4.7 Article

Airborne toluene exposure causes germline apoptosis and neuronal damage that promotes neurobehavioural changes in Caenorhabditis elegans

Journal

ENVIRONMENTAL POLLUTION
Volume 256, Issue -, Pages -

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.envpol.2019.113406

Keywords

Reprotoxicity; Neurotoxicity; Locomotion; Volatile organic compounds; Vapor chamber

Funding

  1. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brasil (CAPES) [001]
  2. CNPq [453963/2014-5]
  3. FAPERGS/PqG [18/2551-0000434-0]
  4. CNPq/FAPERGS/DECIT/SCTIEMS/PRONEM [16/2551-0000248-7]
  5. FAPERGS/PRONUPEQ [16/2551-0000526-5]
  6. UNIPAMPA
  7. CAPES
  8. PQ2/CNPq
  9. NIH Office of Research Infrastructure Programs [P40 OD010440]
  10. FAPERGS/PRONUPEQ

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Toluene is a highly volatile organic solvent present in gasoline. Exposure mainly occurs by absorption via the pulmonary tract and easily reaches the central nervous system, which causes toxic effects. Toluene toxicity has been described but not well established. The present work aimed to evaluate the effects of airborne exposure to toluene, the in vivo model Caenorhabditis elegans was assessed to determine whether nematode could be used to evaluate the effects of exposure to toluene and the possible mechanisms of toxicity of the solvent. Worms at the first or fourth larval stages were exposed to toluene for 48 or 24 h, respectively, in a laboratory-developed vapor chamber at concentrations of 450, 850, 1250 and 1800 ppm. We observed increases in worm mortality and significant developmental delays that occurred in a concentration-dependent manner. An increased incidence of apoptotic events in treated germline cells was shown, which was consistent with observed reductions in reproductive capacity. In addition, toluene promoted significant behavioural changes affecting swimming movements and radial locomotion, which were associated with changes in the fluorescence intensity and morphology of GABAergic and cholinergic neurons. We conclude that toluene exposure was toxic to C. elegans, with effects produced by the induction of apoptosis and neuronal damage. (C) 2019 Elsevier Ltd. All rights reserved.

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