Hafeman D G, Hoekstra W G
J Nutr. 1977 Apr;107(4):656-65. doi: 10.1093/jn/107.4.656.
Dietary vitamin E, selenium (Se), and methionine were tested for their ability to inhibit carbon tetrachloride (CCL4)-induced lipid peroxidation. Peroxidation, in vivo, was monitored by the evolution of ethane, an autoxidation product of omega-3-unsaturated fatty acids. Weanling rats were fed a basal diet low in vitamin E, Se, and sulfur-containing amino acids, or diets individually supplemented with these factors. After 3 to 7 weeks, the rats were injected with CCL4 (ip) and ethane was collected for 9 hours. Cumulative ethane evolution was increased by CCl4 in all groups. Vitamin E, Se, and methionine reduced ethane evolution from CCl4-treated rats by 82%, 74%, and 60%, respectively. The toxicity of CCl4 was decreased in correlation with ethane evolution. Thus, methionine and Se, probably by maintaining intracellular glutathione and glutathione peroxidase, protected against CCl4-induced lipid peroxidation, as did vitamin E. Substitution of cod liver oil, which is rich in omega-3-unsaturated fat, for lard in the basal diet increased CCl4-induced ethane evolution six-fold. Relative inhibition by the dietary supplements was not changed. Thus, the feeding of cod liver oil greatly increased ethane production which facilitated the detection and measurement of lipid peroxidation in vivo.
对膳食中的维生素E、硒(Se)和蛋氨酸抑制四氯化碳(CCL4)诱导的脂质过氧化的能力进行了测试。体内过氧化作用通过乙烷(一种ω-3不饱和脂肪酸的自氧化产物)的释放来监测。给断奶大鼠喂食维生素E、硒和含硫氨基酸含量低的基础日粮,或分别添加这些因素的日粮。3至7周后,给大鼠腹腔注射CCL4,并收集9小时的乙烷。所有组中,CCL4均使乙烷累积释放量增加。维生素E、硒和蛋氨酸分别使CCL4处理的大鼠的乙烷释放量减少82%、74%和60%。CCL4的毒性与乙烷释放量呈负相关。因此,蛋氨酸和硒可能通过维持细胞内谷胱甘肽和谷胱甘肽过氧化物酶,像维生素E一样预防CCL4诱导的脂质过氧化。用富含ω-3不饱和脂肪的鱼肝油替代基础日粮中的猪油,使CCL4诱导的乙烷释放量增加了六倍。膳食补充剂的相对抑制作用没有改变。因此,喂食鱼肝油极大地增加了乙烷产量,这便于在体内检测和测量脂质过氧化。