This document discusses the metabolism of xenobiotics, or foreign compounds, in the body. It describes how xenobiotics undergo two phase biotransformation reactions, with phase 1 involving oxidation, reduction, and hydrolysis, and phase 2 involving conjugation to make compounds more water soluble for excretion. The liver plays a key role in these metabolic reactions through cytochrome P450 enzymes and conjugation enzymes. The document also discusses how reactive oxygen species are generated and the antioxidant systems that help prevent cellular damage from free radicals.
Xenobiotics are foreign compounds to our body. They are more lipophilic and less hydrophilic . So it is quite tough to excrete them out from the body. Hence metabolism of xenobiotic is important.
A comprehensive presentation on Enzymology :Types of Enzyme inhibition & Therapeutic uses for MBBS ,BDS, B Pharm & Biotechnology students to facilitate self- study.
lutathione (GSH) is an antioxidant in plants, animals, fungi, and some bacteria and archaea.Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals. It is a tripeptide with a gamma peptide linkage between the carboxyl group of the glutamate side chain and cysteine. Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion.
Gluconeogenesis: Defined as biosynthesis of glucose from non-carbohydrate precursors
-Gluconeogenesis: an intro
-Thermodynamic Barriers (Each barrier detail explanation)
- Energetics of gluconeogenesis
-Substrates of gluconeogenesis (each substrate and pathway explained)
-Regulation of Gluconeogenesis, hormonal and transcriptional regulation
Xenobiotics are foreign compounds to our body. They are more lipophilic and less hydrophilic . So it is quite tough to excrete them out from the body. Hence metabolism of xenobiotic is important.
A comprehensive presentation on Enzymology :Types of Enzyme inhibition & Therapeutic uses for MBBS ,BDS, B Pharm & Biotechnology students to facilitate self- study.
lutathione (GSH) is an antioxidant in plants, animals, fungi, and some bacteria and archaea.Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals. It is a tripeptide with a gamma peptide linkage between the carboxyl group of the glutamate side chain and cysteine. Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion.
Gluconeogenesis: Defined as biosynthesis of glucose from non-carbohydrate precursors
-Gluconeogenesis: an intro
-Thermodynamic Barriers (Each barrier detail explanation)
- Energetics of gluconeogenesis
-Substrates of gluconeogenesis (each substrate and pathway explained)
-Regulation of Gluconeogenesis, hormonal and transcriptional regulation
By the end of this lecture, students should:
Explain why drug metabolism is essential
Describe the phases of drug metabolism
Explain the role of cytochrome p 450 enzyme system in drug metabolism
Definition
Chemical reactions which occur in the body to change drugs from nonpolar lipid soluble forms to polar water soluble forms that are easily excreted by the kidney.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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
2. Xenobiotics
A xenobiotic (Gk xenos "stranger") is a
compound that is foreign to the body.
Xenobiotics can produce a variety of biological
effects including-
Pharmacological responses
Toxicity
Immunological responses
Cancers
3.
4. Biotransformation Reactions
A process whereby a substance is changed from
one chemical to another chemical by a chemical
reaction within the body.
Consequences
o Changes in solubility characteristics
o Detoxification
o Metabolic activation
6. Detoxification Reactions
Biochemical reactions involved in the conversion of
foreign, toxic and water insoluble molecules to non toxic,
water soluble and excretable forms are called
Detoxification reactions
Purpose
o Converts lipophilic to hydrophilic compounds
o Facilitates excretion
7. Metabolism of Xenobiotics
Two phase of metabolism
Phase 1 Phase 2
Compounds produced in
phase 1 or are converted
by specific enzymes to
various polar metabolites
by conjugation.
They become more water
soluble and easily
excretable.
Alteration of xenobiotic
molecule so as to add a
functional group, which can
be conjugated in phase 2.
10. Role of Liver
Main organ involved
Hepatocytes contain wide variety of enzymes to process
xenobiotics
Enzymes are present in endoplasmic reticulum and to
lesser extent in other organelles
Each enzyme represents a large family of gene product
Each gene product may be induced by different
xenobiotics
11. Phase 1 reactions
Phase I reactions include:
Oxidation
Reduction
Hydrolysis reactions
They are also called Hydroxylation reactions since
they introduce or expose a functional group (e.g., -OH)
that serves as the active center for sequential
conjugation in a phase II reaction.
12. Oxidation
Oxidation of Alcohols- Primary aliphatic and aromatic alcohols are
oxidized to corresponding acids
Methanol Formaldehyde Formic acid
Ethanol Acetaldehyde Acetic acid
Benzoyal Alcohol Benzaldehyde Benzoic acid
16. Phase 1 reactions- Enzymes
Mainly Catalyzed by a class of enzymes referred to
as Monooxygenases, Mixed Function oxidases or
Cytochrome P450s.
Other enzymes of significance are-
o Aldehyde and alcohol dehydrogenase
o Deaminases
o Esterases
o Amidases
o Epoxide hydrolases
18. Properties of Human Cytochrome P450s
o Involved in phase I of the metabolism of innumerable
xenobiotics.
o Involved in the metabolism of many endogenous
compounds.
o They catalyze reactions involving introduction of one atom
of oxygen into the substrate and one into water
o All are haemoproteins.
o Exhibit broad substrate specificity, thus act on many
compounds.
o Extremely versatile catalysts, perhaps catalyze about 60
types of reactions.
19. o Liver contains highest amounts, but found in most if not
all tissues, including small intestine, brain, and lung.
o Located in the smooth endoplasmic reticulum.
o In some cases, their products are mutagenic or
carcinogenic.
o Many have a molecular mass of about 55 kDa.
o Many are inducible, resulting in one cause of drug
interactions.
o Many are inhibited by various drugs or their metabolic
products, providing another cause of drug interactions.
o Some exhibit genetic polymorphisms, which can result
in atypical drug metabolism.
20. Phase 2 - Conjugation
o These reactions involve covalent attachment of small
polar endogenous molecule such as glucuronic acid,
sulfate, or glycine to form water-soluble compounds.
o Conjugation reactions can occur independently or can
follow phase 1(hydroxylation) reactions.
o Conjugation takes place primarily in liver but can occur in
kidney also.
o After conjugation the products are generally rendered
non toxic but in certain conditions they are left unchanged
or become more toxic.
23. o Glucuronidation is the most frequent conjugation reaction.
o UDP-glucuronic acid , is the Glucuronyl donor, which is
formed in the Uronic acid pathway of Glucose metabolism
o Glucuronyl Transferases, present in both the endoplasmic
reticulum and cytosol, are the catalysts.
o The glucuronide may be attached to oxygen, nitrogen, or
sulfur groups of the substrates.
Glucuronidation
24.
25. Sulfation
o The sulfate donor is adenosine 3'-phosphate-5'-
phosphosulfate (PAPS) this compound is called
"active sulfate“
o The enzyme is sulfo transferase
o Compounds which are conjugated with sulphate are
as follows-
• Phenols
• Cresols
• Indole
• Steroids
26. Acetylation
o Acetylation is represented by
where X represents a xenobiotic.
o Acetyl-CoA (active acetate) is the acetyl donor.
o These reactions are catalyzed by acetyltransferases
o Polymorphic types of acetyltransferases exist, resulting
in individuals who are classified as slow or fast
acetylators, and influence the rate of clearance of drugs
from blood.
o Slow acetylators are more subject to certain toxic effects
of drug because the drug persists longer in these
28. Conjugation with Amino acids
Conjugation with Glutamine
Phenyl Acetic acid + Glutamine
Phenyl Acetyl Glutamine
This reaction is important in patients of Phenyl ketonuria,
since excess of Phenyl acetyl glutamine is excreted in
urine, that imparts a mousy odor to the urine.
31. Phase III – further modification and
excretion
o Conjugates and their metabolites can be excreted from
cells in phase III of their metabolism.
o A common example is the processing of glutathione
conjugates to acetylcysteine (mercapturic acid)
conjugates.
32. Factors affecting Biotransformation of drugs
o Prior administration of the drug or Co
administration of other drugs
o Diet
o Hormonal status
o Genetics
o Disease (e.g., decreased in cardiac and
pulmonary disease)
o Age and developmental status
o Functional status of Liver and Kidney
36. A free radical is a molecule or molecular fragment that
contains one or more unpaired electrons in its outer orbit.
Represented by a superscript dot, (R•).
37. ROS: Reactive Oxygen Species
o Oxidation reactions ensure that molecular oxygen is
completely reduced to water. The products of partial
reduction of oxygen are highly reactive, called Reactive
oxygen species or ROS
38. o Superoxide anion radical (O2 -•)
o Hydroperoxyl radical (HOO•)
o Hydrogen peroxide (H2O2)
o Hydroxyl radical (OH•)
o Lipid peroxide radical (ROO•)
o Singlet oxygen ( 1O2)
o Nitric oxide (NO•)
o Peroxy nitrite (ONOO-•).
39. Characteristics of ROS
o Extreme reactivity.
o Short life span.
o Generation of new ROS by chain reaction.
o Damage to various tissues.
40. Generation of Free Radicals
Cellular Metabolism
o Leakage of electrons from ETC
o Due to membrane lipid peroxidation
o Peroxisomal generation-oxidation of O2 & H2O2
o During prostaglandin synthesis
o Production of nitric oxide from arginine
o During phagocytosis
o In the oxidation of heme to bile pigments
o Auto-oxidation (e.g. metal ions, Fe2+, Cu2+ glutathione, ascorbic acid)
41. Environmental Sources
o Result of drug metabolism, Cytochrome P450 related reactions.
o Due to damage caused by ionizing radiations on tissues (X-rays)
o Photolysis of O2 by light
o Photo excitation of organic molecules
o Cigarette smoke
o Alcohol promotes lipid peroxidation.
44. ROS a RNS
Modification of aa,
fragmentation and
aggregation of proteins
Lipid peroxidation DNA damage
Membrane damage
Loss of membrane
integrity
Damage to Ca2+
and other
ion transport systems
Inability to maintain
normal ion gradients
Activation/deactivation of
various enzymes
Altered gene
expression
Depletion of ATP
Lipids Proteins DNA
Cell injury/
Cell death
Damage by ROS/RNS
45.
46. o Chronic inflammation
o Atherosclerosis
o Cardiac diseases
o Cataract
o Respiratory diseases
o Cancer
o Ageing
48. Antioxidants (Scavenger system)
o According to nature and action (enzymatic or non
enzymatic)
o According to location
o In relation to lipid peroxidation
49.
50.
51. o Non-enzymatic antioxidants:
o Nutrient: carotenoids, α-tocopherol ( vit E), selenium &
vitamin C, glutathione, ceruloplasmin
52. Antioxidants in relation to lipid peroxidation:
o Preventive antioxidants that will block the initial
production of free radicals e.g. catalase, glutathione
peroxidase.
o Chain breaking antioxidants that inhibit the
propagative phase of lipid peroxidation e.g.
Superoxide dismutase, vitamin E.
53. According to location:
o Plasma antioxidants: e.g. β-carotene, ascorbic acid,
ceruloplasmin, transferrin.
o Cell membrane antioxidants: e.g. α-tocopherol.
o Intracellular antioxidants: e.g. SOD, catalase, glutathione
peroxidase.