Dietary omega-3 fatty acids do not change resistance of rat brain or liver mitochondria to [Ca.sup.2+] and/or prooxidants

• Published in: Journal of lipids
• Main Authors: Stavrovskaya, Irina G, Bird, Susan S, Marur, Vasant R, Baranov, Sergei V, Greenberg, Heather K, Porter, Caryn L, Kristal, Bruce S
• Format: Journal Article
• Language: English
• Published: John Wiley & Sons, Inc 01.09.2012
• Subjects: Analysis; Health aspects; Mitochondria; Omega-3 fatty acids; Physiological aspects
• DOI: 10.1155/2012/797105
• ISSN: 2090-3030

Omega-3 polyunsaturated fatty acids (n-3 PUFAs) block apoptotic neuronal cell death and are strongly neuroprotective in acute and chronic neurodegeneration. Theoretical considerations, indirect data, and consideration of parsimony lead to the hypothesis that modulation of mitochondrial pathway(s) underlies at least some of the neuroprotective effects of n-3 PUFAs. We therefore systematically tested this hypothesis on healthy male FBFN1 rats fed for four weeks with isocaloric, 10% fatcontaining diets supplemented with 1, 3, or 10% fish oil (FO). High resolution mass spectrometric analysis confirmed expected dietdriven increases in docosahexaenoic acid (DHA, 22:6, n-3) and eicosapentaenoic acid (EPA, 20:5, n-3) in sera, liver and nonsynaptosomal brain mitochondria. We further evaluated the resistance of brain and liver mitochondria to [Ca.sup.2+] overload and prooxidants. Under these conditions, neither mitochondrial resistance to [Ca.sup.2+] overload and prooxidants nor mitochondrial physiology is altered by diet, despite the expected incorporation of DHA and EPA in mitochondrial membranes and plasma. Collectively, the data eliminate one of the previously proposed mechanism(s) that n-3 PUFA induced augmentation of mitochondrial resistance to the oxidant/calcium-driven dysfunction. These data furthermore allow us to define a specific series of follow-up experiments to test related hypotheses about the effect of n-3 PUFAs on brain mitochondria.