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交通空气污染对大鼠子代发育及社交行为的影响

本站小编 Free考研考试/2021-12-30

田宇1,
徐晨露1,
黄丹妮1,
冯钰东2,
陈佳峰2,
刘晨阳2,
金永堂1
1. 环境表观遗传实验室, 杭州 310058;
2. 浙江大学医学部, 杭州 310058
作者简介: 田宇(1995-),女,硕士研究生,研究方向为环境卫生学,E-mail:21718610@zju.edu.cn.
基金项目: 国家自然科学基金项目(81673124)


中图分类号: X171.5


Effects of Traffic-Related Air Pollution on Development and Social Behavior of Offspring Rats

Tian Yu1,
Xu Chenlu1,
Huang Danni1,
Feng Yudong2,
Chen Jiafeng2,
Liu Chenyang2,
Jin Yongtang1
1. Environmental Epigenetics Laboratory, School of Medicine, Zhejiang University, Hangzhou 310058, China;
2. Department of Medicine, Zhejiang University, Hangzhou 310058, China

CLC number: X171.5

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摘要:交通空气污染与儿童自闭症的关联时有报道,但其因果关系仍待进一步探索。为研究出生前后暴露于不同水平的交通空气污染环境对生长发育和自闭症相关社交行为的影响,将Wistar大鼠雌雄1∶1交配,受孕雌鼠根据子代接触交通污染的时间(出生后暴露或胚胎期暴露)及浓度(低、中和高3个水平)分为6组。在子代出生后21~27 d,测量子代的体重、身长及大脑脏器系数,并根据三箱实验评估社交行为,同时检测仔鼠脑组织组蛋白H3第4个赖氨酸(H3K4)的甲基化水平。结果显示,出生前后,尤其是胚胎发育阶段接触较高浓度的交通空气污染物可导致幼鼠体重及大脑湿重较低,身长较短、大脑脏器系数偏高等生长发育特征改变。同时,出生前后较高浓度的交通空气污染物暴露可导致幼鼠出现社交能力下降、社交记忆受损及社交新颖性减弱等典型自闭症样行为改变。虽然组蛋白H3K4甲基化水平与交通空气污染物浓度之间未见统计学关联,但出生后暴露组具有较高的H3K4甲基化水平,提示出生前后接触交通空气污染物可能与自闭症的发生发展有关,而不同暴露时期对脑组织H3K4甲基化水平的影响,为今后进一步探讨自闭症的表观遗传机制提供了线索。
关键词: 交通空气污染/
组蛋白H3K4甲基化/
自闭症/
社交行为

Abstract:It has been reported that the occurrence of autism in children might be associated with traffic-related air pollution, which needs to be further explored. To study the effects of different levels of traffic-related air pollution, Wistar rats were used to study growth development and social behavior after exposure to traffic-related air pollution before and after birth. Wistar rats were mated at the male to female ratio of 1∶1. Pregnant female rats were divided into six groups and then exposed to different concentration of traffic-related air pollutants (i.e., low, medium and high levels) at different time point (i.e., postnatal or embryonic). From the 21st to 27th day after the birth, the body weight, length and brain coefficient of the offspring were measured and social behavior was assessed by three chambers test, while the methylation of histone 3 lysine 4 (H3K4) in brain tissues was detected. The results showed that the offspring rats had lower body weight, shorter body length and higher organ coefficient with higher concentrations of traffic-related air pollutants exposure, especially during the embryonic development. Likewise, typical autistic-like behavioral changes such as decreased social competence, impaired social memory and reduced social novelty in offspring rats can also be observed. Although there was no positive correlation between levels of histone H3K4 methylation and concentration of traffic-related air pollution, the postnatal exposure group had higher level of H3K4 methylation. The above data suggested that traffic-related air pollution might be a potential reason of autism. Moreover, the changes in H3K4 methylation in brain tissues that induced by traffic-related air pollution at different exposure time point could provide an evidence for further study on the epigenetic mechanism of autism.
Key words:traffic-related air pollution/
histone H3K4 methylation/
autism/
social behavior.

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