The persistence of tritiated DNA ([3H]DNA) in the thyroids of rats given propylthiouracil (PTU) or PTU plus thyroxine was compared with that in control animals who received either no drugs or thyroxine alone. When only PTU was given, large goitres developed from which [3H]DNA was lost more rapidly than from thyroids of control animals. Administration of thyroxine with PTU led to only slight thyroidal enlargement, but the persistence of [3H]DNA was similarly reduced.The results suggested that PTU might have a toxic effect, reducing the lifespan of thyroid cells and this was further investigated using monolayer thyroid cultures.Thyroid-stimulating hormone (TSH) accelerated the incorporation of tritiated thymidine ([3H]TdR) into cultures, but when PTU was also given the uptake was retarded. PTU alone was less effective in inhibiting [3H]TdR incorporation.The persistence of [3H]DNA in thyroid cultures was unaffected by PTU and was decreased by TSH. When PTU and TSH were given together there was a greatly increased loss of isotope from the cells.
SUMMARY
Lymphocyte chromosomes of untreated and thyrotoxic patients treated with radioactive iodine have been compared with those of control subjects studied concurrently. Untreated patients had a higher percentage of cells with more than 46 chromosomes. 131I-treated patients who were compared with controls within 2–3 months of therapy had significantly increased incidences of cells containing fewer than 46 chromosomes and cells with chromatid and chromosome aberrations. Patients examined 2–5 yr. after radioactive iodine treatment showed similar changes in lesser degree.
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