Oxidative Stress: Its Impact on Human Health and Disease Onset examines all factors known to elevate oxidative stress (OS) and the mechanism of OS disease causation. Sections cover the causes and prevention of oxidative stress, the types of chemical exposures and environmental factors that precipitate disease, disease hallmarks and biomarkers, disease clusters, disease co-morbidities, free radical attacks at the cellular level, and the Oxidative Stress Index tool, its premise, and how it can be used to identify the primary causes of specific diseases and predict the likelihood of disease onset.
With comprehensive coverage of not only the impact of OS due to chemical exposure but also the consequences of environmental factors, this book is a valuable resource for researchers and scientists in toxicology and environmental science, health practitioners, public health professionals, and others who wish to broaden their knowledge on this topic.
Author(s): Harold Zeliger
Publisher: Academic Press
Year: 2022
Language: English
Pages: 499
City: London
Front Cover
OXIDATIVE STRESS
OXIDATIVE STRESS: ITS MECHANISMS AND IMPACTS ON HUMAN HEALTH AND DISEASE ONSET
Copyright
Dedication
Contents
Preface
I - Oxidative stress and disease
1 - Introduction
1.1 Oxidative stress
1.2 Oxidative stress measuremnt
1.3 Major book topics
References
2 - Chemicals and chemical mixtures
2.1 Historical perspective
2.2 Chemical characteristics–octanol: water partition coefficients
2.3 Lipophilic organic chemicals
2.4 Hydrophilic organic compounds
2.5 Metals
2.6 Nonmetallic inorganic chemicals
2.7 Chemical mixtures
2.8 Traditional toxicology
2.8.1 Toxicological data
2.8.2 Chemical impact
2.9 Chemical mixtures
2.9.1 Additivity
2.9.2 Antagonism
2.9.3 Potentiation
2.9.4 Synergism
2.10 Unanticipated effects of mixtures
2.11 Lipophile–hydrophile mixtures
2.12 Lipophile–lipophile mixtures
2.13 Sequential absorption
2.14 Diseases caused by chemicals
2.15 Chemically caused disease and oxidative stress
References
3 - Particles and fibers
3.1 Introduction
3.2 Particle and fiber sources and content
3.3 Oxidative stress (OS)
3.3.1 Crystalline silica (CS)
3.3.2 Asbestos
3.3.3 Heavy metals
3.3.4 Radionuclides
3.3.5 Fly ash
3.3.6 Plastics
3.4 Dust
References
4 - Air pollution and oxidative stress
4.1 Introduction
4.2 Ambient air pollutants
4.3 Confined air pollutants
4.4 Air pollution and oxidative stress
References
5 - Water and soil pollution
5.1 Introduction
5.2 Water polluting chemicals
5.2.1 Priority pollutants
5.2.2 Agricultural chemicals
5.2.3 Urban runoff
5.2.4 Industrial chemicals
5.3 Chemical reactions in groundwater
5.4 Disinfection bye-products
5.5 Soil pollution
5.6 Plant absorption of soil toxins and bioacculation
5.7 Effects of mixtures
5.8 Oxidative stress from polluted water and soil
References
6 - Alcohol
6.1 Introduction
6.2 Effect of alcohol on nutrients and pharmaceuticals
6.3 Effect of alcohol on toxicities of other chemicals
6.4 Alcohol metabolism
6.5 Alcohol and oxidative stress
References
7 - Tobacco
7.1 Tobacco toxicity: introduction
7.2 Tobacco and cancer
7.3 Tobacco smoke and disease rate synergism
7.3.1 Lung cancer
7.3.2 Noncarcinogenic synergism
7.4 Tobacco and oxidative stress
7.5 Electronic cigarettes
References
8 - Electromagnetic radiation
8.1 Introduction
8.2 The electromagnetic spectrum
8.3 Ionizing radiation
8.4 Ionizing radiation and chemical mixtures
8.5 Ultraviolet radiation
8.6 Ultraviolet radiation and toxic chemical mixtures
8.7 Nonionizing radiation
8.7.1 RF radiation and chemical mixtures
8.7.2 ELF radiation and chemical mixtures
8.8 Visible light radiation
8.9 Radiation and oxidative stress
References
9 - Inflammation
9.1 Introduction
9.2 Acute inflammation
9.3 Chronic inflammation
9.3.1 Persistent infection
9.3.2 Chronic non-infectious diseases
9.3.3 Cancer
9.3.4 Aging
9.3.5 Non-healing wounds
9.3.6 Chronic trauma
9.4 Inflammation and oxidative stress
References
10 - Food
10.1 Introduction
10.2 Uptake from soil and plant surfaces
10.3 Animal ingestion
10.4 Persistent organic pollutants (POPs)
10.5 Mercury in food
10.6 Food preparation. Deliberate incorporation of additive chemicals into food
10.7 Chemical impurities in food - allowable xenobiotics
10.8 Allowable chemical impurities in food
10.9 Artificial colors
10.10 Flavor enhancers
10.11 Esthetic and storage additives
10.12 Volatile organic compounds (VOCs) in food
10.13 Chemicals in food packaging
10.14 Irradiated food
10.15 Chemical preservatives in food
10.16 Food chemicals and oxidative stress
10.17 Dietary choices and oxidative stress
10.17.1 Carbohydrates
10.17.2 Animal protein
10.17.3 Nitrates, nitrites and nitrosamines
10.17.4 Fats
10.17.5 Salt
References
11 - Sleep deprivation
11.1 Introduction
11.2 Temperature extremes
11.3 Sleep apnea
11.4 Circadian cycle interruption
11.5 Prevalent health conditions and lifestyle choices
11.6 Sleep deprivation and oxidative stress
References
12 - Pharmaceuticals
12.1 Introduction
12.2 Pharmaceutical use
12.3 Pharmaceutical adverse drug reactions
12.3.1 ADR effects
12.4 Excipients in pharmaceuticals
12.5 Pharmaceuticals and oxidative stress
References
13 - Psychological stress
13.1 Introduction
13.1.1 Glossary
13.2 Chronic stress and disease
13.3 Psychological stress and oxidative stress
References
14 - Genetics and epigenetics
14.1 Introduction
14.2 Genetics
14.3 Epigenetics
14.4 Chemical environmental and other factors in epigenetic effects
14.5 Role of oxidative stress in genetic and epigenetic effects
References
15 - Aging
15.1 Introduction
15.2 Clinical conditions associated with aging
15.3 Lowering age of disease onset
15.4 Age-related disease and oxidative stress
15.4.1 Cardiovascular disease
15.4.2 Neurodegenerative disease
15.4.3 Psychological stress
15.4.4 Type 2 diabetes
15.4.5 Immune system impact
15.4.6 Cancer
15.5 Hallmarks of aging
15.5.1 Genomic instability
15.5.2 Telomere attrition
15.5.3 Epigenetic alterations
15.5.4 Loss of proteostasis
15.5.5 Deregulated nutrient sensing
15.5.6 Mitochondrial dysfunction
15.5.7 Cellular senescence
15.5.8 Stem cell exhaustion
15.5.9 Altered cellular communication (ACC)
15.6 Summary
References
16 - Diseases and comorbidities
16.1 Introduction
16.2 Systems, organs, oxidative stress and disease
16.3 Diseases associated with oxidative stress
16.4 Multimorbidity
16.5 Conclusion
References
17 - Total oxidative stress and disease
17.1 Introduction
17.2 Diseases and oxidative stress
17.3 Malondialdehyde as an indicator of oxidative stress
17.4 Oxidative stress additivity - infectious disease
17.5 Multimorbidity
17.6 Disease prevention strategies
17.7 Obesity
17.8 Limits to oxidative stress-mediated disease prevention
17.9 Disease onset prediction
17.10 Conclusions
References
18 - Free radicals
18.1 Introduction
18.2 Free radical stability
18.3 The Fenton reaction
18.4 Free radical reactions with DNA
18.5 Free radical reactions with proteins
18.6 Free radical reactions with lipids
18.7 Free radical signaling
18.8 Diseases associated with free radicals
18.9 Antioxidants
18.10 Immune system and free radicals
18.10.1 Exogenous immunocompromising agents
18.10.2 Endogenous immune system free radicals
18.10.3 Autoimmune disease
18.11 Hypothalamus-pituitary-adrenal (HPA) axis
18.12 Summary
References
II - Mechanisms of oxidative stress driven disease
19 - Aging mechanism
19.1 Introduction
19.2 Hallmarks of aging
19.2.1 Genomic instability
19.2.2 Telomere shortening
19.2.3 Epigenetic alterations
19.2.4 Loss of proteostasis
19.2.5 Deregulated nutrient sensing
19.2.6 Mitochondrial dysfunction
19.2.7 Cellular senescence
19.2.8 Stem cell exhaustion
19.2.9 Altered intercellular communication
19.3 Summary
References
20 - Obesity
20.1 Introduction
20.2 Statistics
20.3 Causes of obesity
20.4 Biomarkers of obesity
20.5 Comorbidities
20.6 Obesity, adipose tissue and chemical toxicity
20.6.1 Adipose tissue and persistent organic pollutants
20.6.2 POPs release into the body
20.6.3 Pops as obesogens
20.6.4 Pops as lipotoxins
20.7 Obesity and oxidative stress
20.7.1 Mitochondrial
20.7.2 Enzymes
20.7.3 Other factors
20.8 Psychological impact of obesity
20.9 Summary
References
21 - Cancer
21.1 Introduction
21.1.1 Intristic risks
21.1.2 Non-instristic risks
21.2 Hallmarks of cancer—Hanahan and Weinberg
21.2.1 Emerging hallmarks
21.2.2 Enabling characteristics
21.3 Other hallmarks
21.3.1 Cancer-related inflammation
21.3.2 Systemic hallmarks
21.3.2.1 Primary tumor-metastasis network
21.3.2.2 Global inflammation
21.3.2.3 Immunity inhibition
21.3.2.4 Metabolic changes to cachexia
21.3.2.5 Propensisty to thrombosis
21.3.2.6 Distal metastasis
21.3.3 Additional cancer hallmarks
21.3.4 Cancer hallmark regulation
21.4 Cancer initiation promotion and progression
21.5 Exogenous carcinogens
21.5.1 Mixtures
21.5.2 Total lipophilic load
21.5.3 Sequential absorption
21.5.4 Resonance stabilization
21.6 Metals, metalloids and cancer
21.7 Food and cancer
21.8 Metastasis
21.9 Mechanisms associated with specific cancers
21.9.1 Lung cancer
21.9.1.1 Causes of lung cancer
21.9.1.1.1 Tobacco smoking
21.9.1.1.2 Genetics
21.9.1.1.3 Diet
21.9.1.1.4 Obesity
21.9.1.1.5 Infections
21.9.1.1.6 Biomass, wood and coal smoke
21.9.1.1.7 Outdoor air pollution
21.9.1.2 Occupational chemical exposure
21.9.1.3 Radon
21.9.2 Breast cancer
21.9.3 Prostate cancer
21.9.4 Colorectal cancer
21.9.5 Melanoma
21.9.5.1 Vitamin A
21.9.5.2 Vitamin C
21.9.5.3 Vitamin D
21.9.5.4 Vitamin E
21.9.5.5 Vitamin K
21.9.6 Leukemia
21.9.7 Non-Hodgkin lymphoma
21.9.8 Kidney cancer
21.10 Summary
References
22 - Atherosclerosis
22.1 Introduction
22.2 Hallmark of atherosclerosis
22.3 Atherosclerosis risk factors
22.4 Atherosclerosis progression
22.5 Mechanism of onset
22.6 Oxidative stress and Artherosclerosis
References
23 - Alzheimer's disease
23.1 Introduction
23.2 Hallmarks of Alzheimer’s disease
23.3 Risk factors for Alzheimer’s disease
23.4 Alzheimer’s disease co-morbidity data
23.5 Mechanisms of Alzheimer’s disease onset
References
24 - Type 2 diabetes (T2D)
24.1 Introduction
24.2 Risk factors for type 2 diabetes
24.3 Chemical exposure as a cause of type 2 diabetes
24.3.1 Type 2 diabetes clusters
24.3.2 Lipophilic chemicals shown to cause T2D
24.3.2.1 POPs
24.3.2.2 Plastic exudates
24.3.2.3 Polluted air
24.3.2.4 Tobacco smoke
24.3.2.5 Pharmaceuticals
24.4 Mechanisms of type 2 diabetes onset
24.5 Effects of ROS
24.6 Type 2 diabetes and oxidative stress
24.7 Type 2 diabetes complications
24.8 Diabetes outlook
24.8.1 Aging
24.8.2 Obesity rates
24.8.3 Epigenetics
24.8.4 Diabetes projection
References
25 - Rheumatoid arthritis
25.1 Introduction
25.2 Complications of rheumatoid arthritis
25.3 Biomarkers of rheumatoid arthritis
25.4 Risk factors for rheumatoid arthritis
25.4.1 Age
25.4.2 Gender
25.4.3 History of live births
25.4.4 Genetics/familial history
25.4.5 Race/ethnicity
25.4.6 Obesity
25.4.7 Smoking
25.4.8 Dust inhalation
25.4.9 Gut microbiotica and mucosal inflammation
25.4.10 Peridontal disease
25.4.11 Viral infections
25.4.12 Diet
25.5 Mechanisms of rheumatoid arthritis onset
25.5.1 Triggering
25.5.2 Maturation
25.5.3 Targeting
25.5.4 Fulminant
25.6 Oxidative stress in rheumatoid arthritis
References
26 - Asthma
26.1 Introduction
26.2 Phenotypes of asthma
26.3 Biomarkers of asthma
26.4 Risk factors for asthma
26.4.1 Gender
26.4.2 Ethnicity
26.4.3 Family history
26.4.4 Genetics
26.4.5 Epigenetics
26.4.6 Atopy and allergic sensitizations
26.4.7 Tobacco smoke exposure
26.4.8 Air pollution
26.4.9 Obesity
26.4.10 Diet
26.4.11 Microbial respiratory infections
26.4.12 Antibiotics
26.4.13 Occupational exposure
26.5 Cross sensitization
26.6 Mechanisms of asthma and oxidative stress
26.6.1 Endogenous oxidative stress
26.6.2 Exogenous oxidative stress
26.7 Summary
References
27 - Liver cirrhosis
27.1 Introduction
27.2 Liver fibroproliferative diseases
27.2.1 Alcoholic liver disease (ALD)
27.2.2 Drugs
27.2.3 Chemical solvents and pollutants
27.2.4 Nonalcoholic fatty liver disease (NAFLD)
27.2.5 Hepatitis C
27.3 Oxidative stress and liver disease
References
28 - Chronic kidney disease (CKD)
28.1 Introduction
28.2 Causes of chronic kidney disease
28.3 Hallmarks of chronic kidney disease
28.4 Risk factors for chronic kidney disease
28.5 Mechanisms of chronic kidney disease and oxidative stress
28.5.1 Excess ROS production
28.5.2 Impaired antioxidant defense system
References
29 - Disease comorbidities
29.1 Introduction
29.2 Comorbidity
29.3 Oxidative stress, the common thread
References
III - Disease onset prediction
30 - Oxidative stress index
30.1 Introduction
30.2 Oxidative Stress Index (OSI)
30.3 OSI basis
30.4 Oxidative Stress Index questionnaire
30.4.1 Physical data
30.4.2 Genetics
30.4.3 Prevalent diseases and conditions
30.4.4 Symptoms
30.4.5 Diagnostic data
30.4.6 Pharmaceuticals regularly taken
30.4.7 Diet
30.4.8 Lifestyle
30.4.9 Tobacco and alcohol use
30.5 OSI score and disease
30.6 Additional applications
References
31 - OSI condensed questionnaire
31.1 Introduction
31.2 Age
31.3 Weight
31.4 Preexisting chronic conditions
31.5 Medications regularly taken
31.6 Genetics
31.7 Education level
31.8 Place of residence
31.9 Chronic psychological stress
31.10 Condensed OSI form
31.11 Condensed OSI applications
31.12 Conclusions
References
32 - OSI and Alzheimer's disease
32.1 Introduction
32.2 Alzheimer's disease and oxidative stress
32.3 Alzheimer's disease and dose response relationship (DRR)
32.4 Parameters known to increase likelihood of AD onset
32.5 Late onset AD
32.6 The OSI and AD
32.6.1 Predicting AD onset
32.6.2 Primary AD-causing parameters
32.6.3 AD onset odds
32.7 AD prevention
32.8 Questionnaire use
32.9 Strengths and limitations
32.10 Conclusions
References
33 - OSI public health surveys
33.1 Introduction
33.2 Toxicity as a function of emission distance
33.3 Disease impact as a function of exposure time
33.3.1 PCB exposure in schools
33.3.2 Fly ash toxicity
33.4 Summary
References
34 - Predicting COVID-19 severity
34.1 Introduction
34.2 Oxidative stress and COVID-19 severity
34.3 Oxidative stress index and COVID-19 severity
34.4 Validation of OSI use in predicting COVID-19 severity
34.4.1 Clinical risk score calculation (CRSC)
34.4.2 Comparison of the OSI and the CRSC
34.5 Covid-19 as a cause of oxidative stress
34.6 Summary
References
IV - Prevention
35 - Disease prevention: oxidative stress control, antioxidants, and social factors
35.1 Introduction
35.2 Oxidative stress overproduction control
35.3 Antioxidants
35.3.1 Antioxidant function
35.3.2 Antioxidant categories
35.4 Antioxidants and disease prevention
35.5 Diet
35.6 Treating prevalent illness
35.7 Psychological stress
35.7.1 Alternative stress therapies
35.7.1.1 Sweat lodge participation
35.7.1.2 Environmental chamber use
35.7.1.3 Chinese herbal medicine
35.7.1.4 Accupuncture
35.7.1.5 Yoga
35.7.1.6 Meditation
35.7.1.7 Aromatherapy
35.7.1.8 Hypnosis
35.7.1.9 Pets
35.8 Exercise
35.9 Treating illness
35.10 Inequalities
35.11 Summary
References
36 - Global warming, oxidative stress and disease
36.1 Introduction
36.2 Global warming, oxidative stress
36.2.1 Population
36.2.2 Migration
36.2.3 Energy use
36.2.4 Urbanization
36.2.5 Industrialization and air pollution
36.2.6 Atmospheric and oceanic energy
36.2.6.1 Extreme weather
36.2.7 Air pollution
36.2.8 Water pollution
36.2.9 Increased pesticide use
36.2.9.1 Increased numbers of insects, crop diseases and weeds
36.2.9.2 Increased evaporation of applied pesticides
36.2.9.3 Increased runoff after application
36.2.9.4 Increased loss due to wind
36.2.9.5 Decreased effectiveness
36.2.10 Disease increase
36.2.10.1 Increased pollen counts
36.2.10.2 Spread of infectious diseases
36.2.10.3 Antibiotic resistance
36.2.10.4 Mold growth
36.2.11 Contaminated food
36.2.12 Food quality decline
36.2.13 Absorption of toxins
36.2.14 Increased stress
36.2.15 Species extinction
36.2.15.1 Animal extinction
36.2.15.2 Insect extinction
36.2.15.3 Parasite extinction
36.2.15.4 Fish migration
36.2.15.5 Coral reef destruction
36.2.15.6 Tree population loss
36.3 Stress
36.4 Human extinction?
36.4.1 Lower life expectancy
36.4.2 Loss of life due to extreme weather
36.4.3 Decline in fertility
References
Index
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
Y
Back Cover