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The polyunsaturated nature of n-3 fatty acids makes them prone to oxidative damage. However, it is not clear if n-3 fatty acids are simply a passive site for oxidative attack or if they also modulate mitochondrial reactive oxygen species (ROS) production. The present study used  fat-1  transgenic mice, that are capable of synthesizing n-3 fatty acids, to investigate the influence of increases in n-3 fatty acids and resultant decreases in the n-6∶n-3 ratio on liver mitochondrial H 2 O 2  production and electron transport chain (ETC) activity. There was an increase in n-3 fatty acids and a decrease in the n-6∶n-3 ratio in liver mitochondria from the  fat-1  compared to control mice. This change was largely due to alterations in the fatty acid composition of phosphatidylcholine and phosphatidylethanolamine, with only a small percentage of fatty acids in cardiolipin being altered in the  fat-1  animals. The lipid changes in the  fat-1  mice were associated with a decrease ( p <0.05) in the activity of ETC complex I and increases ( p <0.05) in the activities of complexes III and IV. Mitochondrial H 2 O 2  production with either succinate or succinate/glutamate/malate substrates was also decreased ( p <0.05) in the  fat-1  mice. This change in H 2 O 2  production was due to a decrease in ROS production from ETC complex I in the  fat-1  animals. These results indicate that the fatty acid changes in  fat-1  liver mitochondria may at least partially oppose oxidative stress by limiting ROS production from ETC complex I.

Complex I-Associated Hydrogen Peroxide Production Is Decreased and Electron Transport Chain Enzyme Activities Are Altered in n-3 Enriched fat-1 Mice