Lack of enhancement of bleomycin lung injury in vitamin E-deficient rats

Stephen G. Jenkinson, Charles A. Duncan, Richard A. Lawrence, James F. Collins

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

DNA breakage caused by bleomycin may be due to the formation of bleomycin-ferrous complexes, which activate molecular oxygen to form activated oxygen species or free radicals. If bleomycin administration results in intracellular free radical formation, then peroxidation of cellular membranes may be a prominent mechanism in producing bleomycin lung toxicity. In order to explore this hypothesis, we performed experiments instilling bleomycin intratracheally into vitamin E-deficient and control rats. Exhaled ethane production and formation of lung tissue malonaldehyde were measured as indices of lipid peroxidation. Mortality and serial changes in lung collagen content were also measured to assess increases in lung injury in the vitamin E-deficient rats. No increases in ethane exhalation occurred in the groups receiving bleomycin as compared to the matched controls receiving saline. Lung malonaldehyde was found to increase at 96 hours following bleomycin instillation. No increases in mortality or the formation of lung collagen occurred in vitamin E-deficient rats treated with bleomycin as compared to control rats given bleomycin. These results suggest that vitamin E-deficient rats do not have enhanced lung toxicity following bleomycin instillation and that although free radical activation may be occurring, lipid peroxidation does not appear to be a prominent mechanism in producing bleomycininduced pulmonary toxicity.

Original languageEnglish (US)
Pages (from-to)264-269
Number of pages6
JournalJournal of Critical Care
Volume2
Issue number4
DOIs
StatePublished - Dec 1987

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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