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.

Increased mitochondrial oxidative damage is a feature of diabetes. It has been demonstrated that the enrichment of mitochondrial membranes with low unsaturated‐fatty acids may confer resistance against deleterious effects of ROS on respiratory chain complexes (RCC). Avocado oil is rich in oleic acid, which has beneficial properties in lipid metabolism. Since diabetes is also characterized by dyslipidemia, the aim of this work was to explore if avocado oil may improve dyslipidemia and increase resistance of RCC to ROS. The daily administration of avocado oil to STZ rats at a dose equivalent to 3.5g oleic acid normalized cholesterol and triglycerides levels after 90 days. The activity of complexes III and IV from liver mitochondria of STZ rats was inhibited in 92 and 72% by 25 μM Fe2+ and avocado oil increase their resistance by 67 and 27%, respectively. Fe2+‐induced lipoperoxidation was lowered in STZ rats that consumed avocado oil. These results suggest that avocado oil consumption is beneficial at systemic and subcellular levels probably due to its high oleic acid content. The authors appreciate the financial support from CONACYT (130638 to CCR), PROMEP (PTC‐266 to CCR) and CIC‐UMSNH (2.16 to ASM)

ROS production at mitochondrial complex III (CIII) has been identified as one of the main factors leading to diabetic nephropathy. ROS production at CIII during diabetes occurs due to damage in some of its subunits, being oxidative damage a main contributor for this phenomenon. Thus, the attenuation of the damage in the CIII may serve as an approach to ameliorate diabetic renal dysfunction. Because its antioxidant content, we aimed to investigate whether avocado oil (AO) could decrease both the impairment in CIII and ROS production in kidney mitochondria from STZ‐induced diabetic rats. 90‐days of dietary AO administration prevented the impairment in CIII activity and decreased ROS production when the complex was further damaged by Fe‐induced oxidative stress. Impairment in electron flow through cytochrome c1 subunit was identified as the cause of CIII impairment and avocado oil also prevented this effect. Together, these results suggest that dietary avocado oil decrease the damage in the CIII by avoiding haem c1 destruction, which may be related with the high content of C18:1 and antioxidants in AO. This work was funded by CONACYT (130638 to CCR), and CIC‐UMSNH (CCR) grants.

Diabetes is characterized by an increase in ROS generation and impaired mitochondrial dysfunction in several tissues. Due to its high content of monounsaturated fatty acids (MUFA) and the presence of carotenoid antioxidants, we aimed to test if dietary avocado oil (AO) may attenuate ROS generation in association with a decrease in the peroxidizability index (PI) of membranes from liver and aortic mitochondria. In aortic mitochondria from diabetic rats, 90‐days administration of avocado oil induced both an 8% increment in MUFA content and a 20.6% decrease in PI when compared with the diabetic group. Moreover, a decrease of above 50% in ROS production was detected in mitochondria from the control and diabetic groups treated with AO. Regarding liver mitochondria, ROS production was 81% higher in diabetic mitochondria than in control. However, despite neither MUFA content nor PI was modified by AO treatment, the later decreased ROS generation in diabetic mitochondria at control levels. Together, these results suggest that avocado oil may decrease oxidative stress in different tissues by diverse mechanisms.