Cobilinschi C, Tincu R C, Băetu A E, Deaconu C O, Totan A, Rusu A, Neagu P T, Grințescu I M
"Carol Davila" University of Medicine and Pharmacy - Anesthesiology and Intensive Care - Bucharest, Romania.
Bucharest Emergency Hospital - Anesthesiology and Intensive Care - Bucharest, Romania.
Acta Endocrinol (Buchar). 2021 Apr-Jun;17(2):177-185. doi: 10.4183/aeb.2021.177.
Organophosphate exposure induces many endocrine effects.
In this study we observed the effects of acute stress induced by cholinesterase inhibition on the main hormonal axes.
We included thirteen weanling Wistar rats that were subjected to organophosphate exposure. They were first tested for baseline levels of butyrylcholinesterase, cortisol, free triiodothyronine, thyroxine, thyroid-stimulating hormone and prolactin. Secondly, chlorpyrifos was administered. Next samples were taken to determine the level of all the above-mentioned parameters.
Butyrylcholinesterase was significantly decreased after exposure (p<0.001). Cortisol levels were significantly higher after clorpyrifos administration (358.75±43 241.2±35 nmoL/L)(p<0.01). Although prolactin had a growing trend (450.25±24.65 423±43.4 uI/mL), the results were not statistically significant. Both free triiodothyronine and thyroxine were significantly higher after exposure. Surprisingly, thyroid-stimulating hormone level almost doubled after exposure with high statistical significance (p<0.001), suggesting a central stimulation of thyroid axis. Butyrylcholinesterase level was proportional with thyroid-stimulating hormone level (p=0.02) and thyroxine level was inversely correlated to the cortisol level (p=0.01). Acute cholinesterase inhibition may induce high levels of cortisol, free triiodothyronine, thyroxine and thyroid-stimulating hormone. From our knowledge this is the first study dedicated to the assessment of acute changes of hormonal status in weanling animals after low-dose organophosphate exposure.Conclusion. Acute cholinesterase inhibition may cause acute phase hormonal disturbances specific to shocked patients.
有机磷暴露会引发多种内分泌效应。
在本研究中，我们观察了胆碱酯酶抑制诱导的急性应激对主要激素轴的影响。
我们纳入了13只接受有机磷暴露的断奶Wistar大鼠。首先检测它们的丁酰胆碱酯酶、皮质醇、游离三碘甲状腺原氨酸、甲状腺素、促甲状腺激素和催乳素的基线水平。其次，给予毒死蜱。然后采集样本以测定上述所有参数的水平。
暴露后丁酰胆碱酯酶显著降低（p<0.001）。给予毒死蜱后皮质醇水平显著升高（358.75±43对241.2±35 nmoL/L）（p<0.01）。尽管催乳素有上升趋势（450.25±24.65对423±43.4 uI/mL），但结果无统计学意义。暴露后游离三碘甲状腺原氨酸和甲状腺素均显著升高。令人惊讶的是，促甲状腺激素水平在暴露后几乎翻倍，具有高度统计学意义（p<0.001），表明甲状腺轴受到中枢刺激。丁酰胆碱酯酶水平与促甲状腺激素水平呈正相关（p=0.02），甲状腺素水平与皮质醇水平呈负相关（p=0.01）。急性胆碱酯酶抑制可能会诱导皮质醇、游离三碘甲状腺原氨酸、甲状腺素和促甲状腺激素水平升高。据我们所知，这是第一项致力于评估低剂量有机磷暴露后断奶动物激素状态急性变化的研究。结论。急性胆碱酯酶抑制可能导致休克患者特有的急性期激素紊乱。
