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Physiological concentrations of melatonin inhibit the nitridergic pathway in the Syrian hamster retina
Author(s) -
Sáenz Daniel A.,
Turjanski Adrián G.,
Sacca Geraldine B.,
Marti Marcelo,
Doctorovich Fabio,
Sarmiento María I. Keller,
Estrin Darío A.,
Rosenstein Ruth E.
Publication year - 2002
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1034/j.1600-079x.2002.01880.x
Subject(s) - melatonin , medicine , sodium nitroprusside , endocrinology , hamster , nitric oxide , retinal , nitric oxide synthase , guanosine , trifluoperazine , chemistry , biology , calmodulin , enzyme , biochemistry
In the present work, the effect of melatonin on the hamster retinal nitridergic pathway was examined. When the retinas were incubated in the presence of low concentrations (1 p M –10 n M ) of melatonin for 15 min, a significant decrease of nitric oxide synthase (NOS) activity was observed. However, when crude retinal homogenates were preincubated with melatonin for 15 min, no changes in NOS activity were detected, despite the fact that under the same conditions trifluoperazine, a calmodulin inhibitor, significantly decreased enzymatic activity. Kinetic analysis showed that melatonin decreased the V max of retinal NOS without changes in the K m . On the other hand, low concentrations (100 p M ) of melatonin significantly reduced retinal L ‐arginine influx. A decrease in the V max of L ‐arginine uptake was observed in the presence of melatonin, whereas the K m remained unchanged. Melatonin significantly inhibited the accumulation of cyclic guanosine monophosphate (cGMP) levels induced by both L ‐arginine and sodium nitroprusside (SNP). In summary, the present results indicate that melatonin could be a potent inhibitor of the retinal nitridergic pathway.