Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism causing loss of integrity of lens epithelial cells induced by an overdose of sodium selenite remains to be elucidated. The aim of the present experiment was to search for changes in gene expression in epithelial cells of lenses from rats developing selenite cataract. One day after injection of selenite into 12 day old rats, gene expression in lens epithelial cells was analysed using a commercial DNA array (Atlas Rat 1.2 Array). Changes were confirmed by RT-PCR. Of 1176 genes assayed by hybridization, 91 genes showed differences in expression between normal and selenite lenses. The three genes showing the greatest changes were: cytochrome c oxidase subunit I (COX-I, decrease), gastric inhibitory polypeptide (GIP, decrease), and early growth response protein-1 (EGR-1, increase). Both COX-I and EGR-1 have been reported to be involved with apoptosis. These results suggest that changes in COX-I and EGR-1 expression in lens epithelial cells might play important roles in apoptosis and altered metabolism leading to selenite cataract.
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PMID:Differential gene expression in the lens epithelial cells from selenite injected rats. 1195 Feb 33

Differential expression of apoptotic genes has been demonstrated in selenite-induced cataract. Acetyl-l-carnitine (ALCAR) has been shown to prevent selenite cataractogenesis by maintaining lenticular antioxidant enzyme and redox system components at near normal levels and also by inhibiting lenticular calpain activity. The aim of the present experiment was to investigate the possibility that ALCAR also prevents selenite-induced cataractogenesis by regulating the expression of antioxidant (catalase) and apoptotic [caspase-3, early growth response protein-1 (EGR-1) and cytochrome c oxidase subunit I (COX-I)] genes. The experiment was conducted on 9-day-old Wistar rat pups, which were divided into normal, cataract-untreated and cataract-treated groups. Putative changes in gene expression in whole lenses removed from the rats were determined by measuring mRNA transcript levels of the four genes by RT-PCR analysis, using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an internal control. The expression of lenticular caspase-3 and EGR-1 genes appeared to be upregulated, as inferred by detecting increased mRNA transcript levels, while that of COX-I and catalase genes appeared to be downregulated (lowered mRNA transcript levels) in the lenses of cataract-untreated rats. However, in rats treated with ALCAR, the lenticular mRNA transcript levels were maintained at near normal (control) levels. These results suggest that ALCAR may prevent selenite-induced cataractogenesis by preventing abnormal expression of lenticular genes governing apoptosis.
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PMID:Regulatory effect of acetyl-l-carnitine on expression of lenticular antioxidant and apoptotic genes in selenite-induced cataract. 2006 79