Citation

Bankson DD, Ellis JK, Russell RM. Exp. Gerontol. 1989; 24(2): 127-136.

Affiliation

Department of Medicine, University of North Carolina, Chapel Hill 27599-7005.

Copyright

(Copyright © 1989, Elsevier Publishing)

DOI

unavailable

PMID

2721601

Abstract

Changes in serum, hepatic, and ocular vitamin A levels were followed in 9-month-old Long Evans rats fed either a vitamin-A-free or vitamin-A-sufficient diet for up to 18 months. After 18 months, hepatic total vitamin A fell exponentially from 2542 +/- 433 to 48 +/- 12 micrograms/g wet weight, but these stores maintained normal serum retinol and ocular total vitamin A concentrations in vitamin-A-deprived rats. However, retinal dark-adaptation time, a functional indicator of photoreceptor integrity, was prolonged in elderly vitamin-A-deprived rats as compared to vitamin-A-sufficient controls (p less than 0.05). Aging appeared to be the most important factor that depressed the rate of dark adaptation, with vitamin A status having a secondary effect. The proportion of total ocular retinaldehyde decreased (p less than 0.05) and the concentration of retinyl ester increased (p less than 0.05) in the eyes of 27-month-old vitamin-A-deprived rats compared to age-matched vitamin-A-sufficient animals. Possible mechanisms of visual dysfunction include abnormal retinal rhodopsin recycling caused by a dependence on newly absorbed dietary vitamin A (e.g., chylomicron). Alternatively, in the vitamin-A-deprived rat, decreased hepatic oxidation of pentobarbital (used for electroretinographic anesthesia) could prolong retinal anesthetic exposure and either directly depress neural transmission or indirectly alter transmission by affecting rhodopsin recycling.

Language: en