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目的 了解铅、镉对肾上腺皮质细胞分泌功能的直接毒作用及可能的介导途径。方法原代分离培养的豚鼠肾上腺皮质细胞 ,分别以 0 0 0、6 2 5、12 5 0、2 5 0 0、5 0 0 0和 10 0 0 0 μmol/L氯化镉(CdCl2 )和 0 0 0、12 5 0、2 5 0 0、5 0 0 0和 10 0 0 0 μmol/L醋酸铅 (PbAc)处理细胞 ,在不同孵育时间 (30～2 40min)分别测定培养液皮质醇水平 ,并观察环 磷酸腺苷 (cAMP)与皮质醇分泌的相关性。结果 6 2 5～ 10 0 0 0 μmol/LCdCl2 引起细胞皮质醇分泌水平降低 ,呈现明显的剂量 效应关系 ,且与时间具有协同抑制效应。 12 5 0～ 10 0 0 0 μmol/LPbAc对皮质醇分泌的毒效应呈低剂量轻度抑制、高剂量回复正常的双相反应 ,表现为皮质醇水平在低剂量降低 (12 5 0和 2 5 0 0 μmol/L) ,而高剂量略升高 (10 0 0 0μmol/L) ,且随时间延长其效应愈为明显。cAMP随CdCl2 剂量增加而降低 ,具有剂量 效应关系 ,其变化与CdCl2 抑制皮质醇分泌具有相关性 ;而PbAc对cAMP的作用则表现为低剂量轻微抑制、高剂量升高 ,且与皮质醇分泌的变化相似。结论 在促肾上腺皮质激素存在下 ,CdCl2 可直接抑制皮质醇的合成分泌 ,PbAc对细胞分泌皮质醇功能的毒效应呈低剂量轻微抑制 ,高剂量回复正常 ,甚至诱导的双?
Objective To understand the direct toxic effects of lead and cadmium on the secretion of adrenocortical cells and the possible mediating pathways. Methods Primary cultured guinea pig adrenal cortex cells were treated with 0, 0, 65, 100, 500, 500 and 100 micromol / L cadmium chloride (CdCl2) and 0 The cells were treated with 0, 125, 0, 500, 500 and 10 000 μmol / L lead acetate (PbAc). Cortisol levels were determined at different incubation times (30 ~ 240 min) To observe the relationship between cAMP and cortisol secretion. Results 6 2 5 ~ 10 0 0 0 0 μmol / L CdCl2 caused a decrease in cell cortisol secretion, showing a dose-dependent effect and a synergistic inhibitory effect with time. The toxic effects of 1250-10000 μmol / LPbAc on cortisol secretion were modestly inhibited at low doses and returned to normal biphasic response at high doses, indicating a decrease in cortisol levels at low doses (125 and 25 0 0 μmol / L), while the high dose slightly increased (10 000 μmol / L), and the more obvious the effect with time. cAMP decreased with the dose of CdCl2, with a dose-response relationship, the change was related to the inhibitory effect of CdCl2 on cortisol secretion. However, the effect of PbAc on cAMP was slightly inhibited at low dose and increased at high dose, Similar changes. Conclusions CdCl2 can directly inhibit the synthesis and secretion of cortisol in the presence of ACTH. The toxic effect of PbAc on the secretion of cortisol is slightly inhibited at low dose, returned to normal at high dose, and even induced by double-