Friedman Y, Hladis P, Babiarz-Crowell D, Burke G
Endocr Res Commun. 1979;6(1):71-92. doi: 10.3109/07435807909070885.
Cholera toxin activated beef thyroid cyclic AMP-dependent protein kinase in a dose (0.2 to 8 microgram/ml)-related fashion. Thus, when beef thyroid slices were incubated with toxin (8 microgram/ml) for 90 minutes and then assayed for protein kinase, the activity ratio (i.e. -cyclic AMP/+cyclic AMP) increased from 0.32 +/- 0.02 to 0.77 +/- 0.06. The toxin (5 microgram/ml)-induced increase was abolished by inclusion of ganglioside GM1 in the incubation medium (I50, 0.7 microgram/ml), whereas, gangliosides GD1a and GT1 were without effect. In contrast, TSH-activated protein kinase was unaffected by ganglioside addition. Cholera toxin increased rat thyroid ornithine decarboxylase (ODC) activity in-vitro in a dose (0.1 to 10 microgram/ml)-related fashion [basal, 100 cf cholera toxin (10 microgram/ml), 1500 pmol 14CO2/g tissue/30 min]. The toxin (1 microgram/ml)- (but not TSH-) induced increase in ODC was abolished by inclusion of ganglioside Ga and GT1 were without effect. Cholera toxin stimulation of ODC was inhibited by indomethacin or iodide as are the stimulatory effects of TSH or dibutyryl cyclic AMP. These results demonstrate that although there are differences in the TSH and cholera toxin responses with respect to receptor (ganglioside) interaction, they nevertheless elicit similar intracellular responses in thyroid.
霍乱毒素以剂量（0.2至8微克/毫升）相关的方式激活牛肉甲状腺环磷酸腺苷依赖性蛋白激酶。因此，当将牛肉甲状腺切片与毒素（8微克/毫升）孵育90分钟，然后检测蛋白激酶时，活性比（即 -环磷酸腺苷/ +环磷酸腺苷）从0.32±0.02增加到0.77±0.06。在孵育培养基中加入神经节苷脂GM1（半数抑制浓度，0.7微克/毫升）可消除毒素（5微克/毫升）诱导的增加，而神经节苷脂GD1a和GT1则无作用。相反，促甲状腺激素激活的蛋白激酶不受神经节苷脂添加的影响。霍乱毒素以剂量（0.1至10微克/毫升）相关的方式在体外增加大鼠甲状腺鸟氨酸脱羧酶（ODC）活性[基础值，100 cf霍乱毒素（10微克/毫升），1500皮摩尔14CO2/克组织/30分钟]。加入神经节苷脂Ga可消除毒素（1微克/毫升）诱导的（但促甲状腺激素诱导的未消除）ODC增加，而GT1无作用。吲哚美辛或碘可抑制霍乱毒素对ODC的刺激，促甲状腺激素或二丁酰环磷酸腺苷的刺激作用也受其抑制。这些结果表明，尽管促甲状腺激素和霍乱毒素在受体（神经节苷脂）相互作用方面的反应存在差异，但它们在甲状腺中引发相似的细胞内反应。
