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The effect of an acute dose of biotin at the pre-implantation stage and its relation with female sex steroids in the rat.


An acute dose of biotin (10 mg/100 g body weight) in two subcutaneous injections when given to a rat on day 1 and 2 of pregnancy, caused resorption of fetuses and placentae. Pregnancies under such biotin-treated conditions were maintained by continued estrogen or progesterone therapy. Biotin-treated pregnant rats failed to maintain normal levels of uterine weight, glycogen and protein as well as hepatic protein concomitantly with the loss of pregnancy. Estrogen therapy under such conditions improved all the parameters in these organs including the placenta, but progesterone therapy did not. Glucose-6-phosphate dehydrogenase (G-6-PD) activity in ovary, adrenal, liver and uterus was also reduced following biotin-induced loss of pregnancy which had been improved by estrogen or progesterone therapy. Nevertheless, estrogen was superior to progesterone in stimulating the enzyme activity in these organs excepting the adrenal. As far as the tissue response to biotin, estrogen or progesterone in the nonpregnant rat is concerned, biotin and progesterone exerted a suppressing effect on uterine glycogen and protein and also on liver protein, while estrogen stimulated them. Similarly biotin and progesterone adversely affected G-6-PD activity in all the organs studied except the liver and adrenal. Estrogen stimulated the enzyme activity in all these organs but adrenal. The study suggests that the primary reason for an acute dose of biotin-induced loss of pregnancy is blockage of estrogen production, which probably regulates endogenous progesterone secretion. The associated metabolic derangements are probably secondary to estrogen deficiency and are discussed.

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