1. The Effects of 12(R)Hete and Its Metabolite 8(R)HHDTre on Corneal Endothelial Function
- Author
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G.P. Holley, Henry F. Edelhauser, K. Keven Williams, and Wendell D. Woods
- Subjects
medicine.medical_specialty ,Corneal endothelium ,genetic structures ,Cytochrome ,biology ,ATPase ,Metabolite ,Endogeny ,Metabolism ,eye diseases ,chemistry.chemical_compound ,medicine.anatomical_structure ,Endocrinology ,chemistry ,Cornea ,Internal medicine ,cardiovascular system ,biology.protein ,medicine ,lipids (amino acids, peptides, and proteins) ,sense organs ,Corneal epithelium - Abstract
The purpose of this presentation is twofold: (1) to summarize our studies as to the direct effect of 12(R)HETE, 8(R)HHDTrE on the corneal endothelium, and (2) to illustrate the diffusion and metabolism of 12(R)HETE by the cornea. Our data has shown that 12(R)HETE causes corneal swelling in a dose-dependent manner when perfused directly to the corneal endothelium. As reported by Schwartzman et al, 12(R)HETE is one of the major cytochrome P450-dependent arachidonate metabolites of the corneal epithelium and is an endogenous inhibitor of Na+/K+ATPase. Contact lens-induced hypoxic stress has also been shown to stimulate the endogenous formation of 12(R)HETE by the corneal epithelium. This increased formation of 12(R)HETE was found to correlate to increased corneal thickness and to changes in the corneal endothelial structure.These results suggest that 12(R)HETE produced by the corneal epithelium might be capable of diffusing across the cornea and affecting endothelial function.
- Published
- 1997
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