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  • Title: Cadmium inhibits EGF-induced DNA synthesis but increases cellular glutathione levels in NRK-49F cells.
    Author: Kang YJ, Enger MD.
    Journal: Toxicology; 1991 Mar 11; 66(3):325-33. PubMed ID: 2011856.
    Abstract:
    The effects of cadmium (CdCl2) on epidermal growth factor (EGF) induced DNA synthesis and on cellular glutathione (GSH) content in growth-arrested NRK-49F cells were studied. The cadmium effects were compared with those of L-buthionine-(S,R)-sulfoximine (BSO). EGF at a concentration of 10 ng/ml was found to stimulate DNA synthesis (as judged by [3H]thymidine incorporation) in growth-arrested NRK-49F cells. CdCl2 inhibited this EGF-induced DNA synthesis in a dose-dependent fashion. It also increased significantly cellular GSH content in both growth arrested and EGF-stimulated NRK-49F cells. This effect of CdCl2 was contrary to that of BSO, which depleted cellular GSH. Although BSO both inhibited EGF-induced DNA synthesis and decreased cellular GSH content in EGF-stimulated NRK-49F cells, these two BSO effects showed dissimilar dose dependencies. BSO and CdCl2 together inhibited EGF-induced DNA synthesis in NRK-49F cells in an additive fashion. These results demonstrate that cadmium inhibition of EGF-induced DNA synthesis in NRK-49F cells is not due to an effect on cellular GSH content. Both cadmium and BSO inhibit EGF-induced DNA synthesis in NRK-49F cells, but probably through different mechanisms. Although GSH may be involved in regulation of DNA synthesis, BSO-induced inhibition of EGF-stimulated DNA synthesis in NRK-49F cells does not in its dose-dependency correlate with GSH depletion.
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