Inhibition of receptor-mediated apoptosis upon Bcl-2 overexpression is not associated with increased antioxidant status.
Bcl-2 is reported to augment the antioxidant capacity of cells and this is hypothesized to contribute to the anti-apoptotic activity of this oncoprotein. We generated a number of stable Jurkat cell lines expressing varying levels of Bcl-2, and showed a strong correlation between Bcl-2 levels and resistance to Fas-mediated apoptosis. While individual differences could be detected, there was no overall correlation between Bcl-2 and the expression and activity of superoxide dismutases, catalase, glutathione peroxidases, thioredoxin, thioredoxin reductases, and peroxiredoxins. Cells transfected with Bcl-2 averaged 70% more glutathione than parental cells, but there was no correlation between glutathione and resistance to apoptosis. This challenges the hypothesis that the anti-apoptotic properties of Bcl-2 are linked to a global increase in antioxidant status.
Thomson
Susan J
SJ
Free Radical Research Group, Department of Pathology, University of Otago, P.O. Box 4345, Christchurch, New Zealand.
Cox
Andrew G
AG
Cuddihy
Sarah L
SL
Pullar
Juliet M
JM
Hampton
Mark B
MB
D000975:Antioxidants / Q000378:metabolism*; D017209:Apoptosis; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D019169:Jurkat Cells; D010088:Oxidoreductases / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis* / Q000235:genetics; D014162:Transfection; D019014:fas Receptor / Q000378:metabolism
D000975:Antioxidants; D019253:Proto-Oncogene Proteins c-bcl-2; D019014:fas Receptor; D006861:Hydrogen Peroxide; D010088:Oxidoreductases; D005978:Glutathione