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Respiratory plasticity after perinatal hyperoxia is not prevented by antioxidant supplementation
Author(s) -
Miller Brooke M.,
Fergusson Elizabeth K.,
Bavis Ryan W.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1444-d
Subject(s) - hyperoxia , antioxidant , oxidative stress , reactive oxygen species , respiratory system , medicine , saline , endocrinology , anesthesia , room air distribution , chemistry , lung , biochemistry , physics , thermodynamics
Chronic perinatal hyperoxia impairs carotid body development and attenuates the hypoxic ventilatory response (HVR) in rats. These effects could be caused by overproduction of reactive oxygen species (ROS) during the hyperoxic exposure. To test this hypothesis, rat pups were given daily injections of a potent antioxidant, manganese (III) tetrakis (1‐methyl‐4‐pyridyl) porphyrin pentachloride (5–10 mg/kg, i.p.), throughout two weeks of developmental hyperoxia (60% O 2 ); controls were injected with saline. Adult carotid body volume and HVR were reduced in hyperoxia‐treated rats ( P <0.05), however there were no apparent effects of antioxidant supplementation on either variable (drug and drug × hyperoxia effects, all P >0.05). Further, protein carbonyl concentrations, measured by ELISA, were normal in blood samples collected after 48 hours or 8 days of hyperoxia ( P >0.05), indicating minimal oxidative stress in the hyperoxic rat pups. Taken together, these results suggest that hyperoxia influences respiratory control development through mechanisms other than overproduction of ROS. Supported by NCRR grant P20 RR‐016463.