Int. J. Dev. Biol. 41: 283 - 289 (1997)
© UPV/EHU Press

Carbon monoxide and the embryo.

M A Robkin

Department of Environmental Health, School of Public Health and Community Medicine, University of Washington, Seattle 98195, USA. robkin@u.washington.edu

ABSTRACT Mammals are homeotherms and expend considerable energy maintaining their body temperatures. The temperature of a mammalian embryo on the other hand is maintained by the mother and the embryo can devote its metabolic energy to growth and development. The mammalian embryo is acting as a poikilotherm and its energy needs are thus considerably less than if it were a comparably sized homeotherm. The energy requirements of the preimplantation rat embryo are generated by anaerobic metabolism. As it grows, aerobic metabolism develops. In culture, the addition of carbon monoxide to the perfusing gas for early rat embryos has a much smaller effect than decreasing the oxygen concentration. Carbon monoxide appears to be a relatively mild toxicant until the embryo is much larger, is depending much more on transport of oxygen by red blood cells, and the fraction of required metabolic energy produced by anaerobic metabolism has become quite small. The effect from smoking during gestation may be either by the concomitant reduction in food intake or a more direct toxic effect from some components in the smoke. Carbon monoxide does not seem to be the culprit. The possible mitigating effect of a compensatory increase in fetal hematocrit in response to any hypoxia must also be considered. Humans have no yolk sac placenta as rodents do, but if the switch from anaerobic to aerobic metabolism is correlated with the stage of development, then carbon monoxide exposure should not represent any significant risk to the human embryo until later in gestation.