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Glucagon과 insulin이 glutathione 항상성에 미치는 영향: 세포신호전달체계 및 glutathione transport system의 역할
김봉희,오정민,윤강욱,김충현,김상겸,Kim, Bong-Hee,Oh, Jung-Min,Yun, Kang-Uk,Kim, Chung-Hyeon,Kim, Sang-Kyum 환경독성보건학회 2007 환경독성보건학회지 Vol.22 No.3
It has been reported that hepatic glutathione (GSH) levels are decreased in diabetic patients, and glucagon increases hepatic efflux of GSH into blood. The signaling pathways responsible for mediating the glucagon effects on GSH efflux, however, are unknown. The signaling pathways involved in the regulation of GSH efflux in response to glucagon and insulin were examined in primary cultured rat hepatocytes. The GSH concentrations in the culture medium were markedly increased by the addition of glucagon, although cellular GSH levels are significantly decreased by glucagon. Insulin was also increased the GSH concentrations in the culture medium, but which is reflected in elevations of both cellular GSH and protein. Treatment of cells with 8-bromo-cAMP or dibutyryl-cAMP also resulted in elevation of the GSH concentrations in the culture medium. Pretreatment with H89, a selective inhibitor of protein kinase A, before glucagon addition markedly attenuated the glucagon effect. These results suggest that glucagon changes GSH homeostasis via elevation of GSH efflux, which may be responsible for decrease in hepatic GSH levels observed in diabetic condition. Furthermore, the present study implicates cAMP and protein kinase A in mediating the effect of glucagon on GSH efflux in primary cultured rat hepatocytes.
인슐린 매개성 Microsomal Epoxide Hydrolase의 발현증가에서 Akt의 역할
김상겸,김봉희,오정민,윤강욱,김충현,강건욱,Kim, Sang-Kyum,Kim, Bong-Hee,Oh, Jung-Min,Yun, Kang-Uk,Kim, Chung-Hyeon,Kang, Keon-Wook 대한약학회 2007 약학회지 Vol.51 No.5
The present study examines the effect of dominant-negative Akt on the insulin-mediated microsomal epoxide hydrolase (mEH) induction in rat hepatocytes. We also assessed the role of insulin in the expression of soluble epoxide hydrrolase (sEH). Insulin increased mEH levels and the enzyme activities, whereas sEH protein expression was unaffected by insulin. The specific PI3K inhibitors or p70 S6 kinase inhibitor ameliorated the insulin-mediated increase in mEH protein levels. Infection with adenovirus expressing dominant-negative and kinase-dead mutant of Akt1 effectively inhibited the insulin-mediated increase in mEH expression and mEH activity. These results suggest that mEH and sEH are differentially regulated by insulin and PI3K/Akt/p70S6K are active in the insulin-mediated regulation of mEH expression.
Tetrabromobisphenol-A가 처리된 랫드의 간에서 항산화활성 평가
이상윤(Sang yoon Lee),윤강욱(Kang Uk Yun),박선홍(Sun Hong Park),정선기(Sun Ki Jung),강건욱(Keon Wook Kang),정태천(Tae Cheon Jeong),김형식(Hyung Sik Kim),정혜광(Hye Gwang Jeong),김봉희(Bong Hee Kim),김상겸(Sang Kyum Kim) 환경독성보건학회 2009 환경독성보건학회지 Vol.24 No.4
Hepatic antioxidant defense systems were examined in rats treated with tetrabromobisphenol-A (TBBPA), a brominated flame retardant, at the doses of 0, 250, 500 and 1,000 ㎎/㎏ for four weeks. Hepatic ratio of glutathione disulfide to glutathione (GSH) and levels of malondialdehyde, oxidative stress markers were not changed in rats treated with TBBPA. Hepatic expression of antioxidant enzymes including GSH peroxdiase-1 (GPX-1)/GSH reductase (GR), alpha-, mu- and pi-class glutathione-S-transferase (GST) and gamma-glutamylcysteine ligase catalytic subunit was determined using immunoblot analysis. Alpha-class GSTs, GPX-1 and GR levels were significantly decreased in rats treated with TBBPA at the dose of 500 or 1,000 ㎎/㎏. These results show that TBBPA results in down-regulation of hepatic expression of antioxidant enzymes related with GSH, suggesting the liver in TBBPA-treated rats may be more sensitive to oxidants.
김봉희(Bong-Hee Kim),오정민(Jung Min Oh),윤강욱(Kang Uk Yun),김충현(Chung Hyeon Kim),김상겸(Sang Kyum Kim) 한국독성학회 2007 Toxicological Research Vol.23 No.3
Although taurine (2-aminoethanesulfonic acid) can inhibit oxidative stress in both animal and epidemiological studies, it is obscure whether taurine directly scavenges oxy-radicals or indirectly regulates oxidant production and/or antioxidant defense system. The reason for this discrepancy remains unknown but may be due, in part, to the lack of a validated assay system for evaluating oxy-radical scavenging capacity. The antioxidant activities of taurine and hypotaurine (2-aminoethanesulfinic acid), a precursor of taurine, against peroxyl radicals, hydroxyl radicals and peroxynitrites were determined by the total oxy-radical scavenging capacity (TOSC) assay and cell-based assay using H4IIE cells. tert-Butylhydroperoxide or hydrogen peroxide-induced cell toxicity determined by MTT assay was markedly inhibited by 10 mM taurine or hypotaurine. The tert-butylhydroperoxide- or hydrogen peroxide-induced changes in oxidative stress markers, such as cellular glutathione and malondialdehyde, were ameliorated by 10 mM taurine or hypotaurine. However, specific TOSC values calculated from the slope of the linear regression for taurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were all less than 1 TOSC/mM. On the other hand specific TOSC values for hypotaurine against peroxyl radicals, hydroxyl radicals or peroxynitrites were 48, 2096, or 69 TOSC/mM, respectively. These results suggest that taurine protects cells against oxidative insults, which is not ascribed to directly scavenging activity of taurine against oxy-radicals. These results support the idea that the oxidation state of sulfur in antioxidants may be a determinant of oxy-radical scavenging capacity.