ArticleToxicology reports2023
A study to demonstrate the potential of Anabolic Androgen Steroid to activate oxidative tissue damage, nephrotoxicity and decline endogenous antioxidant system in renal tissue of Adult Wistar Rats.
Article in Toxicology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2025Review
- Ferrite chitosan curcumin nanoparticles alleviate nandrolone decanote induced liver toxicity in male albino rats.Scientific reports · 2025Article
- Ameliorating and therapeutic impact of nano ferrite-chitosan-curcumin nanoparticles against nandrolone decanote induced renal toxicity, inflammation, and oxidative stress in male rats.Toxicology research · 2025Article
- Protective effects of allicin against stanozolol-induced cardiotoxicity: Physiological and histopathological evidence in a rabbit model.Animal models and experimental medicine · 2025Article
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2 authors.
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Abstract
Anabolic Androgenic steroids (AAS) are abused and reports have been made on their deleterious effects on various organs. It is imperative to report the mechanism of inducing oxidative tissue damage even in the presence of an intracellular antioxidant system by the interaction between lipid peroxidation and the antioxidant system in the kidney. Twenty (20) adult male Wistar rats used were grouped into: A- Control, BOlive oil vehicle, C- 120 mg/kg of AAS orally for three weeks, and D- 7 days withdrawal group following 120 mg/kg/ 21days of AAS intake. Serum was assayed for lipid peroxidation marker Malondialdehyde (MDA) and antioxidant enzyme -superoxide Dismutase (SOD). Sectioned of kidneys were stained to see the renal tissue, mucin granules, and basement membrane. AAS-induced oxidative tissue damage, in the presence of an endogenous antioxidant, is characterized by increased lipid peroxidation and decreased SOD level which resulted in the loss of renal tissue cells membrane integrity which is a characteristic of the pathophysiology of nephron toxicity induced by a toxic compound. However, this was progressively reversed by a period of discontinuation of AAS drug exposure.
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