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DOI: 10.1177/107155760000700502 Chronic Hypoxia and Developmental Regulation of Cytochrome C Expression in Rats
Center for Perinatal Biology, Department of Pharmacology and Physiology, Loma Linda University School of Medicine, Loma Linda, California
Center for Perinatal Biology, Department of Pharmacology, Loma Linda University School of Medicine, Loma Linda, California; lzhang{at}som.llu.edu Objective: To test the hypothesis that chronic hypoxia upregulates cytochrome c expression in heart, brain, and liver of fetal and maternal rats. Methods: Time-dated pregnant Sprague-Dawley rats were divided into normoxic and hypoxic (48 hours of 10.5% oxygen from days 19 to 21) groups, and were killed on day 21. Tissue levels of cytochrome c in heart, brain, and liver were determined by using monoclonal antiserum for cytochrome c. Results: Chronic hypoxia caused a decrease in fetal body weight (5.3 ± 0.1 to 4.7 ± 0.1 g) and an increase in heart/body weight ratio (0.0048 ± 0.0001 to 0.0061 ± 0.0002). Cytochrome c levels were 4-, 2.6-, and 13-fold higher in heart, liver, and brain, respectively, of the mother than of the fetus. Chronic hypoxia did not change cytochrome c levels in maternal tissues but caused a 70% increase and 54% decrease in cytochrome c levels in the fetal heart and liver, respectively. No difference was observed in the fetal brain. Conclusions: The results suggest that expression of cytochrome c is tissue specific and developmentally regulated. Chronic hypoxia showed differential regulation of cytochrome c levels both developmentally and tissue specifically. The increased sensitivity of cytochrome c in fetal tissue to chronic hypoxia is likely to represent a fetal adaptive mechanism to the stress of chronic hypoxia.
Key Words: Mitochondria adaptation fetus heart
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