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1 March 2003 The Antiapoptotic Effect of Low-dose UVB Irradiation in NIH3T3 Cells Involves Caspase Inhibition
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Abstract

UVB irradiation is a well-known apoptosis induction factor. However, we have previously found that low doses of UVB irradiation inhibited apoptosis induced by both serum starvation and lack of extracellular matrix, involving a significant inhibition of caspase-3/7 activation. In this study, we report on the relationship between the UVB-induced antiapoptotic effect and caspase-3/7 inhibition by reactive oxygen species (ROS). The UVB-induced antiapoptotic effect was partially prevented by an antioxidant agent, N-acetylcysteine. A ROS-generating agent, menadione and a pro-oxidant agent, H2O2 also showed an effect that was similar to the UVB-induced antiapoptotic effect, indicating that ROS contributed to the antiapoptotic effect. UVB irradiation significantly suppressed caspase-3/7 activation, which was caused by the inhibition of proteolysis and not by the inhibition of enzymatic activity itself. The prevention of proteolysis was also confirmed by both the following results: one is the inhibition of in vitro caspase-3/7 and -9 activation in cell lysates exposed to UVB in the presence of cytochrome c and dATP, which was caused by the production of ROS, and the other is the inhibition of in vitro caspase-3/7 activation in the presence of active caspase-9. These results showed that the inhibition of the caspase cascade downstream mitochondria by ROS production, leading to a significant inhibition of caspase-3/7 activation, was one of the causes of the antiapoptotic effect by small doses of UVB irradiation.

Yuko Ibuki and Rensuke Goto "The Antiapoptotic Effect of Low-dose UVB Irradiation in NIH3T3 Cells Involves Caspase Inhibition," Photochemistry and Photobiology 77(3), 276-283, (1 March 2003). https://doi.org/10.1562/0031-8655(2003)077<0276:TAEOLD>2.0.CO;2
Received: 16 August 2002; Accepted: 1 December 2002; Published: 1 March 2003
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