Different effects of hypercalcemic state induced by Walker tumor (HWCS 256) and 1,25 (OH)D3 intoxication on rat thyroid C cells. An ultrastructural, immunocytochemical, and biochemical study.
Two different models of chronic C cell stimulation by the hypercalcemic state were compared with respect to their morphology, immunocytochemistry, and biochemistry. In the chronic hypercalcemic state due to the HWCS 256 strain of the Walker tumor C cells show signs of degeneration such as vacuolation, on day 7 after tumor implantation. On day 10 tumor induced hypercalcemia leads to irreversible cell damage with karyopyknosis and karyorrhexis. These morphological changes are accompanied by a decline in radioimmunologically measurable calcitonin content of the thyroid and by the loss of response to acute stimulation of C cells. In contrast, in the hypercalcemic state due to 1,25(OH)2D3 intoxication we find an almost complete degranulation of C cells but no signs of degeneration or cell damage, although the thyroid calcitonin content and the calcitonin secretion capacity is greatly reduced. Tumor induced cachexia as a reason for C cell damage in tumor bearing rats could be excluded. Other possible reasons, such as acute overstimulation and tumor factors acting directly on C cells are discussed.
D000818:Animals; D002100:Cachexia / Q000378:metabolism; D002116:Calcitonin / Q000097:blood; D002117:Calcitriol / Q000506:poisoning*; D002279:Carcinoma 256, Walker / Q000150:complications / Q000378:metabolism*; D005260:Female; D006651:Histocytochemistry; D006934:Hypercalcemia / Q000139:chemically induced / Q000209:etiology / Q000378:metabolism*; D007120:Immunochemistry; D051381:Rats; D013961:Thyroid Gland / Q000166:cytology* / Q000378:metabolism / Q000648:ultrastructure
D002116:Calcitonin; D002117:Calcitriol