In a study involving cultured human ARPE19 cells and primary cultures of human fetal (hf)RPE (retinal pigment epithelial) cells pre-treated with R-alpha-lipoic acid were found to be protected against the toxic effects of acrolein, a toxicant found in cigarette smoke to which the cells were exposed. The authors conducted these experiments to better understand the relationships between cigarette smoking, oxidant injury, and age-related macular degeneration. The first part of the study established the toxic effects of acrolein on ARPR19 cells. When cells were exposed to acrolein over 50 mu M (24 hours), decreases were found in cell viability, mitochondrial potential, GSH, antioxidant capacity, Nrf2 expression, and enzyme activity, while increases were found in oxidant levels, protein carbonyls, and calcium. When cells were exposed to lower doses of acrolein (10 to 100-fold lower doses), but continuously over 8 or 32 days, similar toxic effects were observed. When the cells were pre-treated with R-alpha-lipoic acid, they were protected against the toxic effects of acrolein exposure. Similar results were found in the human fetal RPE cells. The results of this study suggest that, "acrolein-induced oxidative mitochondrial dysfunction is reduced by lipoic acid." Furthermore, the authors conclude, "These experiments indicate that mitochondria-targeted antioxidants such as lipoic acid may be an effective strategy for reducing or preventing chronic oxidant-induced RPE degeneration in vivo from a variety of sources, including cigarette smoke." Vitasearch Comment: The immense versatility of this powerful antioxidant never ceases to amaze us. It holds the potential for numerous preventative and therapeutic applications in nutritional medicine.
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