It is important to the preservation and restoration of other antioxidant
species, e.g. vitamin C and vitamin E
42. Biomarkers
The tissue destruction can be assessed by measuring the levels of markers
for lipid peroxidation, protein damage, DNA damage, and
anti-oxidants
Biomarkers of lipid peroxidation
• Conjugated dienes,
• Thiobarbituric acid reactive substances (notably MDA),
• Isoprostanes,
• Ethane/pentane,
• Other volatile hydrocarbons
44. Biomarker for protein damage
• The carbonyl assay measures protein carbonyl (PC) groups
• PC has a major advantage over lipid peroxidation product as the marker
of oxidation stress as Oxidized proteins are more stable
• PC forms early and circulates in blood for longer period
• But carbonyls are not specific biomarkers of ROS damage
• Acrolein • Protein-bound aldehyde that has been widely
used to measure oxidative damage
45. Biomarkers of DNA damage
• Products of hydroxyl radical attack on DNA bases (purines) and pyrimidines)
and carbohydrate moieties (deoxyribose)
• can be measured by various methods (high-
pressure liquid chromatography: Gas or liquid),
liquid chromatography or antibody methods
• No individual reaction product should be used as
the sole index of DNA damage
• But despite this, 8-hydroxydeoxyguanosine is
frequently used as a biomarker for DNA damage.
48. Evidence for the presence and role of ROS in periodontal tissue damage
The majority of tissue destruction in periodontitis is considered to be the result of an
aberrant inflammatory/immune response to microbial plaque adjacent to the
gingival margin and to involve prolonged release of neutrophil enzymes and ROS.
Most published work in the periodontal literature has focused on markers of ROS
reactions with lipids.
Till date, only thiobarbituric acid reactive substances and MDA have been
investigated in chronic periodontitis
All the published studies have suggested that patients with chronic periodontitis
have higher levels of lipid peroxidation than periodontally healthy controls.
49. The GCF concentrations of MDA/4-hydroxyalkanal were 200-to-400-fold
higher than the respective saliva concentrations in patients with chronic
periodontitis, which reflected a substantially higher amount of ROS activity
(thus lipid peroxidation) in GCF than saliva, but total anti-oxidant capacity
was comparable in GCF than saliva
Akalin FA, Baltacioğlu E, Alver A, Karabulut E. Lipid peroxidation levels and total oxidant
status in serum, saliva and gingival crevicular fluid in patients with chronic periodontitis. J
Clin Periodontol 2007;34:558-65
50. Wei et al. measured the lipid peroxidation levels, total oxidant status, and
superoxide dismutase in serum, saliva, and GCF in chronic periodontitis
patients before and after periodontal therapy.
Found that the levels of total oxidative status (TOS) and super oxide
dismutase (SOD) values were significantly higher in the chronic
periodontitis group than in the healthy control group (P < 0.05)
Post-periodontal therapy, serum, saliva, and GCF ,TOS and SOD levels
significantly decreased compared to basal levels (P < 0.05),
Wei D, Zhang XL, Wang YZ, Yang CX, Chen G. Lipid peroxidation levels, total oxidant
status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic
periodontitis patients before and after periodontal therapy. Aust Dent J
2010;55:70-8.
51. In a recent study, Diacron-reactive oxygen metabolites (D-ROM),
anti-oxidant potential, C-reactive protein (CRP), interleukin-6,
and lipid profiles were determined with high-sensitivity
assays in serum.
Patients with severe periodontitis exhibited higher D-ROM levels and lower
total anti-oxidant capacity compared with healthy control individual and D-
ROM levels were positively correlated with CRP.
D’Aiuto F, Nibali L, Parkar M, Patel K, Suvan J, Donos N. Oxidative stress, systemic
inflammation, and severe periodontitis.
J Dent Res 2010;89:1241-6
52. The majority of published data on oxidative damage to DNA has been
reported by a Japanese group who investigated 8 hydroxydeoxyguanosine
levels in saliva by enzyme-linked immunosorbent-assay.
These studies demonstrated that levels of 8-hydroxydeoxyguanosine in
samples from subjects with chronic periodontitis were significantly higher
than those from periodontally healthy controls
Takane M, Sugano N, Iwasaki H, Iwano Y, Shimizu N, Ito K. New biomarker evidence of
oxidative DNA damage in whole saliva from clinically healthy and periodontally diseased
individuals.
J Periodontol 2002;73:551-4
53. Factors to account for when contemplating antioxidant
approaches to therapy
• There should be evidence of excess ROS production associated with the
presence of disease (ideally locally to the diseased tissues)
• There should be evidence of ROS-mediated tissue damage either by:
• (a) Direct effects of ROS activity (biomarkers) measured locally;
• (b) Indirect effects of ROS activity via hyperinflammation as a result of local
redoxsensitive transcription factor activity and subsequent imbalances of
pro- and antiinflammatory cytokine behavior
• There should be clear mechanistic links between oxidative stress, the observed
tissue damage and the mode of activity of the candidate antioxidant;
• Supplementation with the antioxidant should reduce the incidence of disease at
the affected site or tissues;
54. • Supplementation with the antioxidant should reduce disease recurrence;
• Subjects with the disease should have a demonstrable local deficiency of
the antioxidant, or of total antioxidant capacity
• Subjects without disease should have no antioxidant deficiency
• Restoration of the antioxidant level locally should improve clinical
measures of disease
• Adjunctive use of the antioxidant with traditional therapies should provide
improved treatment outcomes over non-surgical therapy alone;
• Markers of local ROS activity should decrease with antioxidant therapy.
55. CONCLUSION
Oxidative stress lays at the heart of the periodontal tissue damage that results
from host–microbial interactions, either as a direct result of excess ROS
activity/antioxidant deficiency or indirectly as a result of the activation of
redox-sensitive transcription factors and the creation of a pro-inflammatory
state
It is now evident that significant relations are present between
oxidant status and periodontal status
But it is still not clear whether this event is the cause or a result of
periodontitis
56. As we know Smoking, infection, UV light, high temperature, etc., play an
important role in generation of free radicals, so one should avoid exposure
to these agents.
Consumption of nutrients with anti-oxidant ability like Vitamin-C and E, β-
carotene, selenium, and manganese should be encouraged, as they help
in fighting oxidative insults to the periodontal tissue.
Adjunctive use of anti-oxidants with traditional therapies should be
considered to improve treatment outcome of various surgical and non-
surgical periodontal therapies
So…..
57. References
• The role of reactive oxygen and antioxidant species in periodontal tissue
destruction., Periodontology 2000, Vol. 43, 2007, 160–232
• Reactiveoxygenspeciesand antioxidantsininflammatory diseases.,
JClinfenodontcil1997;24:2S7-296
• Oxidative injury and inflammatory periodontal diseases: the challenge of anti-
oxidants to free radicals and reactive oxygen species, t Rev Oral Biol Med,
10(4):458-476 (1999)
• Butyrate induces reactive oxygen species production and affects cell cycle
progression in human gingival fibroblasts, J Periodont Res 2013; 48: 66–73
• Reactive oxygen species in periodontitis., Journal of Indian Society of
Periodontology- Vol 17, Issue 4, Jul-Aug 2013
• Relationship Between Periodontal Condition and Plasma Reactive Oxygen
Metabolites in Patients in the Maintenance Phase of Periodontal Treatment, J
Periodontol 2008;79:2136-2142.
• Short-Term Effects of Non-Surgical Periodontal Treatment on Plasma Level of
Reactive Oxygen Metabolites in Patients With Chronic Periodontitis., J
Periodontol 2009;80:901-906.