ABSTRACT
Mouse renal carcinoma (renca) cells growing exponentially in foetal bovine serum (1%) supplemented with selenium (1 microM, sodium selenite) were exposed to oxidative insult. It was found that glutathione peroxidase activity increased (44%), while the activities of catalase, glutathione disulfide reductase, and level of total glutathione did not change due to selenium supplementation. Selenium supplementation made renca cells susceptible to tert-butylhydroperoxide induced cell death, while it did not affect the viability when the cells were exposed to hydrogen peroxide. It suggested that the contribution of glutathione peroxidase in antioxidant defense mechanism of renca cells was possibly not crucial and the function of catalase might be important especially against hydrogen peroxide.
Subject(s)
Animals , Carcinoma, Renal Cell/pathology , Cell Survival/drug effects , Kidney Neoplasms/pathology , Mice , Selenium/administration & dosage , Tumor Cells, Cultured , tert-Butylhydroperoxide/toxicityABSTRACT
In this study whether extracellular Ca++ is essential to produce an increase of tension of isolated rat duodenum by ACh, 5-HT, AVP and KCl-, was examined. KCl- and AVP-evoked contractions were almost totally prevented by Ca++ removal from bath solution. The increase of tension of isolated duodenum caused by ACh or 5-HT was totally prevented after adding nifedipine, a Ca++ channel blocker, into Ca free solution. Our results suggest that ACh or 5-HT utilizes intracellular as well as extracellular sources of Ca++ to produce contraction in rat duodenum, whereas AVP-or KCl evoked contraction was mainly due to influx of Ca from extracellular sources.