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α‐tocopherol improves impaired physiology of rat type II pneumocytes isolated from experimentally injured lungs
Author(s) -
Müller B.,
Hochscheid R.,
Seifart C.,
Barth P. J.
Publication year - 2000
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2000.00730.x
Subject(s) - physiology , medicine , biology
Background Oxidant stress delivered by nitrogen dioxide (NO 2 ) inhalation impairs the function of extracellular surfactant as well as surfactant phospholipid metabolism in type II pneumocytes. Because protection against oxidant stress is important to normal lung function, the lung contains a variety of antioxidants, including vitamin E. Whether administration of this antioxidant during NO 2 inhalation attenuates NO 2 ‐induced alterations in phospholipid metabolism in type II pneumocytes has not been studied. Methods We exposed rats to identical NO 2 body doses (720 p.p.m. x h) using continuous, intermittent, or repetitive protocols. During exposure periods, the animals received daily intramuscular injections of vitamin E (25 mg kg −1 ). We isolated type II pneumocytes from NO 2 ‐exposed rats and evaluated them for cell yield and viability, as well as for synthesis and secretion of phosphatidylcholine (PC) as measures of surfactant metabolism. Results The yield of type II pneumocytes was significantly elevated from animals that had been exposed continuously to NO 2 whereas in intermittently and repeatedly exposed rats, cell yield was similar to yield from control animals. Viability of the isolated cells was similar in controls and all NO 2 exposure protocols. Vitamin E treatment of the NO 2 ‐exposed rats neither changed cell yield nor cell viability. Phospholipid de novo synthesis, as estimated by choline incorporation into PC, was increased most after continuous NO 2 inhalation whereas in the other conditions there was only a slight increase. Vitamin E administration further increased phospholipid synthesis; this difference reached statistical significance only in the case of intermittent NO 2 exposure. Secretion of phosphatidylcholine from type II cells was only reduced after continuous NO 2 inhalation and administration of the antioxidant reduced the impairment. Conclusion Because vitamin E appears to preserve the ability of type II pneumocytes isolated from NO 2 ‐exposed rats to synthesize and secrete surfactant lipid, we conclude that administration of vitamin E may mitigate NO 2 ‐induced lung injury.