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Objective: To investigate the effect of ascorbic acid [vitamin C (VC)] on liver damage parameters in the lead-exposed mice, when given in combination with thiamine [vitamin B1 (VB(1))] at different concentrations., Methods: Sixty-six male mice were randomly assigned into 11 groups (n = 6). Mice in Group I were supplied with only the tap water as the drinking water; mice in Group II were provided with a tap water containing 0.2% lead acetate; mice in Group III-XI were given different dose of VC (140, 420, 1260 mg kg(-1) bw) and VB(1) (10, 30, 90 mg kg(-1) bw) according to 3 x 3 factorial design by oral gavages, along with ingestion of 0.2% lead acetate. After 42 test days, DNA damage of liver cells was assessed using single-cell gel electrophoresis. The apoptosis rate of liver cells was determined by flow cytometry. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in blood and the level of reduced glutathione (GSH) in liver cells were measured based on individual biochemical reactions., Results: Compared with the Group I, sub-chronic lead ingestion (Group II) resulted in a significant decrease of Hb, GSH-P(X), SOD in blood and GSH level in liver cells; lead exposure induced also a significant increase in DNA damage and apoptosis of liver cells (P < 0.05). Supplementation with VC and VB(1), however, reversed these effects. The best effective combination was VC (420 mg kg(-1) bw) and VB(1) (10 mg kg(-1) bw), followed by the combination of VC (420 mg kg(-1) bw) and VB(1) (30 mg kg(-1) bw). But no reversion was shown in the combination of the highest combination of VC (1260 mg kg(-1)) and VB(1) (90 mg kg(-1))., Conclusions: These findings strongly indicated that combination of VC and VB(1) can lessen the damage to liver cells from oxidative stress induce by lead, but the antioxidant effects are dependent on their concentrations.

Background: Lead is a ubiquitous environmental and industrial pollutant that may have toxic effects on the male reproductive system. We explored the mechanism and examine the impacts of combined administration of ascorbic acid and thiamine at different levels on apoptosis in the testes of lead-exposed mice., Methods: Seventy-five male mice were randomly divided into 5 groups (15 mice/group): control, lead-treated and vitamin-treated group (low, middle and high dose) with ascorbic acid (140, 420, 1260 mg/kg) and thiamine (10, 30, 90 mg/kg ) by oral gavage daily. All lead-exposed animals received 0.2% lead acetate in drinking water. DNA damage of testicular cells was assessed by SCGE; the levels of TGFbeta1 and caspase-3 were detected by immunohistochemistry; apoptotic cell was determined by TUNEL., Results: Compared with control group, the expressions of TGFbeta1 and caspase-3, apoptotic index (AI) and DNA damage were increased significantly in lead-exposed group (P<0.05). After intervention of low and middle doses vitamin, the incidence of DNA damage and the number of apoptotic cells in testis were obviously lower than the lead-exposed group (P<0.05) and the impaired tissues were ameliorative. However, simultaneous supplementation of ascorbic acid and thiamine at the highest dose promoted testicular cell apoptosis via increased expressions of TGFbeta1 and caspase-3., Conclusions: The combination treatment with thiamine and ascorbic acid at lower doses effectively inhibited testicular cells from apoptosis by lead acetate, but higher doses could aggravate the testicular lesion.