Zinc, cadmium, metallothionein, and progesterone: do they participate in the etiology of pregnancy induced hypertension?
Cadmium, a toxic heavy metal, has been incriminated in the etiology of essential hypertension. Zinc, an essential micronutrient necessary for growth, competes with cadmium for binding sites in biochemical processes; zinc deficiency states (i.e. pregnancy and low protein diet) might expose an individual to increased risk of cadmium toxicity. The increased sensitivity to cadmium during pregnancy could also be related to the effect of progesterone on zinc and cadmium metabolism through the actions of metallothionein (MT). MT is a low molecular weight protein believed to function in cadmium detoxification. Several studies in lab animals have documented a late gestation drop of maternal MT levels. This was thought to be due to rising progesterone levels. If there is also a late gestation drop in human maternal MT, then the propensity toward maternal cadmium toxicity would be enhanced. Therefore, we propose that when a zinc deficient woman becomes pregnant and is exposed to both the nutritional demands of the fetus and to the influence of progesterone, she will be likely to develop the manifestations of cadmium toxicity (i.e. hypertension, proteinuria, edema, etc.).
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D008668:Metallothionein / Q000378:metabolism; D008954:Models, Biological; D011225:Pre-Eclampsia / Q000209:etiology / Q000378:metabolism; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology* / Q000378:metabolism; D011374:Progesterone / Q000378:metabolism; D015032:Zinc / Q000172:deficiency*
D002104:Cadmium; D011374:Progesterone; D008668:Metallothionein; D015032:Zinc