Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nickel sulfate (2.0 mg/100 g.b.wt) dissolved in double-distilled water was administered (i.p.) on alternate days for ten doses to normal protein-fed and protein-restricted Wister strain albino rats (b.wt. 160 +/- 5 g). Two groups were used: one with normal protein diet, whereas the other with protein-restricted diet served as control. Twenty-four hours after the last treatment, the animals were sacrificed by decapitation. Tissues such as the testes, seminal vesicles, epididymis (Cauda and Caput) and prostate were dissected out, wiped clean, and stored at -20 degrees C until analysis. Lactate dehydrogenase (LDH) activities, glutamate oxaloacetate transaminase (GOT) activities, glycogen content, cholesterol content, and total protein content of the testes were estimated. Nickel sulfate administration significantly decreased the body weight of both normal protein-fed and protein-restricted groups of animals; the organ weights were also decreased. Significant decrease of LDH activity was observed, but GOT activity was not altered significantly. Testicular glycogen and cholesterol increased significantly in both experimental groups, but total protein content decreased. Nickel sulfate seems to have an adverse effect on the male reproductive system in both groups of animals fed with normal protein (18% casein) diet and protein restricted (5% casein) diet.
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PMID:Alteration of testicular biochemistry during protein restriction in nickel treated rats. 949 62

This study was designed to determine the toxic effects of nickel sulfate on the biochemical and elemental profile of liver in protein deficient rats. Nickel sulfate in the dose of 800mg/l in drinking water was administrated to Sprauge Dawley (S.D) normal control as well as protein deficient rats for a total duration of eight weeks. The effects of nickel treatment and protein deficiency when given separately and in combination were studied on rat liver marker enzymes like Alkaline phosphatase (ALP),Glutamate oxaloacetate transaminase (GOT), Glutamate pyruvate transaminase (GPT) and also on the status of essential elements in rat liver. Protein deficient, Ni treated as well as combined protein deficient and nickel treated rats showed significant reductions in the body weight and hepatic protein contents as compared to normal control rats. Hepatic alkaline phosphatase activity and alanine aminotransferase showed a significant elevation in rats subjected to protein deficiency, nickel treatment and combined protein deficiency and nickel treatment. As regards to hepatic levels of aspartate aminotransferase a significant elevation was observed in protein deficient and nickel treated protein deficient animals. Nickel administration to normal and protein deficient rats has resulted in a significant increase in concentrations of nickel, phosphorus and sulfur in liver tissue. The concentration of zinc and copper in liver tissue decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals. Tissue iron concentrations were found to be decreased in protein deficient animals, but the concentrations of iron got elevated significantly in nickel treated and nickel treated protein deficient animals. It has been observed that selenium got decreased significantly in protein deficient, nickel treated and nickel treated protein deficient animals when compared to normal animals. The elevation of selenium in nickel treated protein deficient animals was also significantly higher when compared to protein deficient animals.
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PMID:Ineffectiveness of nickel in augmenting the hepatotoxicity in protein deficient rats. 1633 21