Do organic solvents induce changes in the dopaminergic system? Positron emission tomography studies of occupationally exposed subjects
Do organic solvents induce changes in the dopaminergic system? Positron emission tomography studies of occupationally exposed subjects
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DOI：
10.1007/s004200050204
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发表时间：
1997-09-01
影响因子：
3
通讯作者：
Langstrom, B
中科院分区：
文献类型：
--
作者：
Edling, C;Hellman, B;Langstrom, B
目的：本研究的目的是测试的假设，长期职业暴露于有机溶剂可能会影响多巴胺的水平和营业额man. Methods：一项研究进行了17例神经精神症状，由于职业溶剂暴露，和11名健康的非暴露男性志愿者（对照）。正电子发射断层扫描（PET）用于评估纹状体多巴胺能功能，使用L-[C-11]多巴，[C-11]诺米芬辛和[C-11]雷氯必利作为示踪剂。结果如下：与未暴露的对照组相比，职业暴露于有机溶剂的受试者的多巴胺合成率显着增加。在控制暴露组和对照组之间的年龄差异后，溶剂暴露的影响变得不那么明显，从+32%（P = 0.009）降至+25%（P = 0.07）。关于[C-11]诺米芬辛的结合没有差异。诊断为中毒性脑病和未诊断为中毒性脑病的患者在L-[C-11]多巴、[C-11]诺米芬辛和[C-11]雷氯必利的壳核摄取方面没有差异。结论：这些数据支持这一假设，即长期暴露于有机溶剂可能会增加大脑中多巴胺的合成速率，而不会影响突触前末梢或突触后多巴胺受体的数量。
Objectives: The objective of this study was to test the hypothesis that long-term occupational exposure to organic solvents may effect the levels and turnover of dopamine in man. Methods: A study was performed on 17 patients with neuropsychiatric symptoms due to occupational solvent exposure, and 11 healthy non-exposed male volunteers (controls). Positron emission tomography (PET) was used to assess striatal dopaminergic function, using L-[C-11]DOPA, [C-11]nomifensine and [C-11]raclopride as tracers. Results: The rate of dopamine synthesis was significantly increased among subjects with occupational exposure to organic solvents compared with non-exposed controls. After controlling for the difference in age between exposed and controls, the effect of solvent exposure became less apparent and was reduced from +32% (P = 0.009) to +25% (P = 0.07). There were no differences with regard to the binding of [C-11]nomifensine. Patients with and without the diagnosis of toxic encephalopathy did not differ with regard to their putaminal uptake of L-[C-11]DOPA, [C-11]nomifensine and [C-11]raclopride. Conclusion: The data support the hypothesis that long-term exposure to organic solvents may increase the rate of dopamine synthesis in the brain without affecting the number of presynaptic terminals or postsynaptic dopamine receptors.