Effect of polychlorinated biphenyl (PCB) on the thyroid gland of rats. Ultrastructural and biochemical investigations

Abstract

Polychlorinated biphenyls (PCB) produced ultrastructural lesions in thyroid follicular cells and reductions in serum thyroxine levels in rats that were time- and dose-dependent. The acute effects (4 week) of PCB (50 and 500 ppm) consisted of an accumulation of lysosomal bodies and colloid droplets in follicular cells with abnormalities of microvilli on the luminal surface. The chronic administration (12 week) of PCB (50 and 500/250 ppm) resulted in a striking distention of many follicular cells with large lysosomal bodies with strong acid phosphatase activity and colloid droplets, blunt and abnormally branched microvilli, and mitochondrial vacuolation. These ultrastructural alterations in follicular cells were associated with a highly significant reduction in serum thyroxine with both the low and the high dose of PCB. Follicular cells remained responsive to the lowered thyroxine level after feeding PCB for 4 and 12 weeks and underwent moderate compensatory hypertrophy and hyperplasia. Thyroid follicles were smaller than in controls and were lined by more columnar cells that occasionally formed papillary projections into the colloid. Residual ultrastructural alterations persisted for 12 weeks following cessation of feeding the compound, and serum thyroxine levels were significantly lower than in control rats. However, 35 weeks after discontinuing PCB, thyroid follicular cells were similar to those in controls and serum thyroxine levels had returned to normal. The striking ultrastructural lesions in follicular cells produced by feeding PCB to rats appeared to contribute to the lowering of serum thyroxine levels, in combination with the known stimulation of peripheral thyroxine metabolism by these compounds. Certain metabolic alterations produced by PCB intoxication in experimental animals and human beings may be related to an alteration in thyroid function.