Arsenic induces transgenerational behavior disorders in Caenorhabditis elegans and its underlying mechanisms
Arsenic induces transgenerational behavior disorders in Caenorhabditis elegans and its underlying mechanisms
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砷诱导秀丽隐杆线虫跨代行为障碍及其机制
DOI：
10.1016/j.chemosphere.2020.126510
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发表时间：
2020
期刊：
影响因子：
8.8
通讯作者：
Wu Hong-Mei
中科院分区：
文献类型：
--
作者：
Zhang Xiong;Zhong Hai-Qing;Chu Zhong-Wei;Zuo Xiang;Wang Li;Ren Xiao-Li;Ma Hao;Du Ruo-Yi;Ju Jing-Juan;Ye Xiao-Lei;Huang Chen-Ping;Zhu Jian-Hong;Wu Hong-Mei
本研究旨在探讨砷对秀丽隐杆线虫行为的影响。elegans）和跨代效应。将同步化的秀丽隐杆线虫（P代）暴露于0、0.2、1.0和5.0 mM NaAsO 2中，并将后续世代（F1和F2）维持在新鲜线虫生长培养基（NGM）上。在同步化后0、12、24、36、48、60和72 h记录行为和生长。结果表明，砷对大鼠头部甩动、身体弯曲、运动速度、波长、幅度等行为指标均有影响，且影响从24 h开始积累，并持续至整个暴露期。行为障碍具有代际性，表现形式各异，其中头部撞击和身体弯曲反应最敏感，但反应在代际间逐渐下降。砷暴露24 h至60 h对秀丽隐翅虫的生长（体长、体宽和体面积）均产生抑制作用，但72 h时处理组与对照组无差异。砷可引起秀丽隐杆线虫多巴胺能神经元的剂量依赖性变性，并抑制BAS-1和CAT-2的表达。砷暴露可诱导GCS-1、GSS-1和SKN-1的表达。总体而言，慢性砷暴露损害的行为，并有跨代效应。头部甩动和身体弯曲反应最敏感。砷致大鼠行为障碍可能与氧化应激引起的多巴胺能神经元变性有关。
The present study aimed to identify the effects of arsenic on behaviors inCaenorhabditis elegans (C. elegans)and the transgenerational effects. The synchronizedC. elegans(P generation) were exposed to 0, 0.2, 1.0, and 5.0 mM NaAsO2and the subsequent generations (F1 and F2) were maintained on fresh nematode growth medium (NGM). The behaviors and growth were recorded at 0, 12, 24, 36, 48, 60, and 72 h post synchronization. The results demonstrated that arsenic affected various indicators regarding the behavior (head thrash, body bend, movement speed, wavelength, amplitude and so on) and in general the effects started to accumulate from 24 h and lasted throughout the exposure. The behavior impairments were transgenerational with varying patterns, amongst the head thrash and body bend responded most sensitively though the responses gradually declined across generations. Arsenic exposure inhibited the growth (body length, body width, and body area) in PC. elegansfrom 24 h to 60 h, however there was no difference between treatments groups and the control at 72 h. Arsenic led to a dose-dependent degeneration of dopaminergic neurons inC. elegans, and inhibition of BAS-1 and CAT-2 expressions. The expressions of GCS-1, GSS-1, and SKN-1 were induced by arsenic exposure. Overall, chronic arsenic exposure impaired the behaviors and there were transgenerational effects. The head thrash and body bend responded most sensitively. Arsenic induced behavioral disorders might be attributed to degeneration of dopaminergic neurons which was associated with oxidative stress.