[Effect of exogenous nitric oxide on antioxidants from mice infected with ].

OBJECTIVE

To study the effect of exogenous nitric oxide donor sodium nitroprusside (SNP) on antioxidant enzymes activities and lipid peroxidation of mice infected with .

METHODS

BALB/c mice were infected with separated by the digestion method. Forty-two days post-infection, the peripheral blood and hepatic tissue from the infected or normal mice were collected. Then 4 groups were set：liver homogenate from infected mice + SNP (Group A), liver homogenate from normal mice + SNP (Group B), peripheral blood from infected mice + SNP (Group C), and peripheral blood from normal mice + SNP (Group D). The final concentrations of SNP in each group were set as 0 (blank control), 2, 5, 10 μmol/L and 30 μmol/L, respectively. After reacting with SNP at 37 ℃ for 30 min, the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities, and malondialdehyde (MDA) concentration were examined and compared.

RESULTS

The levels of SOD, CAT, GSH-Px and MDA concentration in the liver and the blood from the mice infected with were significantly higher than those of the normal ones (all < 0.05). When reacted with 10 μmol/L and 30 μmol/L SNP, the SOD, GSH-Px, and CAT activities in Group A and B decreased significantly (all < 0.05), while the liver MDA concentration reacted with 2-30 μmol/L SNP increased obviously (all < 0.05). As reacted with 30 μmol/L SNP, the activities of blood SOD, GSH-Px, and CAT in Group C and D decreased, while the MDA concentration in blood still increased (all < 0.01). When the SNP concentration was in the range of 2-30 μmol/L, there were a negative correlation between the SNP concentrations and SOD, GSH-Px, and CAT activities, as well as a positive correlation with the MDA concentration in the liver and blood from the mice infected with (all < 0.05).

CONCLUSIONS

infection could cause oxidative damage to mice, and increase SOD, GSH-Px, and CAT activities. Nitric oxide released from SNP can decrease antioxidase activities, and inhibit the antioxidant capacity of mice infected with .