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Fig. 1. Hypoxia causes growth retardation, lethality and apoptosis. (A) Western blot analysis. Protein extracts at stages 21 and 25 from embryos exposed to 21%, 10% and 5% O2 were studied by Western blot using anti-phopsho-p38-MAPK and anti-p38-MAPK. Anti-tubulin alpha antibodies were used as a loading control. A 5% O2 exposure caused a strong cellular stress during the embryonic development. (B) Densitometric quantification of phospho-p38-MAPK from immunoblots in the different experimental conditions as described in material and method. (C) Growth of embryos at 21 in functions of time and of oxygen rate. Less oxygen is available more the retardation is important and hypoxic embryos maintained their delay. (D) Lateral view of embryos 42 hours after fertilization. When control embryos were stage 30, embryos exposed to 10% O2 were stage 28 and embryos exposed to 5% O2 were stage 25. (E) Embryo survival in function of oxygen level. Moderate hypoxia permits survival but strong hypoxia causes significant embryonic death. (F) Stage 25 embryos were sectioned (n=15) and TUNEL stained. Positive cells werecounted on frontal sections of control and hypoxic embryos. The average of positive cells per embryos is compared on the graph. Apoptosis was promoted with hypoxia. *P<0.05; **P<0.005; ***P<0.001. Scale bar = 400 μm. Image published in: Hidalgo M et al. (2012) Copyright © 2012. Image reproduced with permission of the Publisher, The Company of Biologists Ltd. Larger Image Printer Friendly View

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