OXIDATIVE STRESS-INDUCED BY CHRONIC ADMINISTRATION OF SODIUM DICHROMATE [CR(VI)] TO RATS

Chromium occurs in the workplace primarily in the valence forms Cr(III ) and Cr(VI), Recent studies have demonstrated that sodium dichromate [Cr(VI)] induces greater oxidative stress as compared with Cr(III), as indicated by the production of reactive oxygen species by peritoneal macrophages and hepatic mitochondria and microsomes, and enhanced excr etion of urinary lipid metabolites and hepatic DNA-single strand break s (SSB) following acute oral administration of Cr(III) and Cr(VI), We have therefore examined the chronic effects of sodium dichromate dihyd rate [Cr(VI); 10 mg (33.56 mu mol)/kg/day] on hepatic mitochondrial an d microsomal lipid peroxidation, enhanced excretion of urinary lipid m etabolites including malondialdehyde (MDA), formaldehyde (FA), acetald ehyde (ACT), acetone (ACON) and propionaldehyde (PROP), and hepatic DN A damage over a period of 90 days, The maximal increases in hepatic li pid peroxidation and DNA damage were observed at approximately 45 days of treatment, Maximum increases in the urinary excretion of MDA, FA, ACT, ACON and PROP were 3.2-, 2.6-, 4.1-, 3.3- and 2.1-fold, respectiv ely, while a 5.2-fold increase in DNA-SSB was observed, The results cl early indicate that chronic sodium dichromate administration induces o xidative stress resulting in tissue damaging effects which may contrib ute to the toxicity and carcinogenicity of hexavalent chromium.