摘要
为进一步探讨亚硝胺通过过氧化物而致癌的可能途径,以及VB2和β-C联用可能通过抑制脂质过氧化反应而影响亚硝胺致癌的机制,给予二甲基亚硝在(NDMN),同时补充核黄素和β-胡萝卜素,观察大鼠体内抗氧化酶活性和脂质过氧化物含量的变化.结果显示:NDMN可使大鼠血红细胞、肝肾匀浆SOD活性和全血GSH-Px活性下降,血清、肝肾匀浆MDA和血清ROOH产生增多.同时添加核黄素和β-胡萝卜素后,红细胞和肝匀装SOD活性、全血GSH-Px活性显著高于NDMN组.血清、肝匀浆MDA含量和血清ROOH含量显著低于NDMN组.表明该黄素和β-胡萝卜素联用可对抗由NDMN引发的脂质过氧化,提示核黄素和β-胡萝卜素联用有预防NDMN致癌的作用.
篒n order to explore the possible way of carcinogenesis induced by nitrosamines and the inhibition of Lipid peroxidation by VB2 and β-C, the change of anti-oxidase activity andthe content of Lipid peroxide in rats were observed. The results showed that compared withthe control group, the activities of SOD and GSH-Px in NDMN group were significantly decreased (P<0. O5),and the concentration of MDA and ROOH increased(P<0. 05). After thegroup was given VB, and β-C simultaneously, the activities of GSH-Px in blood as well asSOD in RBC and liver were significantly higher than that of NDMN group (P<0. 05), andconcentrations 0f ROOH in serum as well as MDA in serum and liver signifcantly were lowerthan that of NDMN group(P<O.O5). These results suggest that free radicals and lipid peroxidatiion may be involved in carcinogenic development of NDMN and other nitrosamines;VB2 and β-C have the ability to inhibite the lipid peroxidation induced by NDMN.
出处
《实用预防医学》
CAS
1998年第3期133-135,共3页
Practical Preventive Medicine
基金
广东省医药卫生青年科研基金!NO:2230317
中山医科大学学生业余科研基金!NO:2011001联合资助项目