Plasma cysteine, cystine, and glutathione in cirrhosis

Chawla, Rajender K.; Lewis, Frederick W.; Kutner, Michael; Bate, David; Roy, Robert G.B.; Rudman, Daniel

doi:10.1016/0016-5085(84)90069-6

Cited by 174 publications

(76 citation statements)

References 19 publications

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“…A continuous decrease in plasma glutathione is also found in the model of CCl 4 -induced cirrhosis of the rat [14]. In man, a 25% reduction of plasma glutathione is found in patients with compensated cirrhosis [2] while in decompensated cirrhosis the reduction accounts for 48% [14]. These findings suggest a correlation between the decrease of plasma glutathione and the stage of chronic liver damage or cirrhosis.…”

Section: Discussionmentioning

confidence: 68%

“…This assumption derives from the measurement of decreased glutathione plasma in cirrhotic patients [2] and the observation that plasma glutathione is directly related to hepatic glutathione content [1]. A decrease in hepatic glutathione could be caused by an increase of reactive oxygen species that, in turn, can aggravate the inflammatory process leading to liver fibrosis and cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

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Glutathione status in liver and plasma during development of biliary cirrhosis after bile duct ligation

et al. 1998

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We do not know much about the changes that occur in reduced (GSH) and oxidized (GSSG) glutathione in the development of liver cirrhosis. Therefore, we investigated the glutathione redox system during development of liver cirrhosis after bile-duct ligation in rats. We compared the GSH and GSSG content of liver and plasma between bile-duct-ligated rats and sham-operated controls 6 and 24 h and 5, 15, 23, and 38 days after operation. Compared to controls (x +/- SD: 6.07 +/- 0.52 mumol/g wet wt.), liver GSH significantly increased 24 h (+ 37%) and 5 days (+ 53%) after bile-duct ligation. Thereafter, GSH continuously declined to 4.25 +/- 0.64 mumol/g (-31%; P < 0.001) at the end of the observation period after 38 days. The GSH turnover in 5-day bile-duct-ligated rats with high GSH concentrations was not significantly different than in sham-operated controls (16 nmol/min per g after bile-duct ligation and 15 nmol/min per g in controls). GSSG (211 +/- 42 nmol/g wet wt. in controls) was significantly lower 6 and 24 h after bile-duct ligation (-34% and -43%, respectively). Thereafter, GSSG increased and was about 100% higher than in controls after 23 and 38 days. The relation of GSSG to GSH in liver continuously increased from 3.4 to 20.5% after bile-duct ligation. The course of plasma GSH (9.57 +/- 0.79 mumol/l) paralleled hepatic GSH on a lower level: + 14% at day 5, -41% at day 15 and -51% at the end of the observation period. Plasma GSSG (0.99 +/- 0.31 mumol/l) was inversely related to liver GSSG: there were increased concentrations early after bile duct ligation (day 5: + 91%) and reduced concentrations (-44%) at the end of the observation period. Dynamic changes of the glutathione status occur in the development of liver cirrhosis after bile-duct ligation. These changes are consistent with increased oxidative stress in the liver and a deficit of transporting GSSG from the cells into plasma.

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Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Glutathione status in liver and plasma during development of biliary cirrhosis after bile duct ligation

et al. 1998

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“…This provides the basis for the prophylactic use of OTC against a wide variety of changed physiological conditions. Conditions where OTC treatment may be useful include physiological states that adversely affect plasma GSH concentrations, such as hepatic dysfunction [27], or those that affect the epithelial cells which can utilize exogenous GSH for protection [28][29][30][31]. However, clinical trials will be needed to determine the effectiveness of therapeutic OTC treatment in humans.…”

Section: Discussionmentioning

confidence: 99%

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent redox changes in rat’s blood plasma

et al. 2011

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In the present study, we investigated both the age- and heat exposure-related redox changes of blood plasma by analyzing GSH, thiol status and carbonyl groups. Our results clearly indicated that the plasma redox balance shifted toward oxidation during both aging and acute heat exposure. To further confirm this age- and heat exposure-related redox shift, we quantified the changes in thiol content. The total thiol level was found to be significantly decreased in the aged group. A similar pattern can be explained by low levels of serum GSH in old rats compared to young rats. The significance of the present study are the data showing increased oxidative stress in plasma during aging, attributed to a decrease in major antioxidant components in serum. OTC treatment, in relation to C=O regarded as a marker of oxidative damage was probably much more effective in increasing of GSH synthesis than in prevention of protein oxidation.

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“…In addition, hepatic transulphuration pathway is impaired in fibrosis hindering the conversion of methionine to cysteine, which is necessary for GSH synthesis (7). L-carnitine's stimulation of hepatic GSH can be linked to the energy enhancing action by increasing ATP needed for synthesis of GSH (25).…”

Section: Discussionmentioning

confidence: 99%

Comparison of vitamin E, L-carnitine and melatonin in ameliorating carbon tetrachloride and diabetes induced hepatic oxidative stress

et al. 2009

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This study aimed to investigate whether treatments with vitamin E, L-carnitine and melatonin can protect against CCl(4) and diabetes-induced hepatic oxidative stress. Hepatic oxidative stress was performed in rats through 50% v/v carbon tetrachloride (CCl(4)) (1 ml/kg/3 days, i.p.), and through diabetes mellitus induced by streptozotocin (STZ) (40 mg/kg, i.p.). Vitamin E (100 mg/kg/day, i.p), L-carnitine (300 mg/kg/day, i.p.) and melatonin (10 mg/kg/day, i.p.) were injected for a period of 6 weeks. Thereafter, changes in serum glucose level, liver function tests, hepatic malondialdehyde (MDA) content, hepatic reduced glutathione (GSH) content, hepatic superoxide dismutase (SOD) activity, and serum total antioxidant capacity (TAC) level were evaluated. In CCl(4)-induced liver fibrosis, the efficacy order was melatonin > L-carnitine > vitamin E, while in STZ-induced diabetes, the efficacy order was vitamin E > or = melatonin > L-carnitine. In conclusion, these data indicate that low dose of melatonin is more effective than high doses of vitamin E and L-carnitine in reducing hepatic oxidative stress induced by CCl(4) and diabetes. Moreover, the potent effect of vitamin E in ameliorating diabetes can be linked not only to the antioxidant actions, but also to the superior effect in reducing diabetes-induced hyperglycaemia. Meanwhile, potency of L-carnitine was nearly the same in CCl(4) and diabetes-induced liver damage.

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Plasma cysteine, cystine, and glutathione in cirrhosis

Cited by 174 publications

References 19 publications

Glutathione status in liver and plasma during development of biliary cirrhosis after bile duct ligation

Glutathione status in liver and plasma during development of biliary cirrhosis after bile duct ligation

l-2-oxothiazolidine-4-carboxylate influence on age- and heat exposure-dependent redox changes in rat’s blood plasma

Comparison of vitamin E, L-carnitine and melatonin in ameliorating carbon tetrachloride and diabetes induced hepatic oxidative stress

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