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

Qian, Y Jiang, B Flynn, DC Leonard, SS Wang, SW Zhang, Z Ye, JP Chen, F Wang, LY Shi, XL

Y. Qian et al., Cr(VI) increases tyrosine phosphorylation through reactive oxygen species-mediated reactions, MOL C BIOCH, 222(1-2), 2001, pp. 199-204

32

INGLESE

Article

Cell & Developmental Biology

MOLECULAR AND CELLULAR BIOCHEMISTRY

0300-8177 → ACNP

222

1-2

2001

199 - 204

ISI

0300-8177(200106)222:1-2<199:CITPTR>2.0.ZU;2-I

While Cr (VI)-containing compounds are well established carcinogens, the me chanisms of their action remain to be investigated. In this study we show t hat Cr (VI) causes increased tyrosine phosphorylation in human lung epithel ial A549 cells in a time-dependent manner. N-acetyl-cysteine (NAC), a gener al antioxidant, inhibited Cr (VI)-induced tyrosine phosphorylation. Catalas e, a scavenger of H2O2, sodium formate and aspirin, scavengers of hydroxyl radical ((OH)-O-.), also inhibited the increased tyrosine phosphorylation i nduced by Cr (VI). SOD, an inhibitor of superoxide radical (O-2(.-)), cause d less inhibition. ESR study shows that incubation of Cr (VI) with the A549 cells generates (OH)-O-. radical. The generation of radical was decreased by addition of catalase and sodium formate, while SOD did not have any inhi bitory effect. Oxygen consumption measurements show that addition of f Cr ( VI) to A549 cells resulted in enhanced molecular oxygen consumption. These results indicate that Cr (VI) can induce an increase in tyrosine phosphoryl ation. H2O2 and (OH)-O-. radicals generated during the process are responsi ble for the increased tyrosine phosphorylation induced by Cr (VI).