Effects of Dietary Polyunsaturated Fatty Acids on Mitochondria

Abstract

Type and quantity of ingested dietary fat contribute to the onset and progression of chronic diseases such as diabetes, obesity or arteriosclerosis. Attention is increasingly focussing on effective therapies for these diseases as well as functional foods that impede the development of insulin resistance and obesity. Studies provided evidence showing polyunsaturated fatty acids of the omega-3 and the omega-6 families play beneficial roles in prevention and treatment of diseases as diverse as Alzheimer's disease, cancer and cardiovascular diseases such as myocardial infarction, arrhythmia, atherosclerosis and hypertension. Strongest evidence is derived from in vitro experiments on cultured cells and animal-based studies, while the results from clinical studies are inconclusive. After ingestion, polyunsaturated fatty acids are distributed to cells and enriched in cellular membranes, where they influence cellular metabolism and survival. Polyunsaturated fatty acids are involved in various mitochondrial processes including mitochondrial calcium homeostasis, gene expression, respiratory function, ROS production and mitochondrial apoptosis. Therefore, mitochondria play a central role in the mechanisms underlying the protective effects of polyunsaturated fatty acids. The complex mechanisms involved in the effects of polyunsaturated fatty acid on mitochondrial actions depend on structural properties, cellular uptake, shuttling and metabolism, competition with intracellular stores as well as inherent properties of fatty acid metabolites. This review will summarize recent findings on the effects of various types of polyunsaturated fatty acids on mitochondria.

Interaction of Dietary Fatty Acids with Tumour Necrosis Factor Family Cytokines during Colon Inflammation and Cancer

“…Altered CL unsaturation and oxidative susceptibility of the mitochondrial membrane modulate the binding and activities of associated proteins, mainly of the pro- and antiapoptotic proteins of the Bcl-2 family. Changes of mitochondrial transition pore opening, decreased mitochondrial membrane potential, CL oxidation, and the release of proapoptotic cytochrome c and Apaf1 molecules are necessary for the execution of the intrinsic mitochondrial apoptotic pathway [140, 141]. Thus, in colonocytes and colon cancer cells, DHA alone or in combination with other agents can induce apoptosis by promotion of the mitochondrial apoptotic pathway as reported by us and others [131, 133, 142].…”

Effects of 6 weeks of n-3 fatty acids and antioxidant mixture on lipid peroxidation at rest and postexercise

“…The level of practice (trained men versus sedentary) and the supplement-related differences between studies could explain the difference in oxidative responses at baseline after n-3 LCPUFA supplementation (McAnulty et al 2010). Moreover, although n-3 LCPUFAs have beneficial effects in delaying the development of various diseases (Rohrbach 2009), it has been shown that their ingestion can result in increased lipid peroxidation (Guichardant et al 2006). These authors reported that the peroxidation of n-3 LCUFAs, which produces 4-hydroxy-2E-hexenal (4-HHE), is higher than the peroxidation of n-6 LCUFAs, although n-3 FAs are much lower than those of n-6 in most tissues.…”

“…Thus, it appears that the beneficial effect of n-3 PUFA supplementation on oxidative stress is controversial. Rohrbach (2009) reported that PUFAs can modulate ROS generation, but due to the complexity of their actions and the mechanisms involved, their effects are difficult to predict. McAnulty et al (2010) suggested that consumption of n-3 LCPUFAs does not increase peroxidation until a state of high oxidative stress is initiated.…”

“…The results from clinical studies are inconclusive, partially due to study design or heterogeneity in patient background. Moreover, the animal studies used very high concentrations of EPA/DHA, which is rarely the case in humans (Rohrbach 2009). Some authors have suggested that EPA and DHA supplementation in humans is more likely to exert beneficial effects (i.e., anti-inflammatory and immunomodulatory effects) in diseased patients or in those at high risk for disease than in healthy individuals (Kew et al 2003;Sijben and Calder 2007).…”

“…Several studies suggested that the very long-chain n-3 polyunsaturated fatty acids (n-3 LCPUFAs), including eicosapentanoic acid (EPA), docosahexanoic acid (DHA) and alpha-linolenic acid (ALA), have the beneficial effect of delaying the development of various diseases, such as cardiovascular disease, essential hypertension, atherosclerosis, Parkinson's disease, and Alzheimer's disease (Rohrbach 2009). More specifically, it was shown that at sufficiently high intakes, n-3 LCPUFAs decrease the production of cytokines and ROS (Bloomer and Goldfarb 2004;Rohrbach 2009), although their effect upon subsequent oxidative stress is under debate. Venkatraman et al (1998) reported that feeding both n-3 and n-6 to rats increased the activities of cytolosic catalase.…”