Dietary vitamin E and pulmonary biochemical and morphological alterations of rats exposed to 0.1 ppm ozone

C. K. Chow, Charles Plopper, M. Chiu, D. L. Dungworth

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Three groups of 28 1-month-old male Sprague-Dawley rats each were fed a basal vitamin E-deficient diet and supplemented with either 0, 11, or 110 ppm vitamin E for 38 days, and were then exposed to 0 or 0.1 ppm ozone continuously for 7 days. Following ozone exposure, the level of reduced glutathione (GSH) and activities of GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and lactate dehydrogenase (LDH), but not of malic dehydrogenase, were significantly elevated in the lungs of rats fed the vitamin E deficient diet. The level of GSH and activities of GSH peroxidase and G-6-PD were also significantly increased in the lungs of the animal group fed the 11 ppm vitamin E diet, while none of the biochemical measurements made was significantly altered by ozone in the 110-ppm vitamin E diet fed rats. Scanning electron microscope examination revealed that five out of six rats on the vitamin E-deficient diet and four out of six from the 11-ppm vitamin E diet had detectable lesions following ozone exposure, as compared with only one of the six exposed animals from the 110-ppm vitamin E diet. The lesion was restricted to bronchiolar epithelium and alveoli immediately adjacent to the bronchiole-alveolar duct junction. None of the control animals had detectable lesions. The results suggest that exposure to ozone at 0.1-ppm level can produce detectable pulmonary damage, and that dietary vitamin E alters pulmonary susceptibility to ozone exposure.

Original languageEnglish (US)
Pages (from-to)315-324
Number of pages10
JournalEnvironmental Research
Volume24
Issue number2
DOIs
StatePublished - Jan 1 1981

Fingerprint

Ozone
vitamin
Vitamin E
Rats
Nutrition
ozone
Lung
diet
Diet
lesion
Animals
Glucosephosphate Dehydrogenase
Peroxidase
animal
glucose
phosphate
Bronchioles
Malate Dehydrogenase
L-Lactate Dehydrogenase
Ducts

ASJC Scopus subject areas

  • Biochemistry
  • Environmental Science(all)

Cite this

Dietary vitamin E and pulmonary biochemical and morphological alterations of rats exposed to 0.1 ppm ozone. / Chow, C. K.; Plopper, Charles; Chiu, M.; Dungworth, D. L.

In: Environmental Research, Vol. 24, No. 2, 01.01.1981, p. 315-324.

Research output: Contribution to journalArticle

@article{88e0e3b003254617b1ad5a7d6dfef5eb,
title = "Dietary vitamin E and pulmonary biochemical and morphological alterations of rats exposed to 0.1 ppm ozone",
abstract = "Three groups of 28 1-month-old male Sprague-Dawley rats each were fed a basal vitamin E-deficient diet and supplemented with either 0, 11, or 110 ppm vitamin E for 38 days, and were then exposed to 0 or 0.1 ppm ozone continuously for 7 days. Following ozone exposure, the level of reduced glutathione (GSH) and activities of GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and lactate dehydrogenase (LDH), but not of malic dehydrogenase, were significantly elevated in the lungs of rats fed the vitamin E deficient diet. The level of GSH and activities of GSH peroxidase and G-6-PD were also significantly increased in the lungs of the animal group fed the 11 ppm vitamin E diet, while none of the biochemical measurements made was significantly altered by ozone in the 110-ppm vitamin E diet fed rats. Scanning electron microscope examination revealed that five out of six rats on the vitamin E-deficient diet and four out of six from the 11-ppm vitamin E diet had detectable lesions following ozone exposure, as compared with only one of the six exposed animals from the 110-ppm vitamin E diet. The lesion was restricted to bronchiolar epithelium and alveoli immediately adjacent to the bronchiole-alveolar duct junction. None of the control animals had detectable lesions. The results suggest that exposure to ozone at 0.1-ppm level can produce detectable pulmonary damage, and that dietary vitamin E alters pulmonary susceptibility to ozone exposure.",
author = "Chow, {C. K.} and Charles Plopper and M. Chiu and Dungworth, {D. L.}",
year = "1981",
month = "1",
day = "1",
doi = "10.1016/0013-9351(81)90161-4",
language = "English (US)",
volume = "24",
pages = "315--324",
journal = "Environmental Research",
issn = "0013-9351",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Dietary vitamin E and pulmonary biochemical and morphological alterations of rats exposed to 0.1 ppm ozone

AU - Chow, C. K.

AU - Plopper, Charles

AU - Chiu, M.

AU - Dungworth, D. L.

PY - 1981/1/1

Y1 - 1981/1/1

N2 - Three groups of 28 1-month-old male Sprague-Dawley rats each were fed a basal vitamin E-deficient diet and supplemented with either 0, 11, or 110 ppm vitamin E for 38 days, and were then exposed to 0 or 0.1 ppm ozone continuously for 7 days. Following ozone exposure, the level of reduced glutathione (GSH) and activities of GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and lactate dehydrogenase (LDH), but not of malic dehydrogenase, were significantly elevated in the lungs of rats fed the vitamin E deficient diet. The level of GSH and activities of GSH peroxidase and G-6-PD were also significantly increased in the lungs of the animal group fed the 11 ppm vitamin E diet, while none of the biochemical measurements made was significantly altered by ozone in the 110-ppm vitamin E diet fed rats. Scanning electron microscope examination revealed that five out of six rats on the vitamin E-deficient diet and four out of six from the 11-ppm vitamin E diet had detectable lesions following ozone exposure, as compared with only one of the six exposed animals from the 110-ppm vitamin E diet. The lesion was restricted to bronchiolar epithelium and alveoli immediately adjacent to the bronchiole-alveolar duct junction. None of the control animals had detectable lesions. The results suggest that exposure to ozone at 0.1-ppm level can produce detectable pulmonary damage, and that dietary vitamin E alters pulmonary susceptibility to ozone exposure.

AB - Three groups of 28 1-month-old male Sprague-Dawley rats each were fed a basal vitamin E-deficient diet and supplemented with either 0, 11, or 110 ppm vitamin E for 38 days, and were then exposed to 0 or 0.1 ppm ozone continuously for 7 days. Following ozone exposure, the level of reduced glutathione (GSH) and activities of GSH peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase (G-6-PD), and lactate dehydrogenase (LDH), but not of malic dehydrogenase, were significantly elevated in the lungs of rats fed the vitamin E deficient diet. The level of GSH and activities of GSH peroxidase and G-6-PD were also significantly increased in the lungs of the animal group fed the 11 ppm vitamin E diet, while none of the biochemical measurements made was significantly altered by ozone in the 110-ppm vitamin E diet fed rats. Scanning electron microscope examination revealed that five out of six rats on the vitamin E-deficient diet and four out of six from the 11-ppm vitamin E diet had detectable lesions following ozone exposure, as compared with only one of the six exposed animals from the 110-ppm vitamin E diet. The lesion was restricted to bronchiolar epithelium and alveoli immediately adjacent to the bronchiole-alveolar duct junction. None of the control animals had detectable lesions. The results suggest that exposure to ozone at 0.1-ppm level can produce detectable pulmonary damage, and that dietary vitamin E alters pulmonary susceptibility to ozone exposure.

UR - http://www.scopus.com/inward/record.url?scp=0019859891&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019859891&partnerID=8YFLogxK

U2 - 10.1016/0013-9351(81)90161-4

DO - 10.1016/0013-9351(81)90161-4

M3 - Article

AN - SCOPUS:0019859891

VL - 24

SP - 315

EP - 324

JO - Environmental Research

JF - Environmental Research

SN - 0013-9351

IS - 2

ER -