Journal
FOOD AND CHEMICAL TOXICOLOGY
Volume 145, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2020.111593
Keywords
Ionic liquids; C8min; AR42J-B13; B-13; B-13/H; Glycolysis; Lactate
Categories
Funding
- Newton-Mosharafa Fund
- UK-based LIVErNORTH charity
- UK National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Chemical and Radiation Threats and Hazards
- Public Health England (PHE)
- UK Engineering and Physical Sciences Research Council (EPSRC) [EP/P030548/1]
- EPSRC [EP/P030548/1] Funding Source: UKRI
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Recent studies have identified the 8C alkyl chain methylimidazolium ionic liquid 1-octy1-3-methylimidazolium in the environment and its potential to trigger the auto-immune liver disease primary biliary cholangitis. The toxicity of a range of methylimidazolium ionic liquids were therefore examined. Oxygen consumption was rapidly inhibited, with potency increasing with alkyl chain length. This preceded caspase 3/7 induction and DNA fragmentation. Time- and dose-dependent loss of dye reduction capacities reflected these effects, with a >700 fold difference in potency between 2C and 10C alkyl chain liquids. None of the ionic liquids directly inhibited mitochondrial complexes I-IV or complex V (F0F1-ATPase). However, dithionite reduction and ESR spectroscopy studies indicate a one electron reduction of oxygen in the presence of a methylimidazolium ionic liquid, suggesting methylimidazolium ionic liquids function as mitochondrial electron acceptors. However, only longer chain ionic liquids form a non-aqueous phase or micelle under aqueous physiological conditions and lead to increases in reactive oxygen species in intact cells. These data therefore suggest that the longer chain methylimidazolium liquids are toxic in sensitive liver progenitor cells because they both readily integrate within the inner mitochondrial membrane and accept electrons from the electron chain, leading to oxidative stress.
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