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At least 1,153 records · Page 64Linked to original sources
PubMed1985

A comparison of the mutagenicity of soluble trivalent chromium compounds with that of potassium chromate.

The mutagenic potential of water soluble complexes of trivalent chromium with five different amino acids in Salmonella typhimurium strains TA92, TA94, TA98, and TA100 was studied. All complexes were nonmutagenic at concentrations up to 50 mumol/plate in the strains used. In contrast, trivalent chromium chloride was slightly mutagenic in TA98 and a considerable increase in numbers of revertants was observed in TA94. Hexavalent chromium was nonmutagenic in TA98. Strong mutagenic effects were found in TA92, TA94, and TA100. The large difference in mutagenicity between trivalent and hexavalent chromium is discussed with respect to affinity to extracellular phosphate, diffusability through membranes and reactivity with DNA. More definitive statements about the toxicological risks of the water soluble chromium complexes requires additional studies with well defined compounds in test systems specially suited to study metal complexes.

Chemical Phenomena↗
PubMed1990

One-electron reduction of chromate by NADPH-dependent glutathione reductase.

Electron spin resonance (ESR) measurements provide evidence for the formation of Cr(V) intermediates in the enzymatic reduction of Cr(VI) by glutathione reductase (GSSG-R) in the presence of NADPH, indicating an initial single-electron transfer step in the reduction mechanism. Depending on the pH, at least two different Cr(V) species are generated which are relatively long-lived. In addition, we have detected the hydroxyl (.OH) radical formation during the GSSG-R catalyzed reduction of Cr(VI) by spin trapping, employing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) as spin traps. Superoxide dismutase (SOD) causes only a minor effect on the .OH radical and Cr(V) formation, indicating that the O2- is not significantly involved in the reaction mechanism. Catalase enhances the Cr(V) formation and substantially inhibits the .OH radical formation, indicating the involvement of hydrogen peroxide (H2O2) in the reaction mechanism. Addition of H2O2 suppresses Cr(V) and enhances the .OH radical formation. Measurements involving N-ethylmaleimide show that the Cr(V) species, produced enzymatically by the reduction of Cr(VI) by GSSG-R, react with H2O2 to generate .OH radicals, which might participate in the initiation of Cr(VI) carcinogenicity.

Chromates↗
PubMed1987

Effects of vitamin E, vitamin B2 and selenite on DNA single strand breaks induced by sodium chromate (VI).

The effects of vitamin E, vitamin B2 and selenite on DNA single strand breaks induced by Na2CrO4 were examined by alkaline elution. Incubation of Chinese hamster V-79 cells with alpha-tocopherol succinate (vitamin E) for 24 h prior to exposure to Na2CrO4 resulted in a decrease of DNA breaks produced by this compound. However, similar pretreatment with riboflavin (vitamin B2) or Na2SeO3 resulted in an enhanced formation of breaks induced by Na2CrO4. Pretreatment with Na2SeO3 resulted in increased levels of glutathione in these cells while levels of glutathione remained the same with vitamin E or vitamin B2. These results suggest that Na2CrO4 induced DNA breaks appear to be mediated by the formation of free radicals and/or cellular reductive metabolism.

Animals↗
PubMed1996

Riboflavin can decrease the nephrotoxic effect of chromate in young and adult rats.

The influence of 5 mg vitamin B2/100 g b.wt. (B2, riboflavin) on the nephrotoxic effect of 1 or 2 mg Na2Cr2O7/100 g b.wt. (Cr) was investigated in 55- and 10-day-old rats, respectively. Nephrotoxic effect was evaluated by the determination of urinary volume and protein excretion as well as the concentration of blood urea nitrogen (BUN). The concomitant administration of Cr and B2 only in 55-day-old rats increased the nephrotoxicity shown by enhanced proteinuria and BUN. B2, administered 3 h after Cr, was able to diminish Cr nephrotoxicity significantly in 55- and 10-day-old rats. The effect of B2 on Cr nephrotoxicity could be interpreted not by the stimulatory effect of B2 on GSSG reductase, which was abolished by Cr; but by its antioxidant effect.

Age Factors↗