| Abstrakt: |
White Leghorn chickens respond to dietary goitrogenic compounds by forming either colloidal or hyperplastic goiters. Thiourea does not cause increases in DNA above that seen in controls, although thyroid weight increases. This may be due to a secondary toxic effect of thiourea on the chick thyroid, which inhibits cellular replication. Both methimazole- and propylthiouracil- (PTU) fed birds exhibit cellular hyperplasia and increases in DNA amounts beyond control levels. The rapid thyroid growth in methimazole-treated birds from 30 to 70 days of age is partially due to follicular colloid accumulation. Growth of the thyroid in PTU-fed birds is thought to be due to cellular hyperplasia and hypertrophy, since DNA values are greatest in these glands. Histological studies of the thyroid glands confirm the results of DNA and protein assays for all three goitrogen-treated groups. The ultrastructural changes associated with prolonged stimulation of the chick thyroid are an increase in the amount of primary and secondary lysosomes, microvilli, and mitochondria, and a dilation of the endoplasmic reticulum and Golgi apparatus. It is thought that micropinocytosis is a more important endocytotic process during goiter development in the chick than is phagocytosis. |
