Rix E, Raue F, Deutschle I, Ziegler R
Histochemistry. 1984;80(5):503-8. doi: 10.1007/BF00495442.
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.
就形态学、免疫细胞化学和生物化学方面，对高钙血症状态下慢性C细胞刺激的两种不同模型进行了比较。在由Walker肿瘤的HWCS 256菌株引起的慢性高钙血症状态下，肿瘤植入后第7天，C细胞出现空泡化等退化迹象。在第10天，肿瘤诱导的高钙血症导致核固缩和核溶解等不可逆的细胞损伤。这些形态学变化伴随着甲状腺中放射免疫可测量的降钙素含量下降以及C细胞对急性刺激反应的丧失。相比之下，在由1,25(OH)2D3中毒引起的高钙血症状态下，我们发现C细胞几乎完全脱颗粒，但没有退化或细胞损伤的迹象，尽管甲状腺降钙素含量和降钙素分泌能力大大降低。肿瘤诱导的恶病质作为荷瘤大鼠C细胞损伤的原因可以排除。还讨论了其他可能的原因，如急性过度刺激和直接作用于C细胞的肿瘤因子。
