Abstract
To test the hypothesis that glutathione (GSH) peroxidase is an important component of the lung's anti-oxidant defense systems, O2 toxicity was studied in selenium (Se)-deficient rats. Chronic respiratory disease free rats fed a Se-deficient diet or a diet supplemented with Se for 40 days after weaning were exposed to 80% O2 at atmospheric pressures for 3 days. Activities of GSH peroxidase in lungs of Se-deficient rats were markedly lower than corresponding activities in rats supplemented with 0.5 or 2.0 ppm Se. With O2 exposure, 35% of the rats fed the Se-deficient regimen died, whereas all rats fed Se-supplemented diets survived. Lungs from surviving Se-deficient rats exposed to O2 were edematous. The data suggest that the toxic effects of O2 are enhanced in Se-deficient rats and that nutritional factors contribute to lung susceptibility to oxidant-induced damage.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 695-706 |
| Number of pages | 12 |
| Journal | Research Communications in Chemical Pathology and Pharmacology |
| Volume | 16 |
| Issue number | 4 |
| State | Published - 1977 |
Fingerprint
ASJC Scopus subject areas
- Pharmacology
- Toxicology
Cite this
Enhanced lung toxicity of O2 in selenium deficient rats. / Cross, Carroll E; Hasegawa, G.; Reddy, K. A.; Omaye, S. T.
In: Research Communications in Chemical Pathology and Pharmacology, Vol. 16, No. 4, 1977, p. 695-706.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Enhanced lung toxicity of O2 in selenium deficient rats
AU - Cross, Carroll E
AU - Hasegawa, G.
AU - Reddy, K. A.
AU - Omaye, S. T.
PY - 1977
Y1 - 1977
N2 - To test the hypothesis that glutathione (GSH) peroxidase is an important component of the lung's anti-oxidant defense systems, O2 toxicity was studied in selenium (Se)-deficient rats. Chronic respiratory disease free rats fed a Se-deficient diet or a diet supplemented with Se for 40 days after weaning were exposed to 80% O2 at atmospheric pressures for 3 days. Activities of GSH peroxidase in lungs of Se-deficient rats were markedly lower than corresponding activities in rats supplemented with 0.5 or 2.0 ppm Se. With O2 exposure, 35% of the rats fed the Se-deficient regimen died, whereas all rats fed Se-supplemented diets survived. Lungs from surviving Se-deficient rats exposed to O2 were edematous. The data suggest that the toxic effects of O2 are enhanced in Se-deficient rats and that nutritional factors contribute to lung susceptibility to oxidant-induced damage.
AB - To test the hypothesis that glutathione (GSH) peroxidase is an important component of the lung's anti-oxidant defense systems, O2 toxicity was studied in selenium (Se)-deficient rats. Chronic respiratory disease free rats fed a Se-deficient diet or a diet supplemented with Se for 40 days after weaning were exposed to 80% O2 at atmospheric pressures for 3 days. Activities of GSH peroxidase in lungs of Se-deficient rats were markedly lower than corresponding activities in rats supplemented with 0.5 or 2.0 ppm Se. With O2 exposure, 35% of the rats fed the Se-deficient regimen died, whereas all rats fed Se-supplemented diets survived. Lungs from surviving Se-deficient rats exposed to O2 were edematous. The data suggest that the toxic effects of O2 are enhanced in Se-deficient rats and that nutritional factors contribute to lung susceptibility to oxidant-induced damage.
UR - http://www.scopus.com/inward/record.url?scp=0017335548&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0017335548&partnerID=8YFLogxK
M3 - Article
C2 - 860085
AN - SCOPUS:0017335548
VL - 16
SP - 695
EP - 706
JO - Research Communications in Chemical Pathology and Pharmacology
JF - Research Communications in Chemical Pathology and Pharmacology
SN - 0034-5164
IS - 4
ER -