Tsuji Ryozo, Kobayashi Kumiko, Ikeda Maya, Yoshioka Takafumi, Yamada Tomoya, Seki Takaki, Okuno Yasuyoshi, Nakatsuka Iwao, Tsuruo Yoshihiro, Kishioka Shiroh
Environmental Health Science Laboratory, Sumitomo Chemical Co., Ltd., Osaka Japan.
J Appl Toxicol. 2002 Nov-Dec;22(6):423-9. doi: 10.1002/jat.881.
Synthetic pyrethroids are among the most common pesticides and insecticides currently in worldwide use. Eriksson and co-workers postulated that oral exposure of mice to pyrethroids during a neonatal brain growth spurt induces permanent disturbance in the cerebral muscarinic cholinergic receptor (MAChR) and behaviour. However, the scientific basis for these phenomena is now under discussion. The present study was performed to determine whether the experimental findings of Eriksson's study could be reproduced in newborn mice by inhalation. Male and female NMRI mice were exposed to d-allethrin by whole-body inhalation for 6 h per day between postnatal days 10 and 16. Actual concentrations of d-allethrin were 0.43, 1.35, 3.49 and 74.2 mg m(-3) (equivalent to 0.70, 2.2, 5.7 and 120.2 mg kg(-1) day(-1), respectively), and the mass median aerodynamic diameter and geometric log-standard deviation of mist particles ranged from 2.58 to 2.98 micro m and from 1.58 to 2.09 micro m for all groups, respectively. The highest exposure level in the present study (74.2 mg m(-3)) was ca. 13,000 times as high as the concentration used in practice. The MAChR in the three brain areas (cortex, hippocampus and striatum) and motor activity were examined at the ages of 17 days and 4 months. In addition, a water-maze test was performed at the age of 11 months. There was no systemic toxicity interfering with the interpretation of assay results. The neonatal exposure to d-allethrin by inhalation did not induce effects either on the brain MAChR density and motor activity at 17 days and 4 months or on performance in the learning/memory test at the age of 11 months. The effects of allethrins on developmental neurotoxicity that Eriksson and co-workers reported previously were not reproduced in the present study.
合成拟除虫菊酯是目前全球使用最广泛的杀虫剂之一。埃里克松及其同事推测,在新生小鼠脑生长突增期经口接触拟除虫菊酯会导致大脑毒蕈碱型胆碱能受体(MAChR)和行为出现永久性紊乱。然而,这些现象的科学依据目前仍在讨论之中。本研究旨在确定埃里克松研究的实验结果能否通过吸入方式在新生小鼠中重现。在出生后第10天至16天,对雄性和雌性NMRI小鼠进行全身吸入d - 烯丙菊酯处理,每天6小时。d - 烯丙菊酯的实际浓度分别为0.43、1.35、3.49和74.2 mg m(-3)(分别相当于0.70、2.2、5.7和120.2 mg kg(-1) 天(-1)),所有组雾滴颗粒的质量中位空气动力学直径和几何对数标准差分别为2.58至2.98μm和1.58至2.09μm。本研究中的最高暴露水平(74.2 mg m(-3))约为实际使用浓度的13,000倍。在17日龄和4月龄时检测了三个脑区(皮层、海马体和纹状体)的MAChR以及运动活性。此外,在11月龄时进行了水迷宫试验。没有系统毒性干扰测定结果的解释。新生期经吸入接触d - 烯丙菊酯对17日龄和4月龄时的脑MAChR密度和运动活性以及11月龄时学习/记忆测试的表现均未产生影响。本研究未重现埃里克松及其同事之前报道的烯丙菊酯对发育神经毒性的影响。