Alpha-Lipoic Acid May Protect against Effects of Cigarette Smoke - Effects on Cells involved in Macular Degeneration

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Alpha-Lipoic Acid May Protect against the Toxic Effects of Cigarette

Smoke - Effects on Cells involved in Macular Degeneration

Reference: " Acrolein, a toxicant in cigarette smoke, causes oxidative

damage and mitochondrial dysfunction in RPE cells: protection by

®-alpha-lipoic acid, " Jia LH, Liu ZB, et al, Investigative

Ophthalmology and Visual Science, 2007; 48(1): 339-348. (Address:

Children's Hospital Oakland Research Institute, Oakland, California, USA).

Summary: 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. "

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