Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Edificio B-3 Ciudad Universitaria, Morelia, Mich., México.
J Bioenerg Biomembr. 2013 Jun;45(3):271-87. doi: 10.1007/s10863-013-9502-3. Epub 2013 Feb 27.
Impaired complex III activity and reactive oxygen species (ROS) generation in mitochondria have been identified as key events leading to renal damage during diabetes. Due to its high content of oleic acid and antioxidants, we aimed to test whether avocado oil may attenuate the alterations in electron transfer at complex III induced by diabetes by a mechanism related with increased resistance to lipid peroxidation. 90 days of avocado oil administration prevented the impairment in succinate-cytochrome c oxidoreductase activity caused by streptozotocin-induced diabetes in kidney mitochondria. This was associated with a protection against decreased electron transfer through high potential chain in complex III related to cytochromes c + c1 loss. During Fe(2+)-induced oxidative stress, avocado oil improved the activities of complexes II and III and enhanced the protection conferred by a lipophilic antioxidant against damage by Fe(2+). Avocado oil also decreased ROS generation in Fe(2+)-damaged mitochondria. Alterations in the ratio of C20:4/C18:2 fatty acids were observed in mitochondria from diabetic animals that not were corrected by avocado oil treatment, which yielded lower peroxidizability indexes only in diabetic mitochondria although avocado oil caused an augment in the total content of monounsaturated fatty acids. Moreover, a protective effect of avocado oil against lipid peroxidation was observed consistently only in control mitochondria. Since the beneficial effects of avocado oil in diabetic mitochondria were not related to increased resistance to lipid peroxidation, these effects were discussed in terms of the antioxidant activity of both C18:1 and the carotenoids reported to be contained in avocado oil.
线粒体中复合物 III 活性受损和活性氧 (ROS) 生成被认为是导致糖尿病期间肾脏损伤的关键事件。由于鳄梨油含有丰富的油酸和抗氧化剂,我们旨在测试鳄梨油是否可以通过与增加脂质过氧化抗性相关的机制来减轻糖尿病引起的复合物 III 电子传递改变。90 天的鳄梨油给药可预防链脲佐菌素诱导的糖尿病引起的肾脏线粒体中琥珀酸-细胞色素 c 氧化还原酶活性的损害。这与保护细胞色素 c + c1 损失相关的复合物 III 中高势能链电子传递减少有关。在 Fe(2+)-诱导的氧化应激期间,鳄梨油改善了复合物 II 和 III 的活性,并增强了亲脂性抗氧化剂对 Fe(2+)损伤的保护作用。鳄梨油还降低了 Fe(2+)-损伤线粒体中的 ROS 生成。在糖尿病动物的线粒体中观察到 C20:4/C18:2 脂肪酸比例的改变,而鳄梨油处理并未纠正这些改变,尽管鳄梨油仅在糖尿病线粒体中降低了过氧化指数,但它导致了单不饱和脂肪酸总含量的增加。此外,鳄梨油对脂质过氧化的保护作用仅在对照线粒体中一致观察到。由于鳄梨油在糖尿病线粒体中的有益作用与增加的脂质过氧化抗性无关,因此根据 C18:1 的抗氧化活性以及据报道存在于鳄梨油中的类胡萝卜素讨论了这些作用。