Structural Alterations in Retinal Tissues From Rats Deficient in Vitamin E and Selenium and Treated With Hyperbaric Oxygen

Document Type

Article

Publication Date

1-1-1992

Description

Vitamin E and selenium play key roles in preventing in vitro lipid peroxidation and free radical damage to retinal tissues. In this research, we studied the effects of hyperbaric oxygen on retinal structure in rats fed diets deficient in vitamin E and/or selenium. We also correlated any alterations in retinal structure with previously measured alterations in electroretinograms (ERGs). Age-matched rats were fed a basal diet deficient in both vitamin E and selenium (B diet), a basal diet supplemented with vitamin E alone (B+E diet), or selenium alone (B+Se diet), or with both micronutrients (B+E+Se). Half the rats in each group were treated (+ HBO) with hyperbaric oxygen (100% O2 at 3 ATA for 1·5 per hr day, 5 days per week) and half were not (-HBO). We previously found that the rats fed the B diet for 6 weeks and treated with HBO for 4 weeks (B+HBO group) had diminished a-wave ERG amplitudes. At this time point all rats in the B group and half of the rats in the B+E+Se group were killed for the structural studies reported here. Surprisingly, we found no evidence of photoreceptor cell necrosis [i.e. a decreased thickness of the outer nuclear layer (ONL)] in retinas from rats in the B+HBO group despite the diminished amplitude of the a-wave which arises from this retinal layer. Quantitative structural analyses of retinas from rats in the B+HBO, B-HBO, B+E+Se-HBO and B+E+Se+HBO groups also failed to reveal any significant differences in the cell height of the retinal pigmented epithelium (nasal, central or temporal regions) or the number of mitochondria, phagosomas or inclusion bodies in the central retinal pigment epithelium (RPE). The inner nuclear layer (INL) thickness was, however, consistently decreased in all retinal regions for the rats in the B+HBO group. Our previous work also showed that only rats fed the B+Se diet for 17 weeks and treated with HBO for 15 weeks (B+Se+HBO group) showed diminished a-wave and b-wave ERG amplitudes. At this time point rats in the B+E+Se, B+E, and B+Se groups were killed for structural studies reported here. Only rats in the B+Se+HBO group showed a significantly decreased (about 20%) thickness of the central ONL. This evidence of photoreceptor cell necrosis correlated very well with our previous observation of diminished a- and b-wave amplitudes only in the B+Se+HBO group (at week 17). Ultrastructural studies after 17 weeks of feeding the experimental diets revealed two different types of inclusion bodies in the central RPE. On the basis of morphological appearance we have termed these inclusion bodies 'electron-dense' and 'granulated'. The central RPE of rats in the B+Se+HBO and B+Se-HBO groups showed a larger number (P < 0·001) of 'granulated' inclusion bodies and a smaller number (P < 0·001) of 'electron-dense' inclusion bodies than rats in any other diet/treatment group at this time point. In marked contrast, there were no observable 'granulated' inclusion bodies and no significant differences in the number of electron-dense inclusion bodies found in the central RPE from rats in any diet/treatment group after 6 weeks of feeding the experimental diets. Our results are discussed with respect to the potential effects of lipid peroxidation on retinal morphology and on electroretinograms.

Share

COinS