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The Antiapoptotic Effect of Low‐dose UVB Irradiation in NIH3T3 Cells Involves Caspase Inhibition ¶

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.