Kanazawa K, Ashida H, Minamoto S, Natake M
Biochim Biophys Acta. 1986 Oct 24;879(1):36-43.
Radioactive secondary autoxidation products of linoleic acid were administered orally to rats and the incorporation of radioactive substances into lipids was investigated in the liver. The radioactive substances were significantly incorporated into hepatic mitochondrial and microsomal lipids 12 h after the administration. 80% of the radioactivity in mitochondria was detected in neutral lipids. The radioactivity in microsomal neutral lipids significantly decreased and the activity in phospholipids increased 12 h after the administration. On the other hand, contents of lipid peroxide and thiobarbituric acid reactive substances in liver were significantly increased by 40% at 15 h after the administration of the secondary autoxidation products. Activity of marker enzymes used for an indication of the hepatic injury was also elevated. Glutathione peroxidase activity increased 3-fold and catalase activity increased 1.5-fold. Activity of mitochondrial NAD-dependent aldehyde dehydrogenase, however, was decreased by 50%. It seems likely that the secondary autoxidation products orally administered are detoxified in the hepatic mitochondria, metabolized to neutral lipids, and further metabolized to phospholipids in microsomes, while as the incorporated secondary autoxidation products induces hepatic injury by lipid peroxidation.
将亚油酸的放射性二级自氧化产物经口给予大鼠，并研究肝脏中放射性物质向脂质的掺入情况。给药后12小时，放射性物质显著掺入肝线粒体和微粒体脂质中。线粒体中80%的放射性存在于中性脂质中。给药12小时后，微粒体中性脂质中的放射性显著降低，而磷脂中的活性增加。另一方面，给予二级自氧化产物15小时后，肝脏中脂质过氧化物和硫代巴比妥酸反应性物质的含量显著增加40%。用于指示肝损伤的标志物酶的活性也升高。谷胱甘肽过氧化物酶活性增加3倍，过氧化氢酶活性增加1.5倍。然而，线粒体NAD依赖性醛脱氢酶的活性降低了50%。口服给予的二级自氧化产物似乎在肝线粒体中被解毒，代谢为中性脂质，然后在微粒体中进一步代谢为磷脂，而掺入的二级自氧化产物通过脂质过氧化诱导肝损伤。
