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

Abstract Endogenous sulfur dioxide (SO 2 ) 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 2 pathway in mouse retinal tissues and 661w photoreceptor cell and investigated its possible pathophysiological role in the hydrogen peroxide (H 2 O 2 )-induced mouse photoreceptor cell apoptosis. The data showed that endogenous SO 2 pathway including AAT1 expression and SO 2 content was found to be presented in mouse photoreceptor cells. AAT1 protein and SO 2 were mainly distributed in the cytoplasm, while a small amount of AAT1 protein and SO 2 was found in the nucleus of 661W photoreceptor cells. H 2 O 2 significantly decreased the SO 2 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 2 synthesis and mimicked H 2 O 2 -induced apoptosis in 661W cells. In conclusion, the endogenous SO 2 /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.