Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Emerging evidence indicates that impaired mitochondrial fatty acid beta-oxidation plays a key role in liver steatosis. We have recently demonstrated that increased angiotensin (ANG) II causes progressive hepatic steatosis associated with oxidative stress; however, the underlying mechanisms remain unclear. We hypothesized that ANG II causes hepatic mitochondrial oxidative damage and impairs mitochondrial beta-oxidation, thereby leading to hepatic steatosis. We used the Ren2 rat with elevated endogenous ANG II levels to evaluate mitochondrial ultrastructural changes, gene expression levels, and beta-oxidation. Compared with Sprague-Dawley littermates, Ren2 livers exhibited mitochondrial damage and reduced beta-oxidation, as evidenced by ultrastructural abnormalities, decrease of mitochondrial content, percentage of palmitate oxidation to CO(2), enzymatic activities (beta-HAD and citrate synthase), and the expression levels of cytochrome c, cytochrome c oxidase subunit 1, and mitochondrial transcription factor A. These abnormalities were improved with either ANG II receptor blocker valsartan or superoxide dismutase/catalase mimetic tempol treatment. Both valsartan and tempol substantially attenuated mitochondrial lipid peroxidation in Ren2 livers. Interestingly, there was no difference in the expression of key enzymes (ACC1 and FAS) for fatty acid syntheses and their transcription factors (SREBP-1c and ChREBP) between Sprague-Dawley, untreated Ren2, and valsartan- or tempol-treated Ren2 rats. These results document that ANG II induces mitochondrial oxidative damage and impairs mitochondrial beta-oxidation, contributing to liver steatosis.
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PMID:Oxidative stress-mediated mitochondrial dysfunction contributes to angiotensin II-induced nonalcoholic fatty liver disease in transgenic Ren2 rats. 1996 4

Introduction of exotic ticks and pathogens through international animal trade (farm animals and pets) is a serious threat to public health and local fauna. Rapid and correct identification of potential threats is an important step on the way to conduct an efficient control of imported pests. In this report we describe the molecular identification of the neotropic tick Amblyomma rotundatum intercepted from red-footed tortoise (Chelonoides carbonaria), imported to Israel from Florida, USA. Molecular analysis of the ticks conducted upon their identification, revealed that they were infected with Rickettsia bellii. Following their collection, the ticks were examined morphologically and five molecular markers were used to determine their taxonomic identity: cytochrome c oxidase subunit 1 (COX1), cytochrome b (CytB), 12S rRNA, 16S rRNA and internal transcribed sequence 2 (ITS-2). Molecular analysis indicated that all of the collected ticks were Amblyomma rotundatum. Using rickettsial gltA (citrate synthase) gene in real-time PCR analysis we found that approximately 25% of the intercepted ticks (8 of 33) were infected with Rickettsia bellii. It is concluded that accurate and timely identification of imported exotic ticks prevented their introduction to Israel, and that use of molecular tools may further improve the response to such potential threats.
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PMID:Molecular detection of Rickettsia bellii in Amblyomma rotundatum from imported red-footed tortoise (Chelonoides carbonaria). 2586 33