Retina-derived endogenous sulfur dioxide might be a novel anti-apoptotic factor.

Endogenous sulfur dioxide (SO) was found to be generated from the enzymatic reaction catalysed by aspartate transference 1 (AAT1) in the mammals and play importantly biological effects. In the present study, we explored the existence of endogenous SO pathway in mouse retinal tissues and 661w photoreceptor cell and investigated its possible pathophysiological role in the hydrogen peroxide (HO)-induced mouse photoreceptor cell apoptosis. The data showed that endogenous SO pathway including AAT1 expression and SO content was found to be presented in mouse photoreceptor cells. AAT1 protein and SO were mainly distributed in the cytoplasm, while a small amount of AAT1 protein and SO was found in the nucleus of 661W photoreceptor cells. HO significantly decreased the SO content and AAT1 expression, but increased the cleaved caspase-3 protein level and the apoptotic index, and the number of TUNEL-positive cells in the 661W photoreceptor cells. Moreover, an AAT inhibitor HDX treatment inhibited SO synthesis and mimicked HO-induced apoptosis in 661W cells. In conclusion, the endogenous SO/AAT1 pathway is firstly found to be present in mouse photoreceptor cells, and might play an important role in the prevention from mouse photoreceptor cell apoptosis.