Functions of intracellular glutathione in hepatic hydroperoxide and drug metabolism and the role of extracellular glutathione

Sies, Helmut; Wahlländer, A.; Waydhas, Christian; Soboll, Sibylle; Häberle, D. A.

doi:10.1016/0065-2571(80)90022-9

Cited by 67 publications

(18 citation statements)

References 42 publications

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“…In agreement with previous reports on hemoglobin free perfusions [ 1, 3,4] only small amounts of GSH was excreted in bile ( -0.03 nmol . g liver-l .…”

Section: Resultssupporting

confidence: 81%

“…The amount of GSSG excreted in the bile under control conditions was 0.7-0.9 nmol/min g liver which is slightly less than previously reported [4]. During perfusion with arsenite the biliary GSSG content increased (table 1) while the amount in the perfusate was only slightly raised (not shown).…”

Section: Resultscontrasting

confidence: 38%

“…Sies et al [ 1,3] have shown that efflux of GSSG occurs during oxidation of drugs such as hexobarbital and ethylmorphine as well as during hydroperoxide metabolism. In the isolated liver there is also a transport of reduced glutathione (GSH) into the perfusate space [4]. However, it has also been reported that relatively high concentrations of GSH may be excreted in the bile produced in situ ]5a,bl.…”

Section: Introductionmentioning

confidence: 99%

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GSH release in bile as influenced by arsenite

1982

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“…In agreement with previous reports on hemoglobin free perfusions [ 1, 3,4] only small amounts of GSH was excreted in bile ( -0.03 nmol . g liver-l .…”

Section: Resultssupporting

confidence: 81%

Section: Resultscontrasting

confidence: 38%

Section: Introductionmentioning

confidence: 99%

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GSH release in bile as influenced by arsenite

1982

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“…Several studies have demonstrated the significance of GSH in the protection of cells against reactive oxygen species, free radicals, and other toxic compounds (Sies et al, 1980;Chasseaud, 1979) and in the induction of thermotolerance Mitchell, 1983). GSH also functions in regulating the intracellular thio1:disulfide status (Ziegler, 1985) and as a transport form of cysteine (Griffith et al, 1979).…”

mentioning

confidence: 98%

Elevation of intracellular glutathione content associated with mitogenic stimulation of quiescent fibroblasts

Shaw

Chou

1986

Journal Cellular Physiology

158

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The relationship between total glutathione (GSH) content and cell growth was examined in 3T3 fibroblasts. The intracellular GSH level of actively growing cultures gradually decreases as these cells become quiescent by either serum deprivation or high cell density. Upon mitogenic stimulation of sparse, quiescent (G0/G1) cultures with serum, there is a rapid 2.3-fold elevation in intracellular GSH levels which is maximal by 1 h and returns to baseline by 2 h. This is followed by a more gradual increase in GSH content as cells enter the S phase. In addition, the elevation in GSH content is required for maximum induction of DNA synthesis. Treatments that prevent the early increase in intracellular GSH levels do not affect protein synthesis but result in a reversible dose-dependent decrease in the percent of cells capable of entering S phase. These results indicate that GSH may be important in the regulation of cellular proliferation.

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“…The high BLOA values found in diabetes confirm that there is a systemic oxidative insult in this disorder. Cells defense systems counteract this insult by actively excreting GSSG [45], But high levels of GSSG affect the integrity of the glutathione system through the inhibi tion of G6PD activity [36,37], In this way, reduced amounts of NADPH are available for glutathione reductase, so that diminished levels of GSH can react with potential oxi dants before they can interact with the less mobile structural proteins. Thus, when GSH has been exhausted, either by loss from the lens or by oxidation, rapid oxidation of both soluble and membrane-bound proteins takes place [46].…”

Section: Discussionmentioning

confidence: 99%

Systemic Human Diseases as Oxidative Risk Factors in Cataractogenesis

et al. 1988

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In this study we have investigated the oxidative metabolism of red blood cells (RBC), plasma, serum, aqueous humor, and lens of healthy subjects and of age-matched cataractous patients with and without diabetes. Reduced and oxidized glutathione (GSH, GSSG) levels in RBC were similar among the three groups. Plasma levels of GSSG were higher in diabetics than in cataractous and control subjects. No differences in plasma content of GSH were noted among the three groups. The activity of the enzyme glucose-6-phosphate dehydrogenase was significantly diminished in diabetic patients. Controls and cataractous patients showed similar levels of malondialdehyde (MDA). Although not significant, the MDA content in RBC from diabetics was elevated. No differences in plasma levels of vitamin E were noted among the three groups. The biological liquid oxidant activity of serum in diabetic patients was significantly higher than in controls and cataractous patients. GSH levels in aqueous humor were similar in diabetic and nondiabetic cataractous patients. The content of GSSG in aqueous humor was highest in diabetic patients. Control clear lenses showed low levels of MDA. The MDA levels in cataractous lenses from nondiabetic patients were significantly higher than those of controls. In diabetic patients the content of MDA in the lens was approximately twice as high as the cataractous values. Our results seem to demonstrate that oxidative damages could play a role in the pathogenesis of cataract in diabetes.

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Functions of intracellular glutathione in hepatic hydroperoxide and drug metabolism and the role of extracellular glutathione

Cited by 67 publications

References 42 publications

GSH release in bile as influenced by arsenite

GSH release in bile as influenced by arsenite

Elevation of intracellular glutathione content associated with mitogenic stimulation of quiescent fibroblasts

Systemic Human Diseases as Oxidative Risk Factors in Cataractogenesis

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