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Reproduction in whole or in part in any form or medium without express written permission of IDG Communications is prohibited. Copyright 2013 IDG Communications.
ABN 14 001 592 650. All rights reserved. Reproduction in whole or in part in any form or medium without express written permission of IDG Communications is prohibited.Arsenic-induced colon carcinogenesis is associated with alteration in the glutathione system.
Recent studies have demonstrated that arsenic at low concentrations is a potent inducer of colon cancer. The mechanism of arsenic-induced carcinogenesis is not fully understood. In this study, we compared the effects of arsenic treatment alone and in combination with l-buthionine-(S,R)-sulfoximine (BSO) on the proliferation of HT29 cells and the activity of glutathione S-transferases (GST). The results demonstrate that both arsenite and arsenate induce the proliferation of HT29 cells. However, the addition of BSO to cells previously exposed to arsenic failed to stimulate cell proliferation. We found that arsenite and arsenate treatments caused a significant increase in both GST activity and GST-mu. In contrast, the combination of BSO and arsenic caused a decrease in both GST activity and GST-mu. These results demonstrate that arsenic treatment induces cell proliferation and expression of GST-mu, an enzyme that plays an important role in the detoxification of electrophilic and carcinogenic compounds. Our results also indicate that BSO can prevent the arsenic-induced increase in GST activity, a finding which is consistent with the hypothesis that arsenic-induced changes in the glutathione system contribute to the initiation of tumorigenesis.———————- Forwarded by Mike McConnell/HOU/ECT on 05/25/2001
07:36 PM ———————— 384a16bd22

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