Aortic Mitochondria Research Articles

Effect of avocado oil on fatty acid profile and ROS generation in liver and aortic mitochondria from diabetic rats

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.

Differential effects of exercise on aortic mitochondria

Routine exercise is widely recognized as cardioprotective. Exercise induces a variety of effects within the cardiovasculature, including decreased mitochondrial damage and improved aerobic capacity. It has been generally thought that the transient increase in oxidative stress associated with exercise initiates cardioprotective processes. Somewhat paradoxically, increased oxidative stress associated with cardiovascular disease (CVD) risk factors is thought to play an important role in the promotion and development of CVD. Hence, it is possible that CVD risk factors that increase oxidative stress (e.g., hypercholesterolemia) may modulate the cardioprotective effects of exercise. In this regard, the interaction between CVD risk factors and exercise on atherosclerotic lesion development and basal oxidant load is less defined. To determine the influence of preexistent hypercholesterolemia on cardioprotective effects of exercise, atherosclerotic lesion formation, oxidant load, mitochondrial damage, protein nitration (3-nitrotyrosine levels), and mitochondrial enzyme activities were determined in aortic tissues from normocholesterolemic (C57 control) and hypercholesterolemic [apoliprotein E-deficient (apoE(-/-))] mice after 16 wk of regular exercise. In normocholesterolemic mice, regular exercise was associated with decreased mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities. Exercise did not decrease endogenous oxidant load and mitochondrial damage in hypercholesterolemic mice and did not reduce atherosclerotic lesion development. These data are consistent with the notion that CVD risk factors associated with increased oxidative stress can alter the benefits of exercise and that mitochondrial damage appears to be correlated with the cardiovascular effects of exercise.

Mitochondrial ca 2+ metabolism in aortic smooth muscle of swine. effect of mild hypercholesterolemia

The rate of ATP supported Ca 2 uptake by mitochondria isolated from normal swine aorta was found to be influenced by Ca 2+, ATP, protein and H + concentrations. V max was not reached even at 273 μM, the highest [Ca +] tested. Initial rate of uptake at this concentration was 1200 nmoles/min/mg and maximal uptake was 1400 nmoles/mg. At a mitochondrial protein concentration of 90 μg/ml and 118 μM Ca 2+, the pH optimum for uptake was 7.5 and optimal ATP was 1.2-2.3 mM. These conditions were used to investigate Ca 2+ uptake in aortic mitochondria from swine with mild hypercholesterolemia and minimal atherosclerosis. The initial rate of uptake by mitochondria from the hypercholesterolemic swine was significantly less than control (152 ± 13 vs 205 ± 20 nmoles/min/mg). Maximal uptake, however, which occurred by 15 min (519 ± 38 vs 570 ± 42 nmoles Ca 2+/mg protein for hypercholesterolemic vs control) was not significantly different in the two groups. Ca 2+ control of O 2 uptake was slightly, but significantly lower in mitochondria from the experimental swine aortas. Cytochrome oxidase activities were not different, but monoamine oxidase activity was significantly less in the experimental group. Since the amount of aortic atherosclerosis was minimal, it seems unlikely that the changes were brought about by mitochondria from atherosclerotic lesion areas alone. More likely, the hypercholesterolemia had a diffuse effect on aortic smooth muscle cells which in turn altered mitochondrial Ca 2+ uptake.

The presence of the glycerol phosphate shuttle and energy dependent transhydrogenase in aortic mitochondria

A procedure has been devised for isolating tightly coupled mitochondria from the intima-media strip of pig aorta. The mitochondria exhibit respiratory control with succinate, pyruvate-malate, β-hydroxybutyrate or α-glycerol phosphate as substrate. Furthermore, submitochondrial particles from these preparations exhibit an energy-dependent reduction of NADP + by NADH.

INCORPORATION OF TRITIUM FROM SUCCINATE-2,3-H3 INTO LONG CHAIN FATTY ACIDS BY AORTIC MITOCHONDRIA.

SummaryThe mechanism of succinate stimulation of fatty acid synthesis by aortic mitochondria was studied. Tritium, but not carbon, from succinate labeled in positions 2- and 3- is incorporated into long-chain fatty acids in this system. The relative incorporation of tritium in various fatty acids is similar to that of C14 from acetate. Succinate can, therefore, provide protons for the reductive steps. We believe this is a demonstration of energy-requiring reversal of electron flow participating in a synthetic process and another way in which Krebs Cycle acids can influence fatty acid synthesis.