THE EFFECTS OF THYROID AND PARATHYROID DEFICIENCY ON REPRODUCTION IN THE RAT1

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Abstract
Sexually mature female rats were made thyroid-deficient by surgery or by irradiation of the thyroid gland with I131 or At211. Thyroid hormone was replaced with desiccated thyroid, L-thyroxine, or L-triiodothyronine. Supplemental calcium was given orally as calcium gluconate. Animals were mated to test reproductive capacity 2 to 3 months after thyroid removal thus assuring complete elimination of residual thyroid hormone. Thyroid-deficient rats had small litters and fewer pregnancies, only 31% compared to normal, 79% pregnancies. All three forms of thyroid hormone supplement increased the number of conceptions to 84% , and litter sizes were within control limits. Stillbirths, prolonged gestation, and maternal tetany were common in I131 -treated groups as well as in surgically thyroparathyroidectomized rats regardless of whether or not supplemental thyroid hormone was given. In 46% of the cases tested the serum calcium level of I131-treated, thyroxine-supported rats was less than 6 mg% at parturition, whereas the average serum calcium of normal controls was 10.5 mg%. Variable radiation damage to the parathyroid glands of I131-treated animals was observed histologically. There was a rough correlation between the extent of structural parathyroid damage and a lower than normal serum calcium level. Thyroid hormone was shown to be essential for normal fertility and pregnancy, but its role in parturition, if any, could not be demonstrated. The difficult labor observed in the I131-treated rats was considered to be due to parathyroid deficiency.