Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans  

作　　者：LI Yunhui YE Huayue DU Min ZHANG Yanfen YE Boping PU Yuepu WANG Dayong 

机构地区：[1]Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Nanjing 210009, China [2]Department of Genetics and Developmental Biology, Southeast University, Nanjing 210009, China [3]School of Public Health, Southeast University, Nanjing 210009, China [4]College of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China

出　　处：《Journal of Environmental Sciences》2009年第7期971-979,共9页环境科学学报（英文版）

基　　金：supported by the National Natural Sci- ence Foundation of China (No. 30771113, 30870810)and the Program for New Century Excellent Talents in University;provided by the Caenorhabditis Genetics Center (funded by the NIH, National Center for Foundation from Research Resource)

摘　　要：Apart from the liver disruption, embryotoxicity and genotoxicity, microcystin （MC）-LR also could cause neurotoxicity. Nematode Caenorhabditis elegans was explored as a model to study the neurotoxicity. In the present study, we provided evidence to indicate the neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure to C. elegans. As a result, higher concentrations of MC-LR caused significantly severe defects of chemotaxis to NaCl and diacetyl, and thermotaxis. The neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure might be largely mediated by the damage on the corresponding sensory neurons （ASE, AWA, and AFD） and interneuron AIY. The expression levels ofche-1 and odr-7 were significantly decreased （P 〈 0.01） in animals exposed to MC-LR at concentrations lower than 10 μg/L, whereas the expression levels of ttx-1 and ttx-3 could be significantly （P 〈 0.01） lowered in animals even exposed to 1 μg/L of MC-LR. Moreover, both the chemotaxis to NaCl and diacetyl and the thermotaxis were more significantly reduced in MC-LR exposed mutants of che-1（p674）, odr-7（ky4）, ttx-1（p767）, and ttx-3（ks5） than those in exposed wild-type N2 animals at the same concentrations.Apart from the liver disruption, embryotoxicity and genotoxicity, microcystin （MC）-LR also could cause neurotoxicity. Nematode Caenorhabditis elegans was explored as a model to study the neurotoxicity. In the present study, we provided evidence to indicate the neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure to C. elegans. As a result, higher concentrations of MC-LR caused significantly severe defects of chemotaxis to NaCl and diacetyl, and thermotaxis. The neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure might be largely mediated by the damage on the corresponding sensory neurons （ASE, AWA, and AFD） and interneuron AIY. The expression levels ofche-1 and odr-7 were significantly decreased （P 〈 0.01） in animals exposed to MC-LR at concentrations lower than 10 μg/L, whereas the expression levels of ttx-1 and ttx-3 could be significantly （P 〈 0.01） lowered in animals even exposed to 1 μg/L of MC-LR. Moreover, both the chemotaxis to NaCl and diacetyl and the thermotaxis were more significantly reduced in MC-LR exposed mutants of che-1（p674）, odr-7（ky4）, ttx-1（p767）, and ttx-3（ks5） than those in exposed wild-type N2 animals at the same concentrations.

关 键 词：MC-LR CHEMOTAXIS THERMOTAXIS neurotoxicity Caenorhabditis elegans 

分 类 号：S852.65[农业科学—基础兽医学] Q343.1[农业科学—兽医学]