Adaptive response to neurotoxicity on locomotion behavior by severe metal exposure was investigated in Caenorhabditis elegans. Exposure to 2.5μM of metals induced a moderate but significant reduction of locomotion behavior and induction of hsp-16.2::gfp expression. After pre-exposure to 2.5μM of metals, the reduced locomotion behavior induced by subsequent 50 and 100μM of metal exposure were significantly prevented, and the induction of hsp-16.2::gfp expression caused by subsequent 50 and 100μM of metal exposure were significantly suppressed. In contrast, after pre-exposure to 50μM examined metals, the reduced locomotion behavior induced by subsequent 50 and 100μM metal exposure were further decreased, and the noticeable induction of hsp-16.2::gfp expression caused by subsequent severe metal exposure were further enhanced. Therefore, pre-treatment with mild metal exposure can activate the adaptive response to neurotoxicity on locomotion behavior induced by subsequent severe metal exposure in nematodes.

In this study, we investigated the locomotion behavior changes at different developmental stages in Caenorhabditis elegans exposed to metals for 4h. No obvious differences could be observed in young adults exposed to examined metals, and only exposure to 100μM of examined metals could significantly decrease the locomotion behaviors of L4 larvae. Incontrast, exposure to 50 and 100μM of examined metals induced noticeable repression of locomotion behaviors at L1-L3 larval stages, and a significant decrease of locomotion behaviors could be observed in L1 larvae exposed to Pb and Hg, and in L2 larvae exposed to Hgat the concentration of 2.5μM. More over, the L1-, L2-, and L3-larvae exposed to metals for 4h exhibited similar neurobehavioral toxicity manner to L4-larvae exposed to metals for 24h. Therefore, younger larvae showed more severe deficits in neurobehavioral phenotypes than L4 larvae and young adults in metal-expose dnematodes.

We examined the possible multiple defects induced by acute and prolonged exposure to high levels of manganese (Mn) solution by monitoring the endpoints of lifespan, development, reproduction, and stress response. Our data suggest that acute exposure (6 h) to Mn did not cause severe defects of life span, development, and reproduction, similarly, no significant defect could be found in animals exposed to a low concentration of Mn (2.5μmol/L) for 48 h. In contrast, prolonged exposure (48 h) to high Mn concentrations (75 and 200μmol/L) resulted in significant defects of life span, development, and reproduction, as well as the increase of the percentage of population with hsp-16.2::gfp expression indicating the obvious induction of stress responses in exposed animals. Moreover, prolonged exposure (48 h) to high concentrations (75 and 200 μmol/L) of Mn decreased the expression levels of antioxidant genes of sod-1, sod-2, sod-3, and sod-4 compared to control. Therefore, prolonged exposure to high concentrations of Mn will induce the severe defects of life span, development, and reproduction in nematodes possibly by affecting the stress response and expression of antioxidant genes in Caenorhabditis elegans.

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 10μg/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.

Chemotaxis to water-soluble attractants is mainly controlled by ASE sensory neuron whose specification is regulated by che-1 in Caenorhabditis elegans. Our data suggested that exposure to high concentrations of metals, such as Pb, Cu, Ag, and Cr, would result in severe defects of chemotaxis to water-soluble attractants of NaCl, cAMP, and biotin. Moreover, the morphology of ASE neuron structures as observed by relative fluorescent intensities and relative size of fluorescent puncta of cell bodies, relative lengths of sensory endings in ASE neurons, and the expression patterns of che-1 were obviously altered in metal exposed animals when they meanwhile exhibited obvious chemotaxis defects to water-soluble attractants. In addition, the dendrite morphology could be noticeably changed in animals exposed to 150 μmol/L of Pb, Cu, and Ag. Furthermore, we observed significant decreases of chemotaxis to water-soluble attractants in Pb exposed che-1 mutant at concentrations more than 2.5 μmol/L, and in Cu, Ag, and Cr exposed che-1 mutant at concentrations more than 50 μmol/L. Therefore, impairment of the ASE neuron structures and functions may largely contribute to the appearance of chemotaxis defects to water-soluble attractants in metal exposed nematodes.