Molecular Basis for Oxidative Stress Induced by Environmental Toxicants in Nematodes

2019 ◽  
pp. 1-30
Author(s):  
Dayong Wang
Keyword(s):  
Oxidative Stress ◽  
Molecular Basis ◽  
Environmental Toxicants

CRYPTIC CAUSES AND MECHANISMS INVOLVED IN AGEING

INDIAN DRUGS ◽  
2013 ◽  
Vol 50 (01) ◽  
pp. 5-22
Author(s):  
K Challabotla ◽  
◽  
D Banji ◽  
O.J.F Banji ◽  
Chilipi K Reddy
Keyword(s):  
Oxidative Stress ◽  
Developing Countries ◽  
Molecular Basis ◽  
Metabolic Disorders ◽  
Natural Process ◽  
Biological Functions ◽  
Stress Theory ◽  
Biochemical Alterations ◽  
Organ Systems ◽  
The Brain

Ageing is a natural process characterized by progressive deterioration of biological functions. Ageing causes both morphological as well as biochemical alterations in various body organs leading to deterioration of health. Proteins, enzymes and neurotransmitters are affected, which in turn can result in dysregulation of various pathways. WHO has reported that by 2020, three quarters of all deaths in developing countries will be age-associated. Currently more than 300 theories exist to explain the phenomenon of ageing; amongst them the oxidative stress theory of ageing is most studied and accepted for the molecular basis of ageing. All these processes can progress at an unprecedented pace on contact with triggering factors, leading to the development of pathological ageing. The probability of developing neurodegenerative and metabolic disorders is relatively high under such circumstances. This review emphasizes the theories and mechanisms of ageing and an overview on the aspects of age associated biochemical changes and the implications on the brain, liver and various organ systems.

Molecular Basis of Diabetic Peripheral Neuropathy: Role of Oxidative Stress

2015 ◽  
Vol 3 (2) ◽  
pp. 123-124
Author(s):  
Nisha Rani Jamwal ◽  
◽  
Senthil P Kumar. ◽  
Keyword(s):  
Oxidative Stress ◽  
Peripheral Neuropathy ◽  
Diabetic Peripheral Neuropathy ◽  
Molecular Basis

Environmental Toxicants and Carcinogenicity: Role of Oxidative Stress

2021 ◽  
pp. 1-13
Author(s):  
Sanjay Saini ◽  
Jagdish Gopal Paithankar ◽  
Anurag Sharma ◽  
Debapratim Kar Chowdhuri
Keyword(s):  
Oxidative Stress ◽  
Environmental Toxicants

Paternal impacts on development: identification of genomic regions vulnerable to oxidative DNA damage in human spermatozoa

2019 ◽  
Vol 34 (10) ◽  
pp. 1876-1890 ◽  
Author(s):  
M J Xavier ◽  
B Nixon ◽  
S D Roman ◽  
R J Scott ◽  
J R Drevet ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Male Infertility ◽  
Oxidative Damage ◽  
Oxidative Dna Damage ◽  
Human Spermatozoa ◽  
Research Centre ◽  
Environmental Toxicants ◽  
Next Generation ◽  
Genomic Regions

Abstract STUDY QUESTION Do all regions of the paternal genome within the gamete display equivalent vulnerability to oxidative DNA damage? SUMMARY ANSWER Oxidative DNA damage is not randomly distributed in mature human spermatozoa but is instead targeted, with particular chromosomes being especially vulnerable to oxidative stress. WHAT IS KNOWN ALREADY Oxidative DNA damage is frequently encountered in the spermatozoa of male infertility patients. Such lesions can influence the incidence of de novo mutations in children, yet it remains to be established whether all regions of the sperm genome display equivalent susceptibility to attack by reactive oxygen species. STUDY DESIGN, SIZE, DURATION Human spermatozoa obtained from normozoospermic males (n = 8) were split into equivalent samples and subjected to either hydrogen peroxide (H2O2) treatment or vehicle controls before extraction of oxidized DNA using a modified DNA immunoprecipitation (MoDIP) protocol. Specific regions of the genome susceptible to oxidative damage were identified by next-generation sequencing and validated in the spermatozoa of normozoospermic males (n = 18) and in patients undergoing infertility evaluation (n = 14). PARTICIPANTS/MATERIALS, SETTING, METHODS Human spermatozoa were obtained from normozoospermic males and divided into two identical samples prior to being incubated with either H2O2 (5 mm, 1 h) to elicit oxidative stress or an equal volume of vehicle (untreated controls). Alternatively, spermatozoa were obtained from fertility patients assessed as having high basal levels of oxidative stress within their spermatozoa. All semen samples were subjected to MoDIP to selectively isolate oxidized DNA, prior to sequencing of the resultant DNA fragments using a next-generation whole-genomic sequencing platform. Bioinformatic analysis was then employed to identify genomic regions vulnerable to oxidative damage, several of which were selected for real-time quantitative PCR (qPCR) validation. MAIN RESULTS AND THE ROLE OF CHANCE Approximately 9000 genomic regions, 150–1000 bp in size, were identified as highly vulnerable to oxidative damage in human spermatozoa. Specific chromosomes showed differential susceptibility to damage, with chromosome 15 being particularly sensitive to oxidative attack while the sex chromosomes were protected. Susceptible regions generally lay outside protamine- and histone-packaged domains. Furthermore, we confirmed that these susceptible genomic sites experienced a dramatic (2–15-fold) increase in their burden of oxidative DNA damage in patients undergoing infertility evaluation compared to normal healthy donors. LIMITATIONS, REASONS FOR CAUTION The limited number of samples analysed in this study warrants external validation, as do the implications of our findings. Selection of male fertility patients was based on high basal levels of oxidative stress within their spermatozoa as opposed to specific sub-classes of male factor infertility. WIDER IMPLICATIONS OF THE FINDINGS The identification of genomic regions susceptible to oxidation in the male germ line will be of value in focusing future analyses into the mutational load carried by children in response to paternal factors such as age, the treatment of male infertility using ART and paternal exposure to environmental toxicants. STUDY FUNDING/COMPETING INTEREST(S) Project support was provided by the University of Newcastle’s (UoN) Priority Research Centre for Reproductive Science. M.J.X. was a recipient of a UoN International Postgraduate Research Scholarship. B.N. is the recipient of a National Health and Medical Research Council of Australia Senior Research Fellowship. Authors declare no conflict of interest.

scholarly journals Perfluorooctanesulfonic Acid and Perfluorohexanesulfonic Acid Alter the Blood Lipidome and the Hepatic Proteome in a Murine Model of Diet-Induced Obesity

2020 ◽  
Vol 178 (2) ◽  
pp. 311-324
Author(s):  
Marisa Pfohl ◽  
Lishann Ingram ◽  
Emily Marques ◽  
Adam Auclair ◽  
Benjamin Barlock ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Expression Profiles ◽  
Environmental Toxicants ◽  
High Fat ◽  
High Carbohydrate ◽  
Lipid Species ◽  
Perfluorooctanesulfonic Acid ◽  
The Impact ◽  
And Oxidative Stress

Abstract Perfluoroalkyl substances (PFAS) represent a family of environmental toxicants that have infiltrated the living world. This study explores diet-PFAS interactions and the impact of perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic (PFHxS) on the hepatic proteome and blood lipidomic profiles. Male C57BL/6J mice were fed with either a low-fat diet (10.5% kcal from fat) or a high fat (58% kcal from fat) high carbohydrate (42 g/l) diet with or without PFOS or PFHxS in feed (0.0003% wt/wt) for 29 weeks. Lipidomic, proteomic, and gene expression profiles were determined to explore lipid outcomes and hepatic mechanistic pathways. With administration of a high-fat high-carbohydrate diet, PFOS and PFHxS increased hepatic expression of targets involved in lipid metabolism and oxidative stress. In the blood, PFOS and PFHxS altered serum phosphatidylcholines, phosphatidylethanolamines, plasmogens, sphingomyelins, and triglycerides. Furthermore, oxidized lipid species were enriched in the blood lipidome of PFOS and PFHxS treated mice. These data support the hypothesis that PFOS and PFHxS increase the risk of metabolic and inflammatory disease induced by diet, possibly by inducing dysregulated lipid metabolism and oxidative stress.

scholarly journals The Bad, the Good, and the Ugly about Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Marlene Jimenez-Del-Rio ◽  
Carlos Velez-Pardo
Keyword(s):  
Oxidative Stress ◽  
Intracellular Signaling ◽  
Molecular Basis ◽  
Mechanistic Explanation ◽  
Etiologic Factor ◽  
Significant Implication ◽  
Design Strategies ◽  
Pathologic Process ◽  
Intracellular Signaling Pathways ◽  
Cell Death Signaling

Alzheimer’s disease (AD), Parkinson’s disease (PD), and cancer (e.g., leukemia) are the most devastating disorders affecting millions of people worldwide. Except for some kind of cancers, no effective and/or definitive therapeutic treatment aimed to reduce or to retard the clinic and pathologic symptoms induced by AD and PD is presently available. Therefore, it is urgently needed to understand the molecular basis of these disorders. Since oxidative stress (OS) is an important etiologic factor of the pathologic process of AD, PD, and cancer, understanding how intracellular signaling pathways respond to OS will have a significant implication in the therapy of these diseases. Here, we propose a model of minimal completeness of cell death signaling induced by OS as a mechanistic explanation of neuronal and cancer cell demise. This mechanism might provide the basis for therapeutic design strategies. Finally, we will attempt to associate PD, cancer, and OS. This paper critically analyzes the evidence that support the “oxidative stress model” in neurodegeneration and cancer.

scholarly journals Impact of lgt mutation on lipoprotein biosynthesis and in vitro phenotypes of Streptococcus agalactiae

Microbiology ◽  
2009 ◽  
Vol 155 (5) ◽  
pp. 1451-1458 ◽  
Author(s):  
Beverley A. Bray ◽  
Iain C. Sutcliffe ◽  
Dean J. Harrington
Keyword(s):  
Oxidative Stress ◽  
Streptococcus Agalactiae ◽  
Molecular Basis ◽  
Cell Envelope ◽  
Host Cells ◽  
Human Endothelial Cells ◽  
Increased Sensitivity ◽  
Group B

Although Streptococcus agalactiae, the group B Streptococcus, is a leading cause of invasive neonatal disease worldwide the molecular basis of its virulence is still poorly understood. To investigate the role of lipoproteins in the physiology and interaction of this pathogen with host cells, we generated a mutant S. agalactiae strain (A909ΔLgt) deficient in the Lgt enzyme and thus unable to lipidate lipoprotein precursors (pro-lipoproteins). The loss of pro-lipoprotein lipidation did not affect the viability of S. agalactiae or its growth in several different media, including cation-depleted media. The processing of two well-characterized lipoproteins, but not a non-lipoprotein, was clearly shown to be aberrant in A909ΔLgt. The mutant strain was shown to be more sensitive to oxidative stress in vitro although the molecular basis of this increased sensitivity was not apparent. The inactivation of Lgt also resulted in changes to the bacterial cell envelope, as demonstrated by reduced retention of both the group B carbohydrate and the polysaccharide capsule and a statistically significant reduction (P=0.0079) in A909ΔLgt adherence to human endothelial cells of fetal origin. These data confirm that failure to process lipoproteins correctly has pleiotropic effects that may be of significance to S. agalactiae colonization and pathogenesis.

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