Ruidera E, Irazu C E, Rajagopalan P R, Orak J K, Fitts C T, Singh I
Medical University of South Carolina, Charleston 29425.
Lipids. 1988 Sep;23(9):882-4. doi: 10.1007/BF02536209.
The increase in free fatty acids in the ischemic tissue is a consistent observation and these free fatty acids are considered to play a role in the cellular toxicity. To elucidate the cause of higher levels of free fatty acids in ischemic tissue, we examined the catabolism of fatty acids. The beta-oxidation of lignoceric (24:0), palmitic (16:0) and octanoic (8:0) acids and the peroxidation of fatty acids were measured at different times of renal ischemia in whole kidney homogenate. The enzymatic activities for the oxidation of fatty acids decreased with the increase in ischemia time. However, the lipid peroxide levels increased 2.5-fold of control with ischemic injury. Sixty min of ischemia reduced the rate of oxidation of octanoic, palmitic and lignoceric acids by 57, 59 and 69%, respectively. Almost similar loss of fatty acid oxidation activity was observed in the peroxisomes and mitochondria. These data suggest that loss of mitochondrial and peroxisomal fatty acid beta-oxidation enzyme activities from ischemic injury may be one of the factors responsible for the higher levels of free fatty acids.
缺血组织中游离脂肪酸的增加是一个一致的观察结果,这些游离脂肪酸被认为在细胞毒性中起作用。为了阐明缺血组织中游离脂肪酸水平升高的原因,我们研究了脂肪酸的分解代谢。在肾缺血的不同时间,对全肾匀浆中二十四烷酸(24:0)、棕榈酸(16:0)和辛酸(8:0)的β-氧化以及脂肪酸的过氧化进行了测定。脂肪酸氧化的酶活性随着缺血时间的增加而降低。然而,脂质过氧化物水平随着缺血损伤增加至对照的2.5倍。缺血60分钟使辛酸、棕榈酸和二十四烷酸的氧化速率分别降低了57%、59%和69%。在过氧化物酶体和线粒体中观察到几乎相似的脂肪酸氧化活性丧失。这些数据表明,缺血损伤导致线粒体和过氧化物酶体脂肪酸β-氧化酶活性丧失可能是游离脂肪酸水平升高的原因之一。