Tappel A L
Ann N Y Acad Sci. 1980;355:18-31. doi: 10.1111/j.1749-6632.1980.tb21324.x.
Some of the vitamins and many of the metals that are being considered at this symposium interact in lipid peroxidation. Some of these interactions have been studied in vivo. Measurement of in vivo lipid peroxidation in the rat is accomplished by gas chromatographic analysis of pentane, a minor peroxidation product that is exhaled in the breath. In the rat, lipid peroxidation is proportional to dietary polyunsaturated lipids when the animal is deficient in antioxygenic agents. The chain-breaking antioxidant vitamin E is the main protector against in vivo lipid peroxidation. Dietary selenium, through its involvement in the biosynthesis of glutathione peroxidase, functions in a secondary antioxygenic role as a hydroperoxide reducer. In rats fed a vitamin E-deficient diet, injection of some hydroperoxides, iron, or vitamin C leads to initiation of in vivo lipid peroxidation, apparently by decomposing hydroperoxides to free radicals. Carbon tetrachloride, a toxic halogenated hydrocarbon, is metabolized by liver microsomes and initiates in vivo lipid peroxidation in the liver. These examples show that practical information on interactions involving in vivo lipid peroxidation can be obtained by studies that use the pentane method.
本次研讨会所探讨的一些维生素和多种金属在脂质过氧化过程中相互作用。其中一些相互作用已在体内进行了研究。通过对戊烷进行气相色谱分析来测定大鼠体内的脂质过氧化,戊烷是一种呼出的微量过氧化产物。在大鼠中,当动物缺乏抗氧化剂时,脂质过氧化与膳食中的多不饱和脂质成正比。具有断链作用的抗氧化维生素E是体内脂质过氧化的主要保护剂。膳食中的硒通过参与谷胱甘肽过氧化物酶的生物合成,作为氢过氧化物还原剂发挥次要的抗氧化作用。在喂食缺乏维生素E饮食的大鼠中,注射某些氢过氧化物、铁或维生素C会引发体内脂质过氧化,显然是通过将氢过氧化物分解为自由基来实现的。四氯化碳是一种有毒的卤代烃,可被肝微粒体代谢并引发肝脏中的体内脂质过氧化。这些例子表明,通过使用戊烷法的研究可以获得有关体内脂质过氧化相互作用的实用信息。