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Prenatal oxidative stress: I. Malondialdehyde in hypoxic and hyperoxic chick embryos
M K Stock1, K K Silvernail, J Metcalfe
1Heart Research Laboratory, Oregon Health Sciences University, Portland.
Insights
Chick embryos exposed to altered oxygen levels did not show increased lipid peroxidation, suggesting a protective adaptation against oxidative stress. This indicates enhanced antioxidant defenses in response to hyperoxia.
Area of Science:
- Developmental Biology
- Environmental Physiology
- Biochemistry
Background:
- Metabolic rate and oxygen tension correlate with free radical formation.
- Previous studies showed hyperoxia increases chick embryo growth and metabolism.
- Oxidative damage is a concern with increased oxygen exposure.
Purpose of the Study:
- To test if chick embryos adapt to altered prenatal oxygen availability to prevent oxidative damage.
- To investigate lipid peroxidation levels in chick embryos under hypoxia and hyperoxia.
Main Methods:
- Used thiobarbituric acid assay to measure malondialdehyde (MDA), a marker of lipid peroxidation.
- Examined MDA concentrations in liver, chorioallantoic membrane, brain, and heart.
- Exposed chick embryos to hypoxia (15% O2) and hyperoxia (60% O2) late in incubation.
Main Results:
- Liver had higher MDA concentrations than other examined tissues.
- No significant differences in MDA levels were found in embryos exposed to hypoxia or hyperoxia compared to normoxic controls.
- Increased aerobic metabolism from hyperoxia was not accompanied by increased lipid peroxidation.
Conclusions:
- Chick embryos do not exhibit increased lipid peroxidation when exposed to hyperoxia.
- Embryos may adapt to hyperoxia by enhancing antioxidant defenses to mitigate free radical damage.
- Prenatal oxygen availability influences embryonic development and oxidative stress response.
Abstract:
Evidence suggests a positive correlation between metabolic rate (VO2), or ambient oxygen (O2) tension, and the rate of formation of free radicals from O2. We have previously demonstrated that the rates of growth, VO2, protein and DNA accumulation, and the activity of cytochrome oxidase (a key mitochondrial respiratory enzyme), are increased significantly by exposing the chick embryo to 72 h of hyperoxia (60% O2) late in incubation. To test the hypothesis that the chick embryo responds to a prenatal alteration in O2 availability in such a way as to protect its tissues from oxidative damage, we have used the thiobarbituric acid assay to estimate lipid peroxidation (a major form of free radical damage) in selected organs from chick embryos exposed to altered O2 availability. We found significantly higher concentrations of malondialdehyde (MDA, a secondary product of lipid peroxidation) in liver than in chorioallantoic membrane, brain, or heart. However, embryos exposed to brief (72 h) hypoxia (15% O2) or hyperoxia (60% O2) late in incubation, or 48 h of such exposure followed by 24 h of incubation in pure O2, exhibited no significant difference in MDA levels compared to normoxic (21% O2) controls in any of the tissues examined. We conclude that the increase in aerobic metabolism induced in the chick embryo by 3 days of hyperoxia is not accompanied by an increase in lipid peroxidation. We postulate that the chick embryo adapts to hyperoxia in such a way as to escape additional free radical damage, perhaps by increasing the capacity of its antioxidant defenses to compensate for a potential increase in the rate of free radical generation.