T-2 toxin induced nephrotoxicity in Wistar rats
Shafiqur Rahman, Amit Kumar Sharma, Neeraj Singh, Shahid Prawez
Abstract
Shafiqur Rahman, Amit Kumar Sharma, Neeraj Singh, Shahid Prawez
Abstract
The present experiment was designed to elucidate nephrotoxicity induced by feeding of graded doses of T-2 toxin in Wistar rats. A total of 192 male Wistar rats, 4 weeks of age were used for the study and were divided into four groups of 48 rats each receiving different levels of T-2 toxin in feed i.e. groups I- 0.5 ppm, II- 0.75 ppm and III- 1.0 ppm and group IV (control) toxin free diet. The duration of the experiment was 12 weeks and 8 animals each were sacrificed at 2, 4, 6, 8, 10 and 12 weeks intervals. Biochemically, increased levels of BUN and serum creatinine were observed in T-2 treated group rats. Significant increase in oxidative stress enzymes like MDA and decrease in SOD, Catalase and GSH in kidneys potentiated the role of free radicals in causing renal injury in T-2 toxicity. Pathomorphological studies revealed gross changes in kidneys viz, pale, soft and moderately enlarged in a dose and duration dependent manner. The relative weights of kidneys were increased in T-2 treated rats as compared with those in controls. The most consistent histopathological lesions in the kidneys included swollen and vacuolated epithelial cells of PCTs, occasional necrosis with presence of proteinaceous/cellular casts in the lumen along with congestion of intertubular blood vessels, mononuclear cell infiltration in interstitium, swollen parietal epithelial cells of Bowman's capsule and dilatation of DCTs which were more conspicuous at later stages. It was concluded that oxidative stress plays a major role in T-2 toxin induced nephrotoxicity.
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The present experiment was designed to elucidate nephrotoxicity induced by feeding of graded doses of T-2 toxin in Wistar rats. A total of 192 male Wistar rats, 4 weeks of age were used for the study and were divided into four groups of 48 rats each receiving different levels of T-2 toxin in feed i.e. groups I- 0.5 ppm, II- 0.75 ppm and III- 1.0 ppm and group IV (control) toxin free diet. The duration of the experiment was 12 weeks and 8 animals each were sacrificed at 2, 4, 6, 8, 10 and 12 weeks intervals. Biochemically, increased levels of BUN and serum creatinine were observed in T-2 treated group rats. Significant increase in oxidative stress enzymes like MDA and decrease in SOD, Catalase and GSH in kidneys potentiated the role of free radicals in causing renal injury in T-2 toxicity. Pathomorphological studies revealed gross changes in kidneys viz, pale, soft and moderately enlarged in a dose and duration dependent manner. The relative weights of kidneys were increased in T-2 treated rats as compared with those in controls. The most consistent histopathological lesions in the kidneys included swollen and vacuolated epithelial cells of PCTs, occasional necrosis with presence of proteinaceous/cellular casts in the lumen along with congestion of intertubular blood vessels, mononuclear cell infiltration in interstitium, swollen parietal epithelial cells of Bowman's capsule and dilatation of DCTs which were more conspicuous at later stages. It was concluded that oxidative stress plays a major role in T-2 toxin induced nephrotoxicity.
Key concepts: Nephrotoxicity, Toxin, Medicine, Pharmacology, Veterinary medicine, Biology, Kidney, Internal medicine