phosphoric acid/hypoxia

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Role of protein phosphorylation in the inhibition of protein synthesis caused by hypoxia in rat hepatocytes.

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Hypoxia causes a rapid and reversible inhibition of translation in freshly isolated rat hepatocytes. This inhibition is neither due to an ATP loss nor to an increase in cell death. Because protein synthesis is mainly regulated by reversible phosphorylation of initiation and/or elongation factors, we

[Effect of hypobaric hypoxia on the acetate-1-14C incorporation rate in hydrophilic and hydrophobic brain phospholipid components].

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Rats were kept in barochamber for 2 hours at the pressure of 240 mm Hg after subcutaneous administration of (1)14C-acetate. Hypobaric hypoxia caused depression in the incorporation of labeled acetate similar in both phospholipid (PL) components. But the dependence of depression in the metabolic rate

[Phosphoric acid ester poisoned rats after antidote therapy. 2. Determination of serum enzyme activity].

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Paraoxon in doses of one LD50 (0.426 mg/kg), eight times and eighty times LD 50 was applied s.c. to female Sprague-Dawley rats. After 3, 6, 10, 24 and 36--48 h the activities of enzymes GOT, GPT, GLDH, SDH, CPK and ChE were measured, once after i.m. antidote application of Toxogonin only, of

Isolation and identification of an aerobic denitrifying phosphorus removing bacteria and analysis of the factors influencing denitrification and phosphorus removal.

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Excessive emission of plant nutrients (such as nitrogen and phosphorus) into the water body can induce eutrophication. Therefore, how to control eutrophic water efficiently and economically is very important. In the paper, highly efficient aerobic denitrifying phosphorus removing J16 bacteria was

N-methyl-D-aspartate-mediated injury enhances quisqualic acid-stimulated phosphoinositide turnover in perinatal rats.

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Previous work in our laboratory demonstrated that ischemic-hypoxic brain injury in postnatal day 7 rats causes a substantial increase in phosphoinositide (PPI) turnover stimulated by the glutamate analogue quisqualic acid (QUIS) in the hippocampus and striatum. To examine this phenomenon in more

[Metabolomics study of the myocardial tissue of rats of cardiac blood stasis syndrome].

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OBJECTIVE To find out the metabolite profile of rats' myocardial tissue of cardiac blood stasis syndrome (CBSS), and to analyze the metabolic pathway of CBSS rats' myocardial tissue by observing the changes of phenotypes intervened by Yangxin Tongmai Recipe (YTR). METHODS Acute myocardial infarction

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