Nitric oxide and Cataract Research.doc

 PAGE \* MERGEFORMAT 13 Nitric oxide and Cataract Research [Keywords:] Nitric oxide Cataract Research In 1980 Furchgott [1] found that endothelial cells can produce and release endothelium derived relaxing factor (EDRF) and later proved that it contains NO. Then, again in 1986, according to the role of the nature of EDRF and nitric oxide (NO) is very similar put forward and confirmed that EDRF is NO, a physiological role and pathophysiological role of the unique physiological effects. NO (nitric oxide, NO) is an endogenous vasodilator, inflammatory mediators, cell messengers and neurotransmitters. NO In the eye of more and more attention. Its main roles: (1) as a vascular endothelial cell-dependent regulators. (2) acts as a neurotransmitter. (3) enhance the body of non-specific immune defense functions. (4 ) cell protective effect (low concentration) and cytotoxicity (high concentration). NO mainly by L-arginine and molecular oxygen in the NO synthase (nitric oxide synthase, NOS) reaction is one for the L-hydroxy Arginine acid, and then further oxidized into stable end products NO and NO loss of activity. NOS in ocular tissue varies widely, in the eyes of many organizations in both the distribution of NOS. NO in physiological and pathological visual system has been increasingly concerned about the role and began to explore from all angles, is to study the progress of cataract NO cases reviewed. 1 NO distribution, biological characteristics and regulation The distribution of 1.1 NO NO in vivo widespread in various tissues, NO and eye disease study abroad began in 1993, started late compared with other disciplines. Kurenni 1995 reported by NADPH2 lipoic amide dehydrogenase and nitric oxide synthase (NOS) The staining and cellular immunity, the result was the existence of intraocular tissue NOS. such as the outer retina, cone, rod ellipsoid inner segment, outer nuclear layer near the photoreceptor, Mller cells distant conflict, bipolar cells, et