Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenytoin, an anticonvulsant agent used for the treatment of epilepsy has been reported to exhibit toxic side effects on the liver and testes. The present study investigated the protective effects of kolaviron (KV, a bioflavonoid from Garcinia kola seeds) against hepatic and testicular damage in rats exposed to phenytoin. The study consisted of four groups of six rats per group. Group I rats received 2 mL/kg of corn alone while group II received 75 mg/kg of phenytoin (PHT) alone. Groups III and IV were co-treated with kolaviron (200 mg/kg KV) and vitamin E (500 mg/kg VTE), respectively, for 14 days. The antioxidant status, hepatic and reproductive functional parameters were subsequently determined. PHT treatment significantly (p < 0.05) increased superoxide dismutase (SOD) and catalase (CAT) activities, elevated lipid peroxidation (LPO) and hydrogen peroxide (H2O2) levels along with significant reduction in the hepatic and testicular levels of glutathione (GSH). Moreover, PHT exposure elicited significant increases in alkaline phosphatase (ALP) and aspartate aminotransferase (AST) levels. The significant reduction in seminal epithelium thickness and the diameter of seminiferous tubules was accompanied with marked decrease in sperm motility, sperm count, and viability in PHT-treated rats. However, antioxidant status and the functional indices of liver and testes were restored to near control levels in rats co-treated with KV and VTE. In conclusion, KV and VTE protect the liver and testes against functional impairment due to PHT treatment.
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PMID:Modulatory role of kolaviron in phenytoin-induced hepatic and testicular dysfunctions in Wistar rats. 2516 91

Phenytoin is known to induce microsomal enzymes including xanthine oxidase which catalyzes uric acid synthesis with superoxides as byproducts, thus contributing to the oxidative stress of phenytoin hepatotoxicity. To investigate the role of antioxidant vitamins in ameliorating phenytoin induced hepatic changes through possible actions on xanthine oxidase activities as measured by urate concentration. Growing albino rats of Wistar strain were randomly divided into 8 groups of 7 rats each. Group 2, 3, 4, 5, 6, 7 and 8 were treated with phenytoin alone, phenytoin + folic acid, phenytoin + vitamin E, phenytoin + vitamin E + vitamin C, phenytoin + vitamin C, phenytoin + folic acid + vitamin E and phenytoin + vitamin E + vitamin C + folic acid respectively while animals in group 1 were given normal saline to serve as control. Serum concentrations of uric acid, albumin, total protein and the activities of aspartate and alanine aminotransferases (AST and ALT) and catalase were measured spectrophotometrically using appropriate commercial reagent kits. Result showed that administration of phenytoin alone caused significant (p < 0.05) increase in serum levels of globulin, uric acid, AST and ALT activities while the levels of albumin and catalase were reduced significantly (p < 0.05). Supplementation of phenytoin treatment with vitamins resulted in various degrees of protection. However, the elevated level of uric acid in serum was not significantly (p < 0.05) affected by any of the vitamins used and there was no significant correlation between the activities of aminotransferases and uric acid concentration in the vitamin treated animals as was observed between aminotransferases and catalase. The findings in this study suggest that antioxidant vitamins were able to ameliorate phenytoin hepatotoxic effects by improving oxidant radicals removal in the animals but would not inhibit further generation of the superoxides by xanthine oxidase activity and that xanthine oxidase may contribute significantly to the oxidative stress of phenytoin therapy.
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PMID:Urate synthesis and oxidative stress in phenytoin hepatotoxicity: the role of antioxidant vitamins. 2602 63

'Erythema Multiforme associated with Phenytoin And Cranial radiation Therapy' (EMPACT) is a very rare clinic situation and classified in EM-like drug reactions. It can be easily misdiagnosed as acute urticaria or drug eruption in ED. Initial symptoms may resemble a simple skin problem, but diagnosing and early hospitalization of the patients can be lifesaving. Here, we present a man with renal cell cancer and brain metastases who admitted to ED due to fever and generalized rash. His skin lesions beginning from his head and spreading through the torso appeared four days after the end of radiotherapy (11 days after the initial dose of both radiation and oral phenytoin). Inspection showed erythematous lesions on the scalp, neck, torso and arms. These lesions had desquomative character on the scalp. Erythematous maculopapular lesions with the tendency of fusion were also visible on the chest, abdomen, back, on the flexor areas of the arm, forearm and femoral region. Laboratory studies showed normal complete blood counts, high creatinine kinase, creatinine kinase-MB, gamma-glutamyl transpeptidase, aspartate aminotransferase, lactate dehydrogenase, albumin and total protein. After discontinuation of phenytoin and giving H1, H2 receptor blockers and steroid intravenously, he was discharged two weeks later with full recovery.
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PMID:Is this a simple drug eruption to be discharged? 2799 12