Latest News on Induced Oxidative Stress: Dec 2020

Latest News on Induced Oxidative Stress: Dec 2020

Advances in metal-induced oxidative stress and human disease

Detailed studies in the past two decades have shown that redox active metals like iron (Fe), copper (Cu), chromium (Cr), cobalt (Co) and other metals undergo redox cycling reactions and possess the ability to produce reactive radicals such as superoxide anion radical and nitric oxide in biological systems. Disruption of metal ion homeostasis may lead to oxidative stress, a state where increased formation of reactive oxygen species (ROS) overwhelms body antioxidant protection and subsequently induces DNA damage, lipid peroxidation, protein modification and other effects, all symptomatic for numerous diseases, involving cancer, cardiovascular disease, diabetes, atherosclerosis, neurological disorders (Alzheimer’s disease, Parkinson’s disease), chronic inflammation and others. The underlying mechanism of action for all these metals involves formation of the superoxide radical, hydroxyl radical (mainly via Fenton reaction) and other ROS, finally producing mutagenic and carcinogenic malondialdehyde (MDA), 4-hydroxynonenal (HNE) and other exocyclic DNA adducts. On the other hand, the redox inactive metals, such as cadmium (Cd), arsenic (As) and lead (Pb) show their toxic effects via bonding to sulphydryl groups of proteins and depletion of glutathione. Interestingly, for arsenic an alternative mechanism of action based on the formation of hydrogen peroxide under physiological conditions has been proposed. A special position among metals is occupied by the redox inert metal zinc (Zn). Zn is an essential component of numerous proteins involved in the defense against oxidative stress. It has been shown, that depletion of Zn may enhance DNA damage via impairments of DNA repair mechanisms. In addition, Zn has an impact on the immune system and possesses neuroprotective properties. The mechanism of metal-induced formation of free radicals is tightly influenced by the action of cellular antioxidants. Many low-molecular weight antioxidants (ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), glutathione (GSH), carotenoids, flavonoids, and other antioxidants) are capable of chelating metal ions reducing thus their catalytic acitivity to form ROS. A novel therapeutic approach to supress oxidative stress is based on the development of dual function antioxidants comprising not only chelating, but also scavenging components. Parodoxically, two major antioxidant enzymes, superoxide dismutase (SOD) and catalase contain as an integral part of their active sites metal ions to battle against toxic effects of metal-induced free radicals. The aim of this review is to provide an overview of redox and non-redox metal-induced formation of free radicals and the role of oxidative stress in toxic action of metals. [1]

Environmentally induced oxidative stress in aquatic animals

Reactive oxygen species (ROS) are an unenviable part of aerobic life. Their steady-state concentration is a balance between production and elimination providing certain steady-state ROS level. The dynamic equilibrium can be disturbed leading to enhanced ROS level and damage to cellular constituents which is called “oxidative stress”. This review describes the general processes responsible for ROS generation in aquatic animals and critically analyses used markers for identification of oxidative stress. Changes in temperature, oxygen levels and salinity can cause the stress in natural and artificial conditions via induction of disbalance between ROS production and elimination. Human borne pollutants can also enhance ROS level in hydrobionts. The role of transition metal ions, such as copper, chromium, mercury and arsenic, and pesticides, namely insecticides, herbicides, and fungicides along with oil products in induction of oxidative stress is highlighted. Last years the research in biology of free radicals was refocused from only descriptive works to molecular mechanisms with particular interest to ones enhancing tolerance. The function of some transcription regulators (Keap1–Nrf2 and HIF-1α) in coordination of organisms’ response to oxidative stress is discussed. The future directions in the field are related with more accurate description of oxidative stress, the identification of its general characteristics and mechanisms responsible for adaptation to the stress have been also discussed. The last part marks some perspectives in the study of oxidative stress in hydrobionts, which, in addition to classic use, became more and more popular to address general biological questions such as development, aging and pathologies. [2]

Exercise-induced oxidative stress.

The role of exercise in free radical processes is not clear; however, recent evidence suggests that elevated oxygen consumption may increase free radical activity. Direct measurement of free radical signals can be made by electron spin resonance and indirect measures include mitochondrial membrane damage, conjugated dienes, hydroperoxides, thiobarbituric acid reactive substances, short chain hydrocarbons, and oxidized nucleosides. Although exact levels are not known, the type, duration, and intensity of exercise affect biomarkers of free radical activity, as does one’s training status. Oxidative stress associated with exercise-induced free radical activity seems to be better tolerated by trained subjects exercising at moderate intensity. [3]

Protective Potential of Grape Seed Proanthocyandins Extract against Glivec (Imatinib Mesylate) Induced Liver Toxicity and Oxidative Stress in Male Rats

Objectives: Glivec (Imatinib mesylate) an antineoplastic chemotherapeutic agent used in the treatment of many types of cancer. The current study examines the hepatoprotective potential of grape seed proanthocyandins extract (GSPE) against Glivec induced oxidative stress and toxicity in male albino rats.

Materials and Methods: A total of 40 male albino rats were equally divided into four groups; group 1 was control, group 2 was GSPE group (rats received orally GSPE by stomach tube {50 mg/kg BW/twice a week} for four week), group 3 was Glivec group (rats were injected intraperitoneally with Glivec {1 mg /kg B W/twice a week} for four weeks) and group 4 was rats treated with GSPE plus Glivec for four weeks.

Results: LD50 was calculated for Glivec in rats (estimated at 598 mg/kg), presenting confidence limits between 588 and 612 mg/kg body weight. A significant increase in the liver TBARS and aspartate aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and γ-glutamyltransferase (GGT) activities in Glivec group when compared with the control group. On the other hand; a significant decrease in the serum albumin, globulin, total protein, liver superoxide dismutase activity (SOD), catalase (CAT), glutathione S-trasferase (GST) and reduced glutathione (GSH) levels in Glivec group when compared with the control group. Administration of GSPE with Glivec caused a protective and ameliorative effect against Glivec induced liver toxicity.

Conclusions: Treatment with GSPE has a promising role for ameliorating the oxidative stress and hepatic injury induced by Glivec. [4]

Neuroprotective Effect of Convolvulus pluricaulis Methanol Extract on Hydrogen Peroxide Induced Oxidative Stress in Human IMR32 Neuroblastoma Cell Line

Aims: The present study aimed to evaluate and ascertain the protective role of methanolic/ethanolic/water extracts of Convolvulus pluricaulis against H2O2 induced cytotoxicity in IMR32 Neuroblastoma cell line as model system and identify the factor responsible for the protective effect.

Study Design:  Experimental study.

Place and Duration of Study: Department of Molecular Biology and Biochemistry, Guru Nanak Dev University, Amritsar & Department of Biotechnology, DAV College, Amritsar, PuCPab, between August 2010 and March 2012.

Methodology: Firstly, cytotoxic dose of H2O2 ­and non-toxic dose of methanolic, ethanolic and water extracts of C. pluricaulis (CP-MEx, CP-EEx and CP-WEx respectively) was determined by MTT assay. Protective effect of CP-MEx, CP-EEx and CP-WEx was determined using quercetin as a positive control. The expression of IMR32 cytoskeletal marker, Neurofilament (NF-200) and stress markers, Heat shock protein (HSP70) and (glucose regulated protein 75, Grp75) Mortalin studied by immunofluorescence and RT-PCR results. The level of antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase, direct scavenger of free radicals, Glutathione and lipid peroxidation were analysed by their standard procedures.

Results: The results showed that quercetin, CP-MEx, CP-EEx and CP-WEx displayed cytoprotective activity in IMR32 cells. Out of tested extracts CP-MEx significantly decreased hydrogen peroxide-induced cell death. Significant decrease in NF-200, HSP70 and Mortalin expression was observed in CP-MEx+H2O2 treated cultures as compared to H2O2 treated. Catalase, superoxide dismutase, glutathione peroxidase, Glutathione levels significantly increased in Quercetin and CP-MEx treated cultures. Lipid peroxidation was significantly decreased in both Quercetin and CP-MEx treated cultures.

Conclusions: The present work establishes the protective effect of CP-MEx on IMR 32 Human Neuroblastoma cell line which is as much as by quercetin. The cytoprotective effect of CP-MEx was due to induction of antioxidant machinery of the cell hence holds therapeutic value in the treatment and/or prevention of neurodegenerative disorders of oxidative stress. [5]

Reference

[1] Jomova, K. and Valko, M., 2011. Advances in metal-induced oxidative stress and human disease. Toxicology, 283(2-3), pp.65-87.

[2] Lushchak, V.I., 2011. Environmentally induced oxidative stress in aquatic animals. Aquatic toxicology, 101(1), pp.13-30.

[3] Alessio, H.M., 1993. Exercise-induced oxidative stress. Medicine and science in sports and exercise, 25(2), pp.218-224.

[4] Al-Rasheed, N. M., El-Masry, T. A., Tousson, E., Hassan, H. M. and Al-Ghadeer, A. (2017) “Protective Potential of Grape Seed Proanthocyandins Extract against Glivec (Imatinib Mesylate) Induced Liver Toxicity and Oxidative Stress in Male Rats”, Annual Research & Review in Biology, 20(6), pp. 1-9. doi: 10.9734/ARRB/2017/37766.

[5] Dhuna, K., Dhuna, V., Bhatia, G., Singh, J. and Singh Kamboj, S. (2012) “Neuroprotective Effect of Convolvulus pluricaulis Methanol Extract on Hydrogen Peroxide Induced Oxidative Stress in Human IMR32 Neuroblastoma Cell Line”, Biotechnology Journal International, 2(4), pp. 192-210. doi: 10.9734/BBJ/2012/1655.

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