News Update on Oxidative Stress Research: July – 2019

Oxidative stress, antioxidants and stress tolerance

Traditionally, reactive gas intermediates (ROIs) were thought of to be deadly by-products of aerobic metabolism, that were disposed of victimization antioxidants. However, in recent years, it’s become apparent that plants actively manufacture ROIs as signal molecules to regulate processes like programmed death, abiotic stress responses, infectious agent defense and general signal. Recent advances together with microarray studies and also the development of mutants with altered ROI-scavenging mechanisms offer new insights into however the steady-state level of ROIs ar controlled in cells. additionally, key steps of the signal transduction pathway that senses ROIs in plants are known. These raise many intriguing questions about the relationships between ROI signal, ROI stress and also the production and scavenging of ROIs within the totally different cellular compartments. [1]

Oxidative stress: oxidants and antioxidants

An imbalance between oxidants and antioxidants in favour of the oxidants, probably resulting in harm, is termed ‘oxidative stress’. Oxidants are shaped as a standard product of aerobic metabolism however may be created at elevated rates beneath pathophysiological conditions. inhibitor defense involves many ways, each catalyst and non‐enzymatic. within the macromolecule section, tocopherols and carotenes likewise as oxy‐carotenoids are of interest, as are A and ubiquinols. within the liquid section, there are ascorbate, glutathione and different compounds. additionally to the cytoplasm, the nuclear and mitochondrial matrices and living thing fluids are protected. Overall, these low molecular mass inhibitor molecules add considerably to the defense provided by the enzymes enzyme, enzyme and glutathione peroxidases. [2]

Free radicals, metals and antioxidants in oxidative stress-induced cancer

Oxygen-free radicals, a lot of usually called reactive element species (ROS) at the side of reactive element species (RNS) area unit well recognised for taking part in a twin role as each injurious and useful species. The “two-faced” character of ROS is verified by growing body of proof that ROS inside cells act as secondary messengers in living thing signalling cascades, that induce and maintain the oncogenic composition of cancer cells, however, ROS may induce cellular senescence and necrobiosis and may so operate as anti-tumourigenic species. The accumulative production of ROS/RNS through either endogenous or exogenous insults is termed aerophilic stress and is common for several kinds of neoplastic cell that area unit coupled with altered oxidoreduction regulation of cellular signalling pathways. aerophilic stress induces a cellular oxidoreduction imbalance that has been found to be gift in varied cancer cells compared with traditional cells; the oxidoreduction imbalance so could also be associated with oncogenic stimulation. polymer mutation could be a important step in carcinogenesis and elevated levels of aerophilic polymer lesions (8-OH-G) are noted in varied tumours, powerfully implicating such injury within the etiology of cancer. It seems that the polymer injury is preponderantly coupled with the initiation method. This review examines the proof for involvement of the aerophilic stress within the carcinogenesis method. Attention is concentrated on structural, chemical and organic chemistry aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the polymer injury (both mitochondrial and nuclear), the injury to lipids and proteins by free radicals, the development of aerophilic stress, cancer and also the oxidoreduction surroundings of a cell, the mechanisms of carcinogenesis and also the role of signalling cascades by ROS; particularly, ROS activation of AP-1 (activator protein) and NF-κB (nuclear issue alphabetic character B) signal transduction pathways, that successively cause the transcription of genes concerned in cell growth regulative pathways. The role of accelerator (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, element and others) within the method of carcinogenesis furthermore because the inhibitor interactions with varied regulative factors, together with Ref-1, NF-κB, AP-1 also are reviewed. [3]

Oxidative stress and mitochondrial responses to stress exposure suggest that king penguins are naturally equipped to resist stress

Exposure to unpredictable environmental stressors might influence animal health and fitness by inducement aerobic  stress, doubtless through downstream effects of corticoid stress hormones (e.g. corticosterone) on mitochondrial perform. Yet, it remains unclear whether or not species that have evolved in random and difficult environments might gift diversifications to alleviate the results of stress exposure on aerobic  stress. we have a tendency to tested this hypothesis in wild king penguins by work mitochondrial and aerobic  stress responses to acute restraint-stress, and their relationships with baseline (potentially mirroring exposure to chronic stress) and stress-induced increase in glucocorticoid levels. Acute restraint-stress didn’t considerably influence mitochondrial perform. However, acute restraint-stress diode to a major increase in endogenous inhibitor defences, whereas aerobic  injury levels were principally not affected or maybe belittled. High baseline glucocorticoid levels were related to associate degree up-regulation of the glutathione inhibitor system and a decrease in mitochondrial potency. each processes may contribute to stop aerobic  injury, doubtless explaining the negative relationship ascertained between baseline glucocorticoid and plasma aerobic  injury to proteins. whereas stress exposure will represent an aerobic  challenge for animals, protecting mechanisms like up-regulating inhibitor defences and decreasing mitochondrial potency appear to occur in king penguins, permitting them to address their random and difficult surroundings. [4]

P53 Expression in Response to Equigan Induced Testicular Injury and Oxidative Stress in Male Rat and the Possible Prophylactic Effect of Star Anise Extracts

Objectives: Equigan is associate anabolic sex hormone steroid that developed for veterinary use to enhance the food manufacturing animal rate of growth through promoting macromolecule synthesis and muscle growth. the present study aimed to analyze the potential prophylactic result of star anise extracts (SAE) response of to Equigan iatrogenic sex gland injury, aerophilous stress, P53 expression in male rats.

Materials and Methods: Forty male person rats were equally divided into four teams. first management cluster, whereas ordinal cluster were rats receive orally SAE for twelve weeks. third cluster embody rats that injected intramuscularly with Equigan for twelve weeks whereas fourth cluster were co-treated cluster wherever rats injected with Equigan and SAE for twelve weeks.

Results: gonad sections in Equigan treated rat iatrogenic abnormal arrangement of gametogenesis cycles; disturbance and reduce within the spermatogenic cells, several of a syncytial cells were detected with marked decrease in sperms numbers and moderate depleted and degenerated Leydig cells. sex gland immunohistochemical observation once Equigan contractile organ injections showed a major increase of the apoptotic macromolecule p53. Co-administration of SAE with Equigan improved the sex gland injury and P53 alternations.

Conclusions: SAE might scavenge free radicals and turn out useful effects against Equigan injury in gonad and P53 alternations. [5]

Reference

[1] Mittler, R., 2002. Oxidative stress, antioxidants and stress tolerance. Trends in plant science, 7(9), pp.405-410. (Web Link)

[2] Sies, H., 1997. Oxidative stress: oxidants and antioxidants. Experimental Physiology: Translation and Integration, 82(2), pp.291-295. (Web Link)

[3] Valko, M., Rhodes, C., Moncol, J., Izakovic, M.M. and Mazur, M., 2006. Free radicals, metals and antioxidants in oxidative stress-induced cancer. Chemico-biological interactions, 160(1), pp.1-40. (Web Link)

[4] Oxidative stress and mitochondrial responses to stress exposure suggest that king penguins are naturally equipped to resist stress

Antoine Stier, Quentin Schull, Pierre Bize, Emilie Lefol, Mark Haussmann, Damien Roussel, Jean-Patrice Robin & Vincent A. Viblanc

Scientific Reportsvolume 9, Article number: 8545 (2019) (Web Link)

[5] A. El-Masry, T., H. Al-Shaalan, N., Tousson, E., El-Morshedy, K. and Al-Ghadeer, A. (2017) “P53 Expression in Response to Equigan Induced Testicular Injury and Oxidative Stress in Male Rat and the Possible Prophylactic Effect of Star Anise Extracts”, Annual Research & Review in Biology, 14(1), pp. 1-8. doi: 10.9734/ARRB/2017/34318. (Web Link)

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