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© 1995 Oxford University Press

research-article

Chromium(VI)-induced nuclear factor-kcyB activation in intact cells via free radical reactions

Jianping Ye, Xiaoying Zhang, Howard A. Young, Yan Mao 1 and Xianglin Shi 1 2

Laboratory of Experimental Immunology, Biological Response Modifiers Program, National Cancer Institute Fredenck, MD 21702
1Laboratory of Experimental Pathology, National Cancer Institute Bethesda, MD 20892, USA

2To whom correspondence should be addressed

Incubation of chronuum(VI) [Cr(VI)] with cultured Jurkat cells resulted in activation of DNA binding activity of the nuclear factor (NF)-kcyB. In a combination with glutathione reductase, a Cr(VI) reducing agent, Cr(VI) expressed an enhanced activity in induction of NF-kcyB. This activation of NF-kcyB was decreased by a metal chelator, diethylene triaminepentaacetic acid or catalase, but increased by superoxide dismutase. Addition of Mn2+ which reacts with Cr(IV) and inhibits Cr(IV)-mediated hydroxyl radical (OH) generation via Fenton-like reaction, attenuated the activation of NF-kcyB. Sodium formate, an OH radical scavenger, also inhibited the activation. Electron spin resonance measurements showed that the incubation of Cr(VI) with intact Jurkat cells generated reactive Cr(V) intermediate. Glutathione reductase and NADPH enhanced Cr(V) generation. Electron spin resonance spin trapping measurements using 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trapping agent provided evidence that the incubation of Cr(VI) with the Jurkat cells in the presence of glutathione reductase generated OH radicals. H enhanced OH radical generation and also enhanced Cr(V) formation, indicating the role of Cr(IV) in OH radical generation. We conclude that Cr(VI) can activate NF-feB in vitro via Cr(IV)-mediated free radical reactions. We hypothesize that Cr(VI)-mediated NF-kcyB activation may be involved in the mechanism of Cr(VI)-induced carcinogenicity.


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