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EFFECTS OF DIETARY VITAMIN E AND SELENIUM ON LIGHT DAMAGE TO THE RAT RETINA*,†
Author(s) -
Stone William L.,
Katz Martin L.,
Lurie Mark,
Marmor Michael F.,
Dratz Edward A.
Publication year - 1979
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1979.tb07757.x
Subject(s) - erg , lipid peroxidation , retinal pigment epithelium , glutathione peroxidase , retina , vitamin e , antioxidant , medicine , endocrinology , electroretinography , oxidative stress , in vivo , vitamin , chemistry , pigment , retinal , biology , biochemistry , superoxide dismutase , genetics , neuroscience , organic chemistry
—In this study we have investigated effects of dietary supplementation or deficiency in α‐tocopherol (vitamin E) and selenium on acute light stress to albino rats. Selenium, which is an essential component of the enzyme glutathione peroxidase, and α‐tocopherol are thought to be important in preventing in vivo lipid peroxidation. Before light stress, sections of paraffin embedded eyes show an intense yellow autofluorescent pigment localized in the retinal pigment epithelium (RPE) of the deficient rats which is barely visible in tissue sections from the supplemented rats. The fluorescent pigment is thought to be the result of damaging lipid peroxidation reactions. In addition the dcficient rats show increased electroretinogram (ERG) thresholds and decreased ERG‐amplitudes compared to the supplemented rats. Acute 12 h light stress did not produce an increase in autofluorescent pigment in the RPE of the supplemented or deficient rats. The supplemented rats. however. showed marked light damage effects as measured by ERG‐parameters. Contrary to our expectations, the deficient rats showed a lesser amount of light damage to the ERG than the supplemented rats. Our ERG results to date fail to implicate r‐tocopherol levels or glutathione peroxidase activity as major factors in protecting the retina and pigment epithelium from damage after acute light stress.