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Overview:

Exposure to elevated levels of heavy metals such as copper (Cu2+) and cadmium (Cd2+) is toxic to humans and threatens wildlife. A key objective of the field of toxicology is to quantify adverse effects of chemical substances (e.g., environmental pollutants, drugs) on living organisms.

C. elegans is well-validated for toxicological research and recommended by NIH for whole-animal toxicology and safety testing. Strengths of C. elegans include:

  • Chemical effects on C. elegans predict toxic effects in mammals
  • Performing tests on C. elegans reduces the use of mammals in toxicology testing
  • The wealth of knowledge on C. elegans, coupled with powerful gene manipulation technologies, can provide powerful insights into toxic effects on whole organisms and uncover gene/environment interactions.

Introducing the ScreenChip System: a platform for real-time readouts of toxic effects on health

The ScreenChip phenotyping platform can be used to test a wide range chemical toxins on C. elegans.

  • Faster detection of chemical toxins or other adverse stimuli (e.g., oxidative stress, hypoxia) than other whole-animal assays.
  • Direct and reliable quantification of a worm’s physiological health.
  • Recording of neuronal and muscle activity, which may be disrupted by neurotoxins.
  • Comparison of acute vs. chronic exposures, and synergistic effects.
  • Molecular-, cellular- and organ-level responses to toxins can be studied.
  • Access to genes and gene networks involved in defenses against toxic substances or that enhance susceptibility.
  • Developmental studies of toxicants during the C. elegans life cycle, from L1 to adult.

Measuring the heavy metals, copper & cadmium 

Exposure to elevated levels of (copper) Cu2+, e.g., from corroded plumbing systems, is toxic to humans. Copper pollution also threatens aquatic wildlife such as salmon.

Routes of human exposure to cadmium (Cd2+) include fossil fuel combustion, municipal waste incineration, fertilizers, tobacco smoking, contaminated food, and industrial soil and water pollution. Cd2+ contributes to cardiovascular and kidney disease and threatens wildlife.

Fig. 1: Copper toxicity. (A): Dose-dependent inhibition of pharyngeal pumping after 60 min exposure. (B): Same, after 30 min exposure (*, P < 10-5; 2-tailed Mann-Whitney Wilcoxon Test).

Fig. 2: Cadmium toxicity. Same methods as in Fig. 1 (*, P =0.002; 2-tailed Mann-Whitney Wilcoxon Test).

Measuring the organophosphate insecticide, dichlorvos

Like other organophosphates, dichlorvos is a neurotoxin that inhibits acetylcholinesterase, an enzyme involved in synaptic transmission. Environmental contamination results primarily from agricultural uses and aerial spraying; the chemical is banned in Europe.

Health risks from chronic exposure include neurological and cognitive dysfunction, including increased risk for ADHD in children. Dichlorvos is also toxic to honeybees, fish, birds and other wildlife.

Fig. 3. Dichlorvos toxicity. Same methods as Figs. 1 and 2 except worms were cultured for 24 h before recordings (*, P < 10-12; 2-tailed Mann-Whitney Wilcoxon Test).

Key Publications:

  • Caenorhabditis elegans as a model in developmental toxicology. Boyd WA, Smith MV, Freedman JH. Methods Mol Biol. 2012;889:15-24. doi: 10.1007/978-1-61779-867-2_3.
  • Caenorhabditis elegans as a powerful alternative model organism to promote research in genetic toxicology and biomedicine. Honnen S (2017). Arch Toxicol. May;91(5):2029-2044. doi: 10.1007/s00204-017-1944-7.
  • C. elegans: a medium-throughput screening tool for toxicology (2006).
  • Sublethal toxicity endpoints of heavy metals to the nematode Caenorhabditis elegans. Jiang Y et al. (2016). PLoS One, 11(1):e0148014.
  • Evaluation of sublethal effects of dichlorvos upon Caenorhabditis elegans based on a set of end points of toxicity. Jadhav KB, PS Rajini (2009). J Biochem Molecular Toxicology 23(1): 9-17

Unpublished data were provided by JC Weeks, KJ Robinson and WM Roberts. Funding from Oregon BEST.

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