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Phenytoin-induced toxicity in the postnatal cerebellar development in rat: effect of calotropis procera on selective biochemical and haematological variables
Abstract
Phenytoin, an antiepileptic drug is used in managing seizures. Phenytoin-associated oxidative stress causes cellular damage by the generation of free radicals. Vitamin C, a standard antioxidant and Calotropis
procera are believed to scavenge oxygen free radicals. The effect of C. procera extract on haematological and biochemical variables in an in-vivo model was studied. Pregnant rats were administered phenytoin (50 mg/kg
body weight). Extracts of C. procera (300 mg/kg body weight) and vitamin C (200 mg/kg body weight) were administered one hour prior to phenytoin treatment separately, while control animals received tap water only.
The animals had access to food and water ad libitum. Blood was collected from animals on day 50 postpartum for packed cell volume (PCV), haemoglobin (Hb) content and evaluation of levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) evaluation. Lipid peroxidase (LPO) and reduced glutathione (GSH) levels in the cerebellum were assessed as markers of oxidative stress on day 50 postpartum. Phenytoininduced toxicity was associated with increased cerebellar LPO and decreased GSH levels. Increase in ALT and
AST levels in the serum was observed. However, PCV and Hb levels were not affected. LPO, GSH, ALT and AST levels registered a tendency to shift towards normalcy on administration of C. procera and vitamin C to
phenytoin. In conclusion, supplementation with C. procera leaf extract reduced the rate at which phenytoin induced toxicity in developing rat cerebellum postnatally.
procera are believed to scavenge oxygen free radicals. The effect of C. procera extract on haematological and biochemical variables in an in-vivo model was studied. Pregnant rats were administered phenytoin (50 mg/kg
body weight). Extracts of C. procera (300 mg/kg body weight) and vitamin C (200 mg/kg body weight) were administered one hour prior to phenytoin treatment separately, while control animals received tap water only.
The animals had access to food and water ad libitum. Blood was collected from animals on day 50 postpartum for packed cell volume (PCV), haemoglobin (Hb) content and evaluation of levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) evaluation. Lipid peroxidase (LPO) and reduced glutathione (GSH) levels in the cerebellum were assessed as markers of oxidative stress on day 50 postpartum. Phenytoininduced toxicity was associated with increased cerebellar LPO and decreased GSH levels. Increase in ALT and
AST levels in the serum was observed. However, PCV and Hb levels were not affected. LPO, GSH, ALT and AST levels registered a tendency to shift towards normalcy on administration of C. procera and vitamin C to
phenytoin. In conclusion, supplementation with C. procera leaf extract reduced the rate at which phenytoin induced toxicity in developing rat cerebellum postnatally.
