Change of paracellular permeability of ocular surface epithelium by vitamin A deficiency.

Abstract

Dietary vitamin A deficiency in young rabbits caused advanced squamous metaplasia with keratinization of conjunctival epithelium and concomitant reduced paracellular permeability to 3H-mannitol. Both morphologic and permeability changes were reversed with systemic administration of vitamin A. In adult rabbits, vitamin A deficiency caused milder changes of goblet cell loss and increased cellular stratification in conjunction with reduced permeability in the conjunctiva-like epithelium that covers the vascularized cornea after chemical injury with n-heptanol. Topically applied retinoid (tretinoin 0.1%) did not affect the morphology and permeability of the normal corneal or conjunctival epithelium of rabbits that were not vitamin A deficient. These studies showed that altered permeability is associated with the epithelial abnormality during vitamin A deficiency and helped clarify the physiologic function of retinoids in the ocular surface epithelia in the nondeficient state.

• Authors: A J Huang, S C Tseng, K R Kenyon
• Journal: Investigative ophthalmology & visual science (Invest Ophthalmol Vis Sci) Vol. 32 Issue 3 Pg. 633-9 (Mar 1991) ISSN: 0146-0404 [Print] United States
• PMID: 1900498 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Mannitol
• Tretinoin

Topics

• Administration, Topical
• Animals
• Cell Differentiation
• Conjunctiva (metabolism)
• Cornea (metabolism, pathology)
• Epithelium (metabolism)
• Mannitol (metabolism)
• Perfusion
• Permeability
• Rabbits
• Tretinoin (administration & dosage)
• Vitamin A Deficiency (metabolism, prevention & control)