Increased biliary glutathione disulfide release in chronically ethanol‐treated rats

Sies, Helmut; Koch, Osvaldo R.; Martino, Elba E.; Boveris, A

doi:10.1016/0014-5793(79)81346-0

Cited by 236 publications

(94 citation statements)

References 19 publications

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“…Lumenal GSH arises from the bile, by export from the epithelial cells, breakdown of desquamated cells, and diet. Bile contains high levels (1-6 mM) of GSH (43)(44)(45), and this could lead to high local levels of GSH in the small intestine. In the present studies, 0.9 ml of 160 mM GSH was administered by gastric lavage; this would be diluted by the lumenal contents but would be expected to be much higher than the GSH level in the diet.…”

Section: Discussionmentioning

confidence: 99%

Glutathione is required for intestinal function.

Mårtensson

Jain²,

Meister³

1990

Proc. Natl. Acad. Sci. U.S.A.

255

167

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Glutathione (GSH) deficiency produced in mice by giving buthionine sulfoximine leads to severe degeneration of the epithelial cells of the jejunum and colon. This is prevented by giving GSH monoester (orally or i.p.) and also by giving GSH (orally, but not i.p.). The i.p. administration leads to high plasma levels of GSH but does not appreciably increase GSH levels in intestinal mucosa or pancreas. These and previous studies on lens, lung, lymphocytes, liver, heart, and skeletal muscle indicate that there is very little, if any, transport of intact GSH from plasma to these tissues. Cells can use extracellular GSH by a pathway involving its cleavage, uptake of products and intracellular GSH synthesis. Epithelial cells of the gastrointestinal tract may use this pathway and can also take up lumenal GSH (which arises partly from the bile) by a mechanism(s) that may involve transport of dipeptides or of GSH. It is suggested that biliary GSH normally functions in the protection of intestinal mucosa. Administration of GSH may be protective of the gastrointestinal epithelium and may also serve as a good source of cysteine moieties for intracellular GSH synthesis in the gastrointestinal tract and in other tissues. Administration of GSH delivery agents such as GSH esters is more effective than administration of GSH in increasing cellular and mitochondrial levels of GSH.Administration to experimental animals of L-buthionine-SR-sulfoximine (BSO), a transition-state inhibitor of yglutamylcysteine synthetase, leads to decreased synthesis of glutathione (GSH) in many tissues (1-4). Decreased cellular GSH levels and capacity for GSH synthesis sensitize cells to radiation and to certain drugs; these effects provide a potentially useful approach in cancer therapy (5-12). Administration of BSO offers several advantages over other methods of cellular GSH depletion, one of which is that it makes possible the selective decrease of cellular GSH for relatively long periods, thus facilitating study of the effects of GSH deficiency on cell structure and function. Administration of BSO to mice for 9-21 days, without application of stress, led to marked structural changes in skeletal muscle (13), lung (14), and epithelial cells ofnewborn lens (15); such effects were not found in heart (13) and liver (14). Mitochondrial damage is found in tissues affected by ; the mitochondrial levels of GSH in tissues markedly affected by GSH depletion (lung, muscle, lens) were -20%o of the untreated controls, whereas in heart and liver the mitochondrial GSH levels were >40% of the controls. Mitochondrial and other cellular damage was prevented by simultaneous administration of GSH monoester but not by administration of GSH. GSH monoesters can enter cells effectively and are converted to GSH intracellularly (16)(17)(18)(19). In contrast, GSH is poorly transported into cells.These studies were stimulated by the observation (13) that administration of BSO to 28-to 30-g mice for 9-21 days led to a marked decrease in weight gain and that simultaneous ...

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Section: Discussionmentioning

confidence: 99%

Glutathione is required for intestinal function.

Mårtensson

Jain²,

Meister³

1990

Proc. Natl. Acad. Sci. U.S.A.

255

167

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“…One unit of SOD is defined as the amount of enzyme that promotes a 50% inhibition of the cytochrome c reduction at pH 7.8 and 25 o C. CAT activity was quantified at 240 nm by the H 2 O 2 decomposition according to the method of Beutler (1975). GPx activity was assayed by the oxidation of NADPH (linked to GSSG reduction by excess glutathione reductase) at 340 nm, according to Sies et al (1979). The total protein content was determined by method of modified Lowry, using bovine albumin as standard (Peterson, 1977).…”

Section: Methodsmentioning

confidence: 99%

Effects of aerial exposure on antioxidant defenses in the brown mussel Perna perna

Almeida

Bainy

2006

Braz. arch. biol. technol.

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Investigations were carried out to evaluate the antioxidant defenses in digestive gland of mussels Perna perna held in air for 4 hours, exposed to air for 4 hours followed by submersion in water for 30 minutes, and constantly submerged for 4.5 hours. No differences were observed in CAT and GPx activities and in the levels of total GSH. Mussels exposed to air had significantly higher SOD activity, possibly related to a preparative mechanism of defense against oxidative stress during reoxygenation.

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“…Total glutathione (GSH-t) is reported as µmol/g Ginkgo biloba on pregnant diabetic rats www.bjournal.com.br liver and was determined by the method of Tietze (10), as modified by Akerboom and Sies (11). Glutathione peroxidase (GSH-Px) activity is reported as IU/mg protein and was evaluated by the method of Sies et al (12). Catalase (CAT) activity is reported as IU/mg protein and was determined by the method of Beutler (13).…”

mentioning

confidence: 99%

Effect of Ginkgo biloba on the reproductive outcome and oxidative stress biomarkers of streptozotocin-induced diabetic rats

Rudge

Damasceno

Volpato

et al. 2007

Braz J Med Biol Res

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The aim of the present study was to evaluate the effect of Ginkgo biloba treatment (EGb 761, 200 mg kg -1 day -1 ) administered from day 0 to 20 of pregnancy on maternal reproductive performance and on the maternal and fetal liver antioxidant systems of streptozotocin-induced diabetic Wistar rats. On day 21 of pregnancy, the adult rats (weighing approximately 250 ± 50 g, minimum number = 13/group) were anesthetized to obtain maternal and fetal liver samples for superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and total glutathione (GSH-t) determinations. The uterus was weighed with its contents. The diabetic (G3) and treated diabetic (G4) groups of rats presented significant maternal hyperglycemia, reduced term pregnancy rate, impaired maternal reproductive outcome and fetal-placental development, decreased GSH-Px (G3 = G4 = 0.6 ± 0.2) and SOD (G3 = 223.0 ± 84.7; G4 = 146.1 ± 40.8), and decreased fetal CAT activity (G3 = 22.4 ± 10.6; G4 = 34.4 ± 14.1) and GSH-t (G3 = G4 = 0.3 ± 0.2), compared to the non-diabetic groups (G1, untreated control; G2, treated). For G1, maternal GSH-Px = 0.9 ± 0.2 and SOD = 274.1 ± 80.3; fetal CAT = 92.6 ± 82.7 and GSH-t = 0.6 ± 0.5. For G2, G. biloba treatment caused no toxicity and did not modify maternal or fetal-placental data. EGb 761 at the nontoxic dose used (200 mg kg -1 day -1 ), failed to modify the diabetes-associated increase in maternal glycemia, decrease in pregnancy rate, decrease in antioxidant enzymes, and impaired fetal development when the rats were treated throughout pregnancy (21 days).

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Increased biliary glutathione disulfide release in chronically ethanol‐treated rats

Cited by 236 publications

References 19 publications

Glutathione is required for intestinal function.

Glutathione is required for intestinal function.

Effects of aerial exposure on antioxidant defenses in the brown mussel Perna perna

Effect of Ginkgo biloba on the reproductive outcome and oxidative stress biomarkers of streptozotocin-induced diabetic rats

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