AJP - Regulatory, Integrative and Comparative Physiology, Vol 247, Issue 3 520-R526, Copyright © 1984 by American Physiological Society
Endotoxin treatment protects vitamin E-deficient rats from pulmonary O2 toxicity
L. Frank and K. Neriishi
Endotoxin treatment in normal rats has a marked protective effect against
O2 toxicity (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47:
577-581, 1979 and 51: 577-583, 1981), and endotoxin's protective action is
associated with stimulation of the lung's enzymatic antioxidant defense
system (superoxide dismutase, catalase, glutathione peroxidase, and
glucose-6-phosphate dehydrogenase). Vitamin E-deficient animals are
especially sensitive to hyperoxidant stresses, including pulmonary O2
toxicity. In these studies we tested whether endotoxin could reverse the
increased susceptibility of vitamin E-deficient rats to hyperoxic
challenge. We found that untreated vitamin E-deficient rats do succumb more
readily to O2 toxicity [0/11 alive at 72 h in greater than 95% O2, lethal
time for 50% of the animals (LT50) = 50 h] than rats fed a regular diet
(4/14 alive, LT50 = 69 h). In contrast, 15 of 16 vitamin E-deficient rats
treated with endotoxin survived the same O2 exposures (P less than 0.001)
and showed significantly reduced pulmonary edema compared with the other
groups. The endotoxin-treated vitamin E-deficient group was also the only
one to demonstrate significant elevations of all the antioxidant enzymes
during O2 exposure, suggesting that the antioxidant enzyme defenses of the
lung have a more primary and important role in prevention of O2-induced
lung injury than the lipid-associated antioxidant, vitamin E.
