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Cr(VI) increases tyrosine phosphorylation through reactive oxygen species-mediated reactions.

Authors
Qian-Y; Jiang-BH; Flynn-DC; Leonard-SS; Wang-S; Zhang-Z; Ye-J; Chen-F; Wang-L; Shi-X
Source
Mol Cell Biochem 2001 Jun; 222(1-2):199-204
NIOSHTIC No.
20021845
Abstract
While Cr (VI)-containing compounds are well established carcinogens, the mechanisms of their action remain to be investigated. In this study we show that Cr (VI) causes increased tyrosine phosphorylation in human lung epithelial A549 cells in a time-dependent manner. N-acetyl-cysteine (NAC), a general antioxidant, inhibited Cr (VI)-induced tyrosine phosphorylation. Catalase, a scavenger of H2O2, sodium formate and aspirin, scavengers of hydroxyl radical (*OH), also inhibited the increased tyrosine phosphorylation induced by Cr (VI). SOD, an inhibitor of superoxide radical (O2*-), caused less inhibition. ESR study shows that incubation of Cr (VI) with the A549 cells generates *OH radical. The generation of radical was decreased by addition of catalase and sodium formate, while SOD did not have any inhibitory effect. Oxygen consumption measurements show that addition of Cr (VI) to A549 cells resulted in enhanced molecular oxygen consumption. These results indicate that Cr (VI) can induce an increase in tyrosine phosphorylation. H2O2 and *OH radicals generated during the process are responsible for the increased tyrosine phosphorylation induced by Cr (VI).
Keywords
Carcinogens; Lung-cells; Cell-cultures; Antioxidants; Antioxidation; Sodium-compounds
Contact
D. C. Flynn, Cancer Center and Department of Microbiology and Immunology, School of Medicine, West Virginia University, Morgantown, WV 26506
CODEN
MCBIB8
CAS No.
55520-40-6
Publication Date
20010601
Document Type
Journal Article
Fiscal Year
2001
NTIS Accession No.
NTIS Price
Issue of Publication
1-2
ISSN
0300-8177
NIOSH Division
HELD
Source Name
Molecular and Cellular Biochemistry
State
WV
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