Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken to investigate the effect of biphenyl dimethyl dicarboxylate (PMC) on the humoral immunosuppression by ethanol (EtOH) in ICR mice. PMC at a dose of 6 mg/kg was orally administered to mice daily for 28 consecutive days, and the control mice were given vehicle. Mice treated with EtOH were given freely with 20% EtOH instead of water. The results of this study are summarized as follows; a gain of body weight and the relative weights of spleen and liver were significantly increased by combination of PMC and EtOH, as compared with those in mice treated with EtOH alone. Splenic plaque forming cells (PFC) and hemagglutination (HA) titers to sheep red blood cells (SRBC), and the secondary IgG antibody response to bovine serum albumin (BSA) were decreased by the treatment of EtOH alone, then restored to normal level by PMC treatment. The elevations of serum glutamic-pyruvic transaminase (S-GPT) and total protein levels caused by EtOH were reduced to normal level by the combination of PMC and EtOH. In addition, lower serum albumin and A/G ratio were also increased to normal level. These findings indicate that PMC has a protective effect against EtOH-induced humoral immunosuppression.
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PMID:Effect of biphenyl dimethyl dicarboxylate on the humoral immunosuppression by ethanol. 1109 Jun 99

In this study, PMC (2,2,5,7,8-pentamethyl-6-hydroxychromane), a derivative of alpha-tocopherol, dose-dependently (1-10 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated carbon tetrachloride (CCl4) intoxication in mice. Moreover, PMC significantly improved the CCl4-induced increase of hepatic glutathione peroxidase, reductase, and superoxide dismutase activities. PMC also restored the decrement in the glutathione content of hepatic tissues in CCl4-intoxicated mice. Furthermore, it also dose-dependently inhibited the formation of lipid peroxidative products during carbon tetrachloride treatment. Histopathological changes of hepatic lesions induced by carbon tetrachloride were significantly improved by treatment with PMC in a dose-dependent manner. These results suggest that PMC exerts effective protection in chronic chemical-induced hepatic injury in vivo.
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PMID:The protective effects of PMC against chronic carbon tetrachloride-induced hepatotoxicity in vivo. 1172 62