title: Decreased antioxidant defence and increased oxidant stress during dexamethasone-induced apoptosis: bcl-2 prevents the loss of antioxidant enzyme activity.
abstract: When the WEHI7.2 mouse lymphoid cell line was treated with dexamethasone to induce apoptosis the activities and transcript levels of the antioxidant defence enzymes catalase, superoxide dismutase (SOD) and DT-diaphorase exhibited a progressive decrease over 48 hours. Catalase activity was maintained and total SOD and DT-diaphorase activity showed smaller decreases following dexamethasone treatment of WEHI7.2 cells transfected with the bcl-2 oncogene, which protects the cells against apoptosis. Treatment of wild-type WEHI7.2 and bcl-2 transfected cells with a catalase inhibitor, aminotriazole, was not sufficient to induce apoptosis. Antioxidants, including bovine liver catalase, bovine erythrocyte CuZn-SOD, sodium selenite and Trolox, a water soluble vitamin E analogue, as well as hypoxia, inhibited dexamethasone-induced apoptosis. These results suggest that oxidant stress due to the decreased activity of antioxidant defence enzymes may play a role in dexamethasone-mediated lymphoid cell apoptosis and that bcl-2 may prevent apoptosis by maintaining the level of critical antioxidant defence mechanisms, which include catalase.
authors.affiliation: Arizona Cancer Center, Tucson, Arizona.
authors.forename: A F
authors.initials: AF
authors.lastname: Baker
authors.forename: M M
authors.initials: MM
authors.lastname: Briehl
authors.forename: R
authors.initials: R
authors.lastname: Dorr
authors.forename: G
authors.initials: G
authors.lastname: Powis