Induction of antioxidant enzyme activity by hyperoxia (60 % O2) in the developing chick embryo

At premature birth, man and animals are exposed to relatively high oxygen levels, compared with intra-uterine conditions, at a time when their antioxidant enzyme (AOE) system is still immature. Using the chick embryo as a study model, we investigated changes in the AOE system in response to hyperoxi...

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Veröffentlicht in:The Journal of physiology 1998-05, Vol.509 (1), p.289-296
Hauptverfasser: Golde, Jolanda C., Borm, Paul J., Wolfs, Marion C., Rhijnsburger, Els H., Blanco, Carlos E.
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Sprache:eng
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Zusammenfassung:At premature birth, man and animals are exposed to relatively high oxygen levels, compared with intra-uterine conditions, at a time when their antioxidant enzyme (AOE) system is still immature. Using the chick embryo as a study model, we investigated changes in the AOE system in response to hyperoxia applied at different time points during the incubation period. Relations between hyperoxia and AOE activity were studied in selected organs (brain, heart, liver, intestine and lungs) of developing chick embryos (during the second half of the incubation period). Incubated White Leghorn eggs were divided into four groups: control ( n = 100) and three test groups exposed for 48 h to 60 % O 2 on day 10 (test group 1, n = 80), day 14 (test group 2, n = 60) and day 18 (test group 3, n = 30). Superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) enzyme activities were measured in homogenates of the brain, heart, liver, intestine and lungs. Exposure to hyperoxia at different time points during incubation resulted in a 2- to 10-fold increase in SOD activity in all organs except the brain. Catalase and GPx enzyme activities were only induced in test group 1, 48 h after initiation of hyperoxia. In the developing chick embryo, hyperoxia can produce a temporary induction of AOE activity, which is dependent on the AOE, organ, incubation time and time point of exposure.
ISSN:0022-3751
1469-7793
DOI:10.1111/j.1469-7793.1998.289bo.x