The Role of Nitric Oxide in Ocular Surface Cells.
10.3346/jkms.2002.17.3.389
- Author:
Jae Chan KIM
1
;
Gun Sic PARK
;
Jin Kook KIM
;
Young Myeong KIM
Author Information
1. Department of Ophthalmology, College of Medicine, Chung-Ang University, Seoul, Korea. jck50ey@kornet.net
- Publication Type:Original Article
- Keywords:
Cell Survival;
Nitric Oxide;
Nitric-Oxide Synthase (NOS);
Ocular Surface Tissue
- MeSH:
Animals;
Apoptosis/drug effects/physiology;
Aqueous Humor/metabolism;
Blood Proteins/pharmacology;
Cell Survival/drug effects/physiology;
Cells, Cultured;
Epithelium, Corneal/*cytology/*enzymology;
Fibroblasts/cytology/enzymology;
Humans;
Nitric Oxide/biosynthesis/*physiology;
Nitric Oxide Donors/pharmacology;
Nitric Oxide Synthase/metabolism;
Nitric Oxide Synthase Type I;
Nitric Oxide Synthase Type II;
Nitric Oxide Synthase Type III;
Penicillamine/*analogs & derivatives/pharmacology;
Peroxynitrous Acid/biosynthesis;
Rabbits;
Tears/metabolism;
Uveitis/metabolism
- From:Journal of Korean Medical Science
2002;17(3):389-394
- CountryRepublic of Korea
- Language:English
-
Abstract:
The role of nitric oxide (NO) in the ocular surface remains unknown. We investigated the conditions leading to an increase of NO generation in tear and the main sources of NO in ocular surface tissue. We evaluated the dual action (cell survival or cell death) of NO depending on its amount. We measured the concentration of nitrite plus nitrate in the tears of ocular surface diseases and examined the main source of nitric oxide synthase (NOS). When cultured human corneal fibroblast were treated with NO producing donor with or without serum, the viabilities of cells was studied. We found that the main sources of NO in ocular surface tissue were corneal epithelium, fibroblast, endothelium, and inflammatory cells. Three forms of NOS (eNOS, bNOS, and iNOS) were expressed in experimentally induced inflammation. In the fibroblast culture system, the NO donor (SNAP, S-nitroso-N-acetyl-D, L-penicillamine) prevented the death of corneal fibroblast cells caused by serum deprivation in a dose dependent manner up to 500 micrometer SNAP, but a higher dose decreased cell viability. This study suggested that NO might act as a doubleedged sword in ocular surface diseases depending on the degree of inflammation related with NO concentration.
