Thyroid proliferation, body weight, thyrotropin and thyroid hormones in chronic antithyroid (carbimazole) treatment in rats.

O Redmond, AR Tuffery - Journal of Anatomy, 1981 - ncbi.nlm.nih.gov
O Redmond, AR Tuffery
Journal of Anatomy, 1981ncbi.nlm.nih.gov
Male rats (200 g body weight) were either untreated or given carbimazole (0.1 g/100 mg) in
their drinking water for up to 24 weeks. Vincristine sulphate-a metaphase arrest agent-was
used to estimate the mitotic activity of thyroid follicular cells. Measurements of body growth
rate and oxygen consumption showed that the animals were hypothyroid after one week of
treatment. The relationship between body growth and mitotic rate supports the concept of the
thyroid follicular cells as an'expanding'cell population. The mitotic rate (metaphases/10 (4) …
Abstract
Male rats (200 g body weight) were either untreated or given carbimazole (0.1 g/100 mg) in their drinking water for up to 24 weeks. Vincristine sulphate-a metaphase arrest agent-was used to estimate the mitotic activity of thyroid follicular cells. Measurements of body growth rate and oxygen consumption showed that the animals were hypothyroid after one week of treatment. The relationship between body growth and mitotic rate supports the concept of the thyroid follicular cells as an'expanding'cell population. The mitotic rate (metaphases/10 (4) cells. hour+/-SE) rose from the control level of 3.9+/-1.28 to 33.3+/-7.59 after 2 days of treatment and reached a peak of 79.9+/-8.56 on day 5. Thereafter, it declined slowly, but remained significantly greater than control levels until the 16th week of treatment. Changes in mitotic activity were accompanied by characteristic histological changes in the gland. After two days' treatment with carbimazole, the serum concentration of thyrotropin (TSH) was significantly increased and the serum levels of tri-and tetra-iodothyronine were decreased. These results area compared with those of earlier studies and discussed in relation to changes in hormone levels and strongly suggest that TSH is responsible for the hyperplasia of thyroid follicular cells to respond to continued stimulation.
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