5/16/2023 0 Comments Lost in random ending![]() A previous animal study indicated that inadequate vitamin B-6 caused a reduction in the GSH level, as well as the activities of GSH-Px and GSH-Rd in the liver tissue of rats. Since the liver is the main site for the storage and metabolism of vitamin B-6, deficient vitamin B-6 may indirectly interfere with GSH synthesis, and subsequently affect the antioxidant capacities of GSH and its related enzymes. ![]() ![]() However, no oral GSH supplementation has been implicated in liver cirrhosis patients, and the efficacy of oral GSH supplementation on oxidative stress and antioxidant capacities has not yet been determined.Īs the rate-limiting substrate for GSH biosynthesis, cysteine can either be obtained from the diet or through the transsulfuration pathway for the conversion of homocysteine to cysteine via pyridoxal 5′-phsophate (PLP, the physiological coenzyme form of vitamin B-6) acting as an essential coenzyme. The GSH supplemented period appears to be crucial for effectiveness and a minimum of three months is necessary for healthy subjects. Although four weeks supplementation of oral GSH (1000 mg/d) neither changes the erythrocyte GSH concentration nor reduces the level of oxidative stress indicators in healthy adults, the plasma GSH concentration was shown to be significantly increased after three and six months of oral GSH supplementation (1000 mg/d) in healthy subjects. Liver dysfunction appears to impair GSH synthesis, and the increment of GSH status might be effective in maintaining the GSH level and its related antioxidant capacities for patients with liver cirrhosis. observed that patients with non-alcoholic fatty liver disease had significantly lower levels of GSH and GSH-Px activity when compared to healthy controls. Since the liver is the mainstay of total body GSH turnover and accounts for greater than 90% of GSH inflow into the systemic circulation, the endogenous GSH basal appearance rate in cirrhotic patients have been reported to have a 50% reduction compared to healthy subjects, and the GSH appearance rate is significantly correlated with liver function. GSH is mainly synthesized by cysteine, glycine, and glutamate in the liver, and is oxidized to glutathione disulfide (GSSG) via GSH-Px, and is reduced back to GSH by GSH-Rd. Glutathione (GSH) and its related enzymes are well known antioxidants of human body that capture toxic electrophilic xenobiotics and scavenge free radicals. Although the decreased GSH and its related enzyme activity were associated with the severity of liver cirrhosis, vitamin B-6 and GSH supplementation had no significant effect on reducing oxidative stress and increasing antioxidant capacities. High levels of GSH, a high GSH/oxidized GSH ratio, and high GSH-St activity at baseline (Week 0) had a significant effect on low Child–Turcotte–Pugh scores at Week 0, the end of supplementation (Week 12), and the end of follow-up in all patients after adjusting for potential confounders. The median follow-up time was 984 d, and 21 patients were lost to follow-up. ![]() Neither vitamin B-6 nor GSH supplementation had significant effects on indicators of oxidative stress and antioxidant capacities. After the end of supplementation, the condition of patient’s disease severity was followed until the end of the study. In total, 61 liver cirrhosis patients were randomly assigned to placebo, vitamin B-6 (50 mg pyridoxine/d), GSH (500 mg/d), or B-6 + GSH groups for 12 weeks. We followed patients after the end of supplementation to evaluate the association of vitamin B-6 and GSH with disease severity. Since liver cirrhosis is often associated with increased oxidative stress and decreased antioxidant capacities, we conducted a double-blind randomized controlled trial to assess the antioxidative effect of vitamin B-6, GSH, or vitamin B-6/GSH combined supplementation in cirrhotic patients. Vitamin B-6 and glutathione (GSH) are antioxidant nutrients, and inadequate vitamin B-6 may indirectly limit glutathione synthesis and further affect the antioxidant capacities. ![]()
0 Comments
Leave a Reply. |