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Resources » Paper

Li Y et al. (2009) J Environ Sci (China) "Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans."

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  • Comments on Li Y et al. (2009) J Environ Sci (China) "Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans." (0)

  • Overview

    PMID:
    19862965
    DOI:
    10.1016/S1001-0742(08)62370-0
    Status:
    Publication type:
    Journal_article
    WormBase ID:
    WBPaper00035416

    Li Y, Ye H, DU M, Zhang Y, Ye B, Pu Y, & Wang D (2009). Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans. J Environ Sci (China), 21, 971-9. doi:10.1016/S1001-0742(08)62370-0

    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 of che-1 and odr-7 were significantly decreased (P < 0.01) in animals exposed to MC-LR at concentrations lower than 10 microg/L, whereas the expression levels of ttx-1 and ttx-3 could be significantly (P < 0.01) lowered in animals even exposed to 1 microg/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.


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