Several studies have shown the protective effects of dietary enrichment of omega-3 (ω-3) long-chain fatty acids in several animal models of neurodegenerative diseases. Here we investigate if eicosapentaenoic (EPA) and Docosahexaenoic (DHA) acids (ω-3) protect against neurodegeneration mediated by the exposure to a widely used herbicide Paraquat (PQ) (1,1ʹ-dimethyl-4-4ʹ-bipyridinium dichloride), focusing on mitochondrial metabolism using Drosophila melanogaster as a model. Dietary ingestion of PQ for 3 days resulted in the loss of citrate synthase content, respiratory capacity impairment and exacerbated H₂O₂ production per mitochondrial unit related to complex I dysfunction, and high lactate accumulation in fly heads. PQ intoxication lead to 1) the loss of ELAV (embryonic lethal abnormal vision) and α-spectrin, essential proteins of neuronal viability and synaptic stability; 2) increased gamma-secretase activity, an enzyme related to APP release; and 3) increased the amyloid fibrils contents. All these toxic effects induced by PQ were prevented by concomitant dietary ingestion of EPA/DHA, suggesting that a neuroprotective effect of ω-3 also involves mitochondrial protection. In conclusion, concomitant EPA and DHA ingestion protects against PQ-induced neuronal and mitochondrial dysfunctions frequently found in neurodegenerative processes reinforcing its protective role against environmental neurodegenerative diseases.

多项研究表明，膳食补充omega-3（ω-3）长链脂肪酸对神经退行性疾病的几种动物模型具有保护作用。在这里，我们调查二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）（ω-3）是否能防止因广泛使用除草剂百草枯（PQ）（1,1ʹ-二甲基-4-4ʹ-联吡啶二氯化物）介导的神经变性，以果蝇果蝇为模型，专注于线粒体代谢。饮食中摄入PQ 3天导致柠檬酸合酶含量降低，呼吸能力受损和H ₂ O ₂加剧与复杂的I功能障碍和蝇头中高乳酸积累相关的线粒体单位产量。PQ中毒导致1）丧失ELAV（胚胎致死性异常视力）和α-血影蛋白（神经元生存力和突触稳定性的必需蛋白）；2）增强的γ-分泌酶活性，一种与APP释放有关的酶；3）淀粉样蛋白原纤维含量增加。饮食中同时摄入EPA / DHA可以预防PQ诱导的所有这些毒性作用，这表明ω-3的神经保护作用也涉及线粒体保护。总之，同时摄入EPA和DHA可预防PQ诱导的神经退行性过程中常见的神经元和线粒体功能障碍，从而增强了其对环境神经退行性疾病的保护作用。