Vitamin A Against the Acetaminophen- Induced Toxicity in the Renal Cortex of Albino Rats

Background: Acetaminophen (paracetamol; APAP) - induced toxicities have been a major problem in clinical practice. There is no specific treatment for paracetamol poisoning. Vitamin A has shown to have an assisting role in the management of renal inflammatory disorders in animal models as it has anti-inflammatory, antioxidant as well as cytoprotective effect on various renal cell types. Aim of the Work: To evaluate the possible protective effect of vitamin A against APAP -induced acute renal toxicity in rats. Materials and Methods: Forty adult male albino rats were used and divided into five groups including control untreated, control vitamin A (12000 IU/kg b.wt, oral), APAP (lg/kg b.wt, intraperitoneally), APAP+ vitamin A (3000 IU/kg b.wt, oral) and APAP+ vitamin A (12000 IU/kg b.wt, oral). One week after APAP administration, all rats were anaesthetized. Venous blood was collected; serum and plasma were separated for biochemical assessments. The kidneys were also removed and the renal specimens were submitted to biochemical analysis as well as the microscopic examination using both the light and electron microscopy. Results: Acetaminophen treatment induced increased lipid peroxidation in the plasma and renal tissue. Additionally, increased serum BUN and creatinine levels as well as decreased antioxidant catalase activity were detected indicating a possible involvement of oxidative stress in acetaminophen-induced nephropathy. Microscopic examination revealed massive proximal tubular degeneration, luminal cellular debris associated with partial loss of the luminal brush border. Additionally, cortical interstitial vascular congestion and extravasation of red blood cells were observed. Vitamin A treatment markedly reduced paracetamol- induced renal cortical damage in a dose - dependant manner, as evidenced by the improvement of the biochemical measurements and the marked amelioration of renal pathology. Conclusion: Vitamin A may be a choice of preventive treatment against paracetamol- induced renal damage. The mechanism of protection is probably due to its antioxidant properties and the repairing effect on the damaged tubular cells.