Androgenic Anabolic Steroids Perturb Hepatocellular Tissue Damage Mediated by Oxidative Stress in the Presence of Endogenous Antioxidant
Journal Title: Advances in Clinical Toxicology - Year 2024, Vol 9, Issue 1
Abstract
Objective of the study: Anabolic androgenic steroids (AASs) unlawfully misused for their anabolic effects has deleterious effects of major concerns in public health even in the presence of endogenously produced antioxidants. This study is to evaluate the interaction between AAS metabolites and endogenously produced superoxide dismutase (SOD) activity in AAS treatment and AAS abstinence. Materials and Methods: Twenty (20) adult male Wistar used were divided into four (4) groups, A and B served as the positive and negative control given normal saline and olive oil respectively, C and D was given 120mg/kg/bodyweight oral AAS for 21 days while D served as the 7 days withdrawal group after AAS treatment by evaluating histopathological changes in the liver histology, mucin/ glycogen granules, network of reticulum fibers, liver function enzymes; alanine aminotransferase (ALT) and aspartate aminotransferase (AST), lipid peroxidation enzyme malondialdehyde (MDA) and antioxidant enzyme. Results and Discussion: AAS treatment perturbed hepatocellular membrane integrity seen in the increase MDA, AST and ALT activity which caused disruption of the hepatocytes cell integrity attributed to a decline in endogenous SOD. However, AAS withdrawal group gradually reversed AAS mediated heaptocellular pathogenesis associated with progressive elevation of endogenous SOD, decline in MDA and activities of liver function test. Conclusion: AAS mediates hepatic injury through lipid peroxidation and a decline in endogenous antioxidant enzyme, withdrawal of AAS slows down the oxidative damage process when the endogenous antioxidant production increases and mobs off ROS generated by AAS ingested thereby protecting against liver injury and hepato-cellular break down.
Authors and Affiliations
Memudu AE* and Magnut GE
Keywords
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- EP ID EP754421
- DOI 10.23880/act-16000292
- Views 7
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