- page settings
- showhide sidebar
- showhide empty fields
- layout
- (too narrow)
- open all
- close all
- Page Content
- Overview
- External Links
- History
- Referenced
- Tools
- Tree Display
- My WormBase
- My Favorites
- My Library
- Recent Activity
- Comments (0)
history logging is off
Tree Display
My Favorites
My Library
Comments on Kirsten Helmcke et al. (2008) C.elegans Aging, Stress, Pathogenesis, and Heterochrony Meeting "Characterization of effects of methylmercury on Caenorhabditis elegans" (0)
Overview
Kirsten Helmcke, Alexandre Benedetto, David Miller, & Michael Aschner (2008). Characterization of effects of methylmercury on Caenorhabditis elegans presented in C.elegans Aging, Stress, Pathogenesis, and Heterochrony Meeting. Unpublished information; cite only with author permission.
Mercury (Hg) displays neurotoxic effects via unknown molecular mechanisms. Humans are typically exposed to methylmercury (MeHg) upon consumption of seafood from which it is absorbed in the digestive tract to eventually pass through the blood-brain and placental barriers. We hypothesized that C. elegans would be a valuable model for studying the effects of MeHg on the nervous system and for delineating molecular mechanisms of toxicity and genetic susceptibility. Replicate experiments confirm that MeHg is toxic to C. elegans. As expected from studies of other animals in which MeHg toxicity is enhanced by early exposure, L1 larvae (LC50=1.3mM MeHg) are more susceptible than L4 animals (LC50=2.3mM MeHg) to acute treatment (30 min). L4 lethality is enhanced by exposure to MeHg for longer periods (6 hour, LC50=0.43mM MeHg; and 15-hour, LC50=0.34mM MeHg). Inductively coupled plasma-mass spectrometry established that Hg content in worm tissues is correlated with both duration and concentration of MeHg exposure. We have evaluated surviving animals for developmental and reproductive defects. Brood size is not affected by MeHg, but a delay in egg-laying coupled with decreased body size are indicative of developmental delay. While spontaneous and stimulus-induced movement indicated no alterations in behavior, chronically treated L4 animals display decreased swimming rates after exposure to MeHg is terminated. Analysis of cell specific GFP reporters did not detect obvious MeHg-induced changes in morphology or process placement for various neuron classes (dopamine, acetylcholine, or GABA). Quantitative studies in neurotransmitter systems, quantitative behavioral tests, and genetic screens are forthcoming. Our research indicates that C. elegans is a useful tool for studying MeHg toxicity and will allow us to examine molecular mechanisms and genetic susceptibility for the effects of this toxin.