Peer Reviewed Open Access Journal
Methamphetamine (METH), a potent psychostimulant, is widely recognized for its neurotoxic and systemic toxic effects, including oxidative and inflammatory damage to peripheral organs such as the kidney. Excessive METH exposure induces nephrotoxicity characterized by oxidative stress, tubular degeneration, and impaired renal function. Vitamin A, in its active metabolite form (retinoic acid), exhibits strong antioxidant and cytoprotective properties that may counteract drug-induced organ injury. This study investigated the potential protective effect of low-dose of vitamin A on the kidneys of adult male Wistar rats exposed to toxic doses of methamphetamine. Twenty rats were randomly divided into four groups (n = 5): group A (control) feed and water, group B (METH-only; 20g/kg at 3-hour intervals within 12 hours in a day), group C (vitamin A-only; 0.7 mg/kg) while group D (combined METH + vitamin A). All the experimental groups were fed with feed and water. All treatments were administered orally via intubation for 28 consecutive days. After the final administration, animals were anesthetized and sacrificed; kidneys were harvested, fixed in 10% neutral formal-saline and processed for histological examination using Hematoxylin and Eosin (H&E) staining. Results of methamphetamine exposure group showed weight loss, oxidative stress, and notable renal architectural disruptions, including tubular necrosis, glomerular shrinkage, and inflammatory infiltration. However, co-administration of low-dose of vitamin A preserved renal morphology, reduced cellular degeneration, and stabilized biochemical markers of kidney function. The findings of this study suggest that vitamin A confers a nephroprotective effect against methamphetamine-induced renal toxicity, likely mediated through its antioxidant and anti-inflammatory mechanism.
Toxic dose, Vitamin A, Wistar rat, Nephroprotective, Methamphetamine
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