4.5 Article

Caenorhabditis elegans Bicarbonate Transporter ABTS-1 Is Involved in Arsenite Toxicity and Cholinergic Signaling

Journal

CHEMICAL RESEARCH IN TOXICOLOGY
Volume 23, Issue 5, Pages 926-932

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/tx100016e

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Funding

  1. NIH National Center for Research Resources
  2. National Science Council, Taiwan [NSC96-2313-B-002-037, NSC97-2313-B-002-016-MY3]

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Arsenic poisoning affects millions of people worldwide. Although there is accumulating evidence to suggest that the nervous system is a target of arsenic, relatively little information is known regarding its effects on the nervous system. The effects of arsenite on the nervous system in Caenorhabditis elegans were investigated in the present study. We found that abts-1, which encodes a Na+-dependent Cl-/HCO3- transporter, is required to protect C. elegans from arsenite toxicity. The abts-1::GFP transgene is primarily expressed in neurons and the hypodermis, but stronger expression was also observed in the pharynx and body wall muscle cells after exposure to arsenite. The steady-state level of ABTS-1 mRNA increased in response to arsenite exposure. We showed that worms lacking abts-1 are hypersensitive to the paralytic effects of the cholinesterase inhibitor, aldicarb, and the nicotinic acetylcholine receptor agonist, levamisole. We also showed that arsenite enhanced sensitivity to aldicarb and levamisole in abts-1 mutant worms. Our results indicate neuronal effects of arsenite and the ABTS-1 bicarbonate transporter.

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