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Influence of Vitamin B₂ on Formation of Chromium(V), Alkali-labile Sites, and Lethality of Sodium Chromate(VI) in Chinese Hamster V-79 Cells¹

Department of Medical Biochemistry, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830, Japan

The effect of vitamin B₂ on the cellular reduction and cytotoxicity of chromate(VI) was studied using Chinese hamster V-79 cells. Electron spin resonance studies showed that incubation of cells with Na₂CrO₄ resulted in the formation of both chromium(V) and chromium(III) complex and that cellular pretreatment with riboflavin (Vitamin B₂) for 24 h prior to exposure increased the level of chromium(V) complex, but the level of chromium(III) remained unchanged. Analysis of flavin derivatives revealed that pretreatment with vitamin B₂ increased free riboflavin without altering flavin adenine dinucleotide and flavin mononucleotide. In addition, the level of the flavoenzyme glutathione reductase, which is capable of reducing chromate, was unaffected by pretreatment with vitamin B₂. However, treatment of cells with vitamin B₂ and Na₂CrO₄ augmented the inhibition of glutathione reductase attributable to Na₂CrO₄ alone. Using a colony-forming assay, pretreatment with vitamin B₂ resulted in a decrease of cytotoxicity after exposure to the lethal concentration of chromate (15 µM) but did not affect the cytotoxicity at sublethal concentration of this metal (5–7.5 µM). Alkaline elution studies demonstrated that Na₂CrO₄ induced alkali-labile sites in the DNA of cells in a concentration-dependent manner (5–15 µM) and pretreatment with vitamin B₂ resulted in an increase of these DNA lesions at all concentrations of Na₂CrO₄. The results, showing that vitamin B₂ enhances chromate-induced alkali-labile lesions and chromium inhibition of glutathione reductase, might be due to an increase of chromium(V) species, possibly through its ability to directly reduce chromium(VI). The results also suggest that the extent of DNA lesions induced by chromate may not correlate directly with the cytotoxic effects of this metal.

¹ This work was supported in part by the Fukuoka Cancer Society and Chiyoda Mutual Life Foundation.

² To whom requests for reprints should be addressed.

Received 6/19/89. Revised 8/16/89. Accepted 8/21/89.

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