抗坏血酸对染砷小鼠肝脏氧化损伤拮抗作用

Antagonistic effect of ascorbic acid on oxidative damage induced by arsenic in mice

目的研究抗坏血酸(VC)对砷中毒小鼠肝脏中丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的影响。方法用硫代巴比妥酸法测定丙二醛(MDA)含量;用Nitrite-kit法检测SOD活性;用二硫双硝基苯酸(DTNB)比色法测定GSH含量。结果对照组MDA含量为14.87 nmol/(mg.prot),SOD活力为167.49NU/(mg.prot),GSH含量为51.27 nmol/(mg.prot);20μmol/L染砷组小鼠肝脏中MDS含量明显增高,为18.48nmol/(mg.prot),SOD活力明显下降,为125.97 NU/(mg.prot),GSH含量也显著降低,为34.87 nmol/(mg.prot);而抗坏血酸拮抗组小鼠肝脏中MDS含量与单纯染砷组相比明显下降,为16.24 nmol/(mg.prot),但未达到对照组水平;SOD活力明显增高,为138.94 NU/(mg.prot),但未达到对照组水平,GSH含量显著增高,为50.39 nmol/(mg.prot),与对照组比较差异无统计学意义。结论抗坏血酸可拮抗砷对小鼠肝脏的氧化损伤。

Objective To explore the effects of ascorbic acid on the content of MDA, activity of SOD and content of GSH in arsenic poisoning mice. Methods The malonaldehyde （MDA） content was detected by thio-barbituric acid method. Superoxide dismutase （SOD） activity was determined by nitrite-kit. Glutathione （GSH） content was detected by dinitrothiocyanobenzene chromatometry. Results The content of MDA in control group was 14. 87 nmol/mg · prot;SOD activity was 167.49 NU/mg · prot;GSH content was 51.27 mnol/mg ·prot. In 20μnoL/L arsenite treated group,the MDA increased to 18. 48 nmol/mg ~ prot;SOD activity decreased to 125. 97NU/mg · prot;and GSH content decreased to 34. 87 nmol/mg · prot. In the ascorbic acid treated group, the MDA content decreased to 16. 24nmol/mg · prot; SOD activity increased to 138. 94 NU/mg · prot; GSH content increased to 50. 39 nmol/mg · prot. Conclusion Ascorbic acid can alleviate the oxidative damage induced bv arsenic in mice liver.