摘要
In this study,we isolated a polysaccharide from Branchiostoma belcheri (PBB) by enzymatic protein hydrolysis and alcohol precipitation.We investigated the effects of PBB supplementation on DNA oxidation and growth of the transplanted tumor cells Sarcoma (S180) in mice.Sixty healthy Kunming mice weighing between 18 and 25 g were randomly assigned to 6 groups,each consisting of 10 animals.All the mice,except for the blank control group,were inoculated with S180 sarcoma cells into the axilla of the left foreleg.PBB was given to mice by gavage at doses of 0 (model control),25,50,or 100 mg/kg b.w.in 0.2 ml saline for 30 days.The fifth group of S180-mice was given cytoxan (50 mg/kg) by peritoneal injection as a positive control group.The animals had free access to food and water.The mice were sacrificed after the final treatment and blood was quickly collected.Spontaneous and oxidized DNA damage of peripheral lymphocytes induced by H2O2 were analyzed by SCGE.O6-methyl-guanine (O6-MeG) was measured by high-performance capillary zone electrophoresis.The average tumor weights (0.856-1.118 g) of the three PBB groups were significantly lower than that of the model control group (1.836 g) (p<0.05).The tumor inhibition ratios of the PBB groups were 39.1%-53.4% and similar to the cytoxan positive group (57.5%).There were no significant differences in spontaneous DNA damage in peripheral lymphocytes among the groups.The oxidative DNA damage induced by 10 μmol/L H2O2 in the 50 and 100 mg/kg b.w.groups were 246.1 AU and 221.7 AU,respectively,both of which were significantly lower than that in the model group (289.0 AU;p<0.05).The plasma concentrations of O6-MeG in the 25,50,and 100 mg/kg supplemented groups were 2.09 μmol/L,1.86 μmol/L,and 1.63 μmol/L,respectively,all of which were significantly lower than that of the model group (2.67 μmol/L;p<0.05).These results indicated that PBB may have antioxidative activity and thus reduce oxidation-induced DNA damage.
In this study, we isolated a polysaccharide from Branchiostoma belcheri （PBB） by enzymatic protein hydrolysis and alcohol precipitation. We investigated the effects of PBB supplementation on DNA oxidation and growth of the transplanted tumor cells Sarcoma （S180） in mice. Sixty healthy Kunming mice weighing between 18 and 25 g were randomly assigned to 6 groups, each consisting of 10 animals. All the mice, except for the blank control group, were inoculated with S180 sarcoma cells into the axilla of the left foreleg. PBB was given to mice by gavage at doses of 0 （model control）, 25, 50, or 100 mg/kg b.w. in 0.2 ml saline for 30 days. The fifth group of S180-mice was given cytoxan （50 mg/kg） by peritoneal injection as a positive control group. The animals had free access to food and water. The mice were sacrificed after the final treatment and blood was quickly collected. Spontaneous and oxidized DNA damage of peripheral lymphocytes induced by H2O2 were analyzed by SCGE. O6-methyl-guanine （O6-MeG） was measured by high-performance capillary zone electrophoresis. The average tumor weights （0.856-1.118 g） of the three PBB groups were significantly lower than that of the model control group （1.836 g） （p〈0.05）. The tumor inhibition ratios of the PBB groups were 39.1%-53.4% and similar to the cytoxan positive group （57.5%）. There were no significant differences in spontaneous DNA damage in peripheral lymphocytes among the groups. The oxidative DNA damage induced by 10 μmol/L H2O2 in the 50 and 100 mg/kg b.w. groups were 246.1 AU and 221.7 AU, respectively, both of which were significantly lower than that in the model group （289.0 AU; p〈0.05）. The plasma concentrations of O6-MeG in the 25, 50, and 100 mg/kg supplemented groups were 2.09 μmol/L, 1.86 μmol/L, and 1.63 lamol/L, respectively, all of which were significantly lower than that of the model group （2.67 μmol/L; p〈0.05）. These results indicated that PBB may have antioxidative activity and thus reduce oxidation-induced DNA damage.
