Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acidosis is a well established concomitant of tissue ischemia. Acidosis in the pH range 6.0-7.0 is seen in cerebral ischemia and within solid tumors. Extracellular acidosis of pH 6.0 and 6.4 provided essentially complete protection from 48 h serum deprivation induced apoptotic death of cultured primary murine neurons. We tested the effect of p53 using transformed mouse embryo fibroblasts of either p53+/+ or p53-/- genotype. Both were markedly protected from serum deprivation by acidity. Hypoxia induced fibroblast injury was also reduced at pH 6.8. Lower pH resulted in a shift from apoptotic to necrotic morphology after 42 h hypoxia. Acidosis reduces apoptosis of both normal and transformed cells, irrespective of p53 status.
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PMID:Acidosis reduces neuronal apoptosis. 957 83

Information on the change in extracellular ascorbic acid (AA) during the acute period of cerebral ischemia is of great importance in the early therapeutic intervention of the cerebral ischemic injury since AA is known to be involved into most kinds of neurochemical changes in the cerebral ischemia. This study describes a fast and efficient method through integration of in vivo microdialysis with on-line electrochemical detection for continuous monitoring cerebral AA, allowing comparative study of the change in the extracellular AA level in different brain ischemia/reperfusion models. The method exhibits a high specificity for AA measurements, bearing a good tolerance against the fluctuation in the brain anoxia and acidity induced by cerebral ischemia/reperfusion. In the global two-vessel occlusion (2-VO) ischemia model, the striatum AA did not change with statistic significance until 60 min after occlusion and was decreased to be 91+/-3% (n=5, P<0.05) of the basal level (8.05+/-0.23 microM) at the time point of 60 min after occlusion. In the 2-VO ischemia/reperfusion model, AA remained unchanged during the 10 min of ischemia, and was sharply increased to be 267+/-74% (n=5, P<0.05) of the basal level after the initial 15 min of reperfusion, and then decreased to be 122+/-33% (n=5, P<0.05) of the basal level after 50 min of reperfusion. Extracellular AA was largely increased after 5 min of left middle cerebral artery occlusion (LMCAO) and was then gradually increased to be 257+/-49% (n=5, P<0.05) of the basal level after 60 min of LMCAO ischemia. In the LMCAO ischemia/reperfusion model, AA was greatly increased during 10 min of ischemia and then gradually increased to be 309+/-69% (n=5, P<0.05) of the basal level after the consecutive 50 min of reperfusion. The results demonstrated here may be useful for understanding the neurochemical processes in the acute period of cerebral ischemia and could thus be important for neuroprotective therapeutics for cerebral ischemic injury.
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PMID:Comparative study of change in extracellular ascorbic acid in different brain ischemia/reperfusion models with in vivo microdialysis combined with on-line electrochemical detection. 1829 77