Chloric acid(I) affects antioxidant defense of lung epitelial cells

Generation of chloric acid(I) and reactive oxygen and nitrogen species by activated phagocytes is associated with the course of many inflammatory-related lung diseases. Thus, we studied the effects of HOCl on the redox state of A549 cells as well as on the activity of enzymes involved in cell protection against oxidants. Additionally, we determined the ability of plasma antioxidants to prevent the HOCl-induced cytotoxicity to lung epithelial A549 cells. Cell treatment with HOCl at concentrations above 50 μM for 1h resulted in the loss of cell viability. The decrease of GSH concentration and antioxidant capacity of cell extracts was accompanied by an increase of the level of GSSG and the rate of generation of ROS and peroxyl radicals. Hyperpolarization of the mitochondrial membrane was also observed. HOCl at concentrations of 50 μM significantly decreased the activity of all antioxidant enzymes studied in A549 cells. All antioxidants employed protected cells against the action of HOCl, with the efficiency decreasing as follows: albumin>GSH>uric acid>ascorbate>Trolox. HOCl was found to affect the redox state of A549 by oxidation of GSH, inactivation of antioxidant enzymes and increase of ROS generation.