Savolainen H, Pfäffli P
Acta Pharmacol Toxicol (Copenh). 1986 Sep;59(3):209-13. doi: 10.1111/j.1600-0773.1986.tb00156.x.
Male Wistar rats exposed to 5, 10 or 20 p.p.m. 4-methylcyclohexyl-1,6-dicarboxylic acid anhydride vapour for 2-11 weeks showed dose-dependent blood anhydride concentrations. The maximum concentrations were found after two weeks. At five exposure weeks, they were smaller but they did not decrease further thereafter. The change was coincident with increased epoxide hydrase activity in liver. The excretion of 4-methylcyclohexyl-1,6-dicarboxylic acid was detected in the urine. The excretion was linearly related to the exposure in specimens collected during the 10th and 11th week. Brain acetylcholinesterase activity was transiently inhibited by the exposure at the two higher doses while decreased enzyme activity in the isolated spinal cord axons was only found after 11 weeks. This change was simultaneous with increased creatine kinase activity in the cerebellar homogenate. In the occupational setting, acetylcholinesterase activity might only be significantly inhibited in lungs because of the low exposure levels.
将雄性Wistar大鼠暴露于浓度为5、10或20 ppm的4-甲基环己基-1,6-二羧酸酐蒸气中2至11周，结果显示血酐浓度呈剂量依赖性。两周后发现血酐浓度最高。在暴露五周时，血酐浓度较低，但此后不再进一步下降。这一变化与肝脏中环氧水解酶活性增加相一致。在尿液中检测到了4-甲基环己基-1,6-二羧酸的排泄。在第10周和第11周采集的样本中，该排泄量与暴露量呈线性相关。在两个较高剂量下，暴露会使脑乙酰胆碱酯酶活性暂时受到抑制，而仅在11周后才发现分离的脊髓轴突中酶活性降低。这一变化与小脑匀浆中肌酸激酶活性增加同时发生。在职业环境中，由于暴露水平较低，乙酰胆碱酯酶活性可能仅在肺部受到显著抑制。
