This study provides further evidence for the toxicity of hypochlorous acid (HOCl) in mammalian cells. Using the Chinese hamster B14 cell line, a significant decrease in cell viability was demonstrated after exposure to 100-200 microM HOCl for 1 h. Loss of viability was accompanied by a slight increase in DNA damage as shown by the Comet assay and by oxidation of cellular thiols. Exposure of B14 cells, erythrocyte membranes and human serum albumin to HOCl resulted in an extensive protein carbonyl accumulation. Thus, the cytotoxicity of HOCl may be due to both protein damage (carbonyl formation and oxidation of protein thiol groups) and DNA damage. The well-known antioxidant melatonin interacted with the oxidant and significantly protected cells during HOCl exposure, diminishing its cytotoxic effects and reducing protein carbonyl generation.
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