Pineal indoleamines and vitamin E reduce nitric oxide-induced lipid peroxidation in rat retinal homogenates

Citation
Aw. Siu et al., Pineal indoleamines and vitamin E reduce nitric oxide-induced lipid peroxidation in rat retinal homogenates, J PINEAL R, 27(2), 1999, pp. 122-128
Citations number
56
Categorie Soggetti
Physiology
Journal title
JOURNAL OF PINEAL RESEARCH
ISSN journal
07423098 → ACNP
Volume
27
Issue
2
Year of publication
1999
Pages
122 - 128
Database
ISI
SICI code
0742-3098(199909)27:2<122:PIAVER>2.0.ZU;2-5
Abstract
Oxidative damage to retinal cell membranes can lead to sight-threatening oc ular diseases. Pineal indoleamines are naturally located and synthesized in the retina, and they possibly protect the retina from oxidative cell damag e. In this study, we compared the efficacy of three different pineal indole amines (melatonin, N-acetylserotonin, and pinoline) with vitamin E, a well- known antioxidant, against nitric oxide (NO)-induced lipid peroxidation (LP O) in rat retinal homogenates. The possible synergistic effect of these age nts was also studied. Retinal homogenates were incubated with sodium nitrop russide, which releases NO.. The LPO product, malondialdehyde (MDA), provid ed an index of cell damage. The results show that vitamin E and indoleamine s significantly reduced MDA levels in a dose-dependent manner. When vitamin E was combined with the indoleamines, the protection was synergistically e nhanced. In summary, under conditions where cellular homogenates are used ( a) vitamin E and the three pineal indoleamines protected the retinal cells from NO-induced LPO damage; (b) the efficacies of each of these compounds h ad the following relationships: vitamin E > N-acetylserotonin > pinoline > melatonin; (c) vitamin E acted synergistically with indoleamines in combati ng oxidative retinal damage. Whether these same associations would exist in vivo after treatment with these compounds is unknown. The pharmacological potential of indoleamines, possibly in combination with vitamin E, in preve nting retinal pathogenesis deserves further investigation.