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目的观察出生后早期镉暴露对仔鼠生理发育及神经行为发育的影响,探讨相关损伤机制。方法采用生理及神经行为学检测方法。新生ICR仔鼠40只,随机分为氯化镉(Cd Cl_2)2.0、1.0、0.5 mg/kg暴露组和生理盐水对照组,每组10只,从出生后3~13 d进行腹腔注射染毒,隔天1次,末次染毒后24 h检测仔鼠脑组织中丙二醛(MDA)、谷胱甘肽(GSH)含量,部分半脑进行神经病理学检查;剩余动物观察至出生后35 d发育成熟后取脑进行神经病理学检查、称取各脏器质量计算脏器系数。结果 Cd Cl_22.0、1.0 mg/kg组脑组织MDA水平显著增加(P<0.05),2.0 mg/kg组GSH活力低于其他各组(P<0.05);Cd Cl_22.0、1.0 mg/kg组开眼时间延迟(P<0.05),各暴露组旷场探索达标时间显著延迟(P<0.05),Cd Cl_22.0 mg/kg组悬崖回避达标时间有一定影响(P<0.05);脑组织神经病理学检查发现Cd Cl_22.0 mg/kg组大脑皮层椎体细胞排列较对照组稀疏。结论出生后早期接触镉能够诱导小鼠生理及神经行为发育改变。
Objective To observe the effects of early postnatal cadmium exposure on the physiological development and neurobehavioral development of offspring, and to explore the related injury mechanisms. Methods Using physiological and neurobehavioral testing methods. Forty newborn ICR offspring were randomly divided into exposure groups (2.0,1.0,0.5 mg / kg) and saline control groups (CdCl_2), 10 rats in each group. The mice were injected intraperitoneally , The other day, the content of malondialdehyde (MDA) and glutathione (GSH) in the brain tissue of the offspring rats were detected 24 h after the last exposure, and the neuropathological examination was performed on some of the hemispheres. The remaining animals were observed until 35 d after birth Mature brain brain neuropathology examination, weighed the quality of organs calculated organ coefficients. Results The levels of MDA in brain tissue of Cd Cl_22.0 and 1.0 mg / kg groups were significantly increased (P <0.05), and the GSH activities of 2.0 mg / kg group were lower than those of other groups (P <0.05). Cd Cl_22.0 and 1.0 mg / kg (P <0.05). There was a significant delay in exploring open time (P <0.05) in open field of each exposure group, and a certain influence on Cl 12.0 mg / kg (P <0.05) Nephrology examination revealed that the arrangement of vertebral cells in the cerebral cortex of Cd Cl_22.0 mg / kg group was sparse compared with the control group. Conclusions Exposure to cadmium early in life can induce physiological and neurobehavioral changes in mice.