McGee Sean L, Sadli Nadia, Morrison Shona, Swinton Courtney, Suphioglu Cenk
Metabolic Research Unit, The School of Medicine, Deakin University, Geelong, Victoria, Australia.
Cell Physiol Biochem. 2011;28(1):157-62. doi: 10.1159/000331724. Epub 2011 Aug 16.
Zinc accumulation may impair cellular bioenergetics, which is associated with neuronal apoptosis. We simultaneously assessed anaerobic and aerobic metabolism in live cells to characterise this effect and hypothesised that the omega 3 fatty acid docosahexaenoic acid (DHA) would protect against any zinc mediated alterations in bioenergetics. In this study we observed a decrease in cellular oxygen consumption, but not glycolytic rate, following chronic zinc exposure, which was specific for neuronal cells. This was due to impaired ATP turnover, without any other effects on mitochondrial function, and was restored by DHA. DHA had no further effects on bioenergetics. These data suggest that zinc disrupts bioenergetics at a point distal to the respiratory chain, which is restored by DHA.
锌的积累可能会损害细胞生物能量学，这与神经元凋亡有关。我们同时评估了活细胞中的无氧和有氧代谢，以表征这种效应，并假设ω-3脂肪酸二十二碳六烯酸（DHA）可以防止锌介导的生物能量学改变。在本研究中，我们观察到慢性锌暴露后细胞耗氧量下降，但糖酵解速率未下降，这在神经元细胞中具有特异性。这是由于ATP周转受损，对线粒体功能没有任何其他影响，而DHA可使其恢复。DHA对生物能量学没有进一步影响。这些数据表明，锌在呼吸链远端的一个点上破坏了生物能量学，而DHA可使其恢复。
