Modification of gene expression by dietary antioxidants in radiation-induced apoptosis of mice splenocytes

Overexpression of Ref-1 Inhibits Lead-induced Endothelial Cell Death via the Upregulation of Catalase

“…This finding is consistent with a previous report, in which it was demonstrated that catalase levels declined significantly in vascular smooth muscle cells chronically exposed to lead (Ni et al, 2004). Catalase expression can be downregulated by lipopolysaccharide (Clerch et al, 1996), ionizing radiation (Ushakova et al, 1999;Nenoi et al, 2001), and tumor necrosis factor-alpha (Clerch and Massaro, 1992;Chovolou et al, 2003;Lupertz et al, 2008), which stimulated cell death or oxidative stress in the cells. Therefore, in this study, the downregulation of catalase was related to Pb-induced cell death in endothelial cells.…”

In vitro immune response of human peripheral blood cells to vitamins C and E

“…C provides a marked protection from apoptosis. An inhibitory effect of antioxidant vitamins on apoptosis has been observed after exposure of HL-60 myeloid leukemia cells and mouse splenocytes to ionizing irradiation [16,17]. Since oxidative stress may induce abnormal apoptosis, it is conceivable that antioxidants modified programmed cell death by a repair of its effect [18].…”

Vitamin E Regulation of Mitochondrial Superoxide Generation

“…Treatment of the Mn-SOD-overexpressing cells with various ROS-generating systems or inhibition of different H 2 O 2 -detoxifying pathways resulted in an increase in matrix-degrading metalloprotease-1 mRNA levels, and oxidative stress conditions led to a strong induction of c-jun and c-fos mRNA levels leading to a higher transactivation of AP-1 in the Mn-SOD-overexpressing cells [94]. Ushakova et al [95] reported that the antioxidant inhibited TRPM-2 (a marker for programmed cell death) expression both before and after irradiation and the bcl-2 mRNA content steadily increased after irradiation in mouse splenocytes. These data suggest that antioxidant administration decreased the radiation-induced apoptosis and delayed internucleosomal fragmentation of DNA and that radiation-induced alteration of gene expression is, at least in part, determined by ROS.…”