Progression and reversibility of early light-induced alterations in rat retinal rods

Progression and reversibility of early light-induced alterations in rat retinal rods The temporal sequence of ultrastructural changes induced in the rat rod photoreceptor by 80 lux light-stress has been studied. The changes seen were compared with those produced by a much dimmer (3 lux) illumination. Some of the early signs of abnormality were (1) degradation of some disk membranes at the tips of outer segments, (2) disaggregation and detachment of ribosomes, (3) lighter matrices in swollen mitochondria, (4) disappearance of the Golgi apparatus, (5) proliferation of autophagic bodies in the inner segments, and (6) appearance of perimitochondrial membrane whorls in the synaptic terminals. No single change could be identified that would inexorably lead to cell death. The overall picture, however, suggested that an inability of the cell to maintain its anabolic balance is responsible for the pyknosis that occurs when the 80 lux exposure exceeds 12–15 h. All changes were reversible when exposure duration did not exceed 12 h, the normal length of the light cycle for these rats. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cell and Tissue Research Springer Journals

Progression and reversibility of early light-induced alterations in rat retinal rods

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Publisher
Springer Journals
Copyright
Copyright © 1986 by Springer-Verlag Berlin Heidelberg
Subject
Biomedicine; Neurosciences; Endocrinology; Neurology; Cell Biology
ISSN
0302-766X
eISSN
1432-0878
D.O.I.
10.1007/BF00215203
Publisher site
See Article on Publisher Site

Abstract

The temporal sequence of ultrastructural changes induced in the rat rod photoreceptor by 80 lux light-stress has been studied. The changes seen were compared with those produced by a much dimmer (3 lux) illumination. Some of the early signs of abnormality were (1) degradation of some disk membranes at the tips of outer segments, (2) disaggregation and detachment of ribosomes, (3) lighter matrices in swollen mitochondria, (4) disappearance of the Golgi apparatus, (5) proliferation of autophagic bodies in the inner segments, and (6) appearance of perimitochondrial membrane whorls in the synaptic terminals. No single change could be identified that would inexorably lead to cell death. The overall picture, however, suggested that an inability of the cell to maintain its anabolic balance is responsible for the pyknosis that occurs when the 80 lux exposure exceeds 12–15 h. All changes were reversible when exposure duration did not exceed 12 h, the normal length of the light cycle for these rats.

Journal

Cell and Tissue ResearchSpringer Journals

Published: Dec 1, 1986

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