Abstract
While Cr(V) species and .OH radicals have been suggested to play significant roles in the mechanism of chromate-related carcinogenesis, controversy still exists regarding the identity of the Cr(V) species and their role in the generation of .OH radicals. Some recent studies have suggested that the primary Cr(V) species involved is the tetraperoxochromate(V) (CrO8(3-)) ion, which produces .OH radical either on decomposition or by reaction with H2O2. The present study utilized ESR and spin trapping techniques to probe this mechanism. The results obtained show that (i) CrO8(3-) is not formed in any significant quantity in the reaction of chromate with biologically relevant reductants such as glutathione, glutathione reductase, NAD(P)H, ascorbate, vitamin B2, etc. (ii) Decomposition of CrO8(3-), or its reaction with H2O2 does not generate any significant amount of .OH radicals. (iii) The major Cr(V) species formed are complexes of Cr(V) with reductant moieties as ligands. (iv) These Cr(V) complexes generate .OH radicals from H2O2 via Fenton-like reaction. The present study thus disagrees with the recently proposed "tetraperoxochromate(V) theory of carcinogenesis from chromate." Instead, it suggests an alternative mechanism, which might be labeled as "the Cr(V)-complexation-Fenton reaction model of carcinogenesis from chromate.