Plasmatic vitamin C in nontreated hepatitis C patients is negatively associated with aspartate aminotransferase.

OBJECTIVES: To evaluate the possible relationship between aminotransferases levels and markers of oxidative stress in chronic hepatitis C patients. DESIGN AND METHODS: Patients without treatment for hepatitis were divided in to group I (15-39 U/L); group II (41-76 U/L) and group III (81-311 U/L) of activity alanine aminotransferase (ALT). Blood markers of oxidative stress [catalase (CAT), glutathione peroxidase (GPx), thiobarbituric acid-reactive species (TBARS), nonprotein and protein thiol (NP-SH and P-SH) groups and vitamin C] were determined. RESULTS: P-SH and NP-SH levels, TBARS, GPx and CAT were not different between groups. Vitamin C was significantly decreased in groups II (P=0.03) and III (P=0.001) when compared with group I and correlated negatively with aspartate aminotransferase (AST; r=-0.29, P=0.042). CONCLUSION: Vitamin C levels were negatively associated with AST, suggesting that vitamin C could be an additional indicator of hepatitis C severity.

A single high dose of ascorbic acid and iron is not correlated with oxidative stress in healthy volunteers.

Fe (II) is a potential prooxidant in vivo and can induce cellular oxidative stress. Ascorbic acid (AA) is a powerful physiological antioxidant and, in the presence of free Fe (II), can exhibit prooxidant effects in vitro. However, in vivo prooxidant effects of Fe (II) and AA have not yet been indisputably demonstrated. Here we evaluate the potential toxic effect of supplementation of Fe (II) associated with AA. Nine healthy, nonsmoking male volunteers (20-31 years old) participated in the crossover study design. The volunteers were supplemented with either a dose of 2 g of AA, 150 mg of iron carbonyl or 2 g of AA plus 150 mg of iron carbonyl with a washout period of 15 days between each treatment. AA, iron, ferritin, thiobarbituric acid-reactive substances, catalase, delta-aminolevulinic dehydratase and SH thiol groups were measured in the blood of the volunteers. Plasma AA levels were increased at 2, 5 and 24 h after AA or AA plus iron ingestion. Plasma Fe levels were increased at 2 and 5 h in the AA plus iron group. Erythrocyte malondialdehyde levels decreased at 5 and 24 h after AA and 5 h after AA plus iron ingestion. Catalase activity from erythrocytes was increased 5 h after supplementation with AA plus iron. There was no significant difference between groups in the other biochemical parameters evaluated. Thus, the present study does not support the hypothesis that the combination of high plasma concentrations of AA and iron, or iron alone, could cause in vivo oxidative damage after a single supplementation dose.