Chemical toxicology of reactive species in the atmosphere: two decades of progress in an electron acceptor and an electrophile

J Toxicol Sci. 2016;41(Special):SP37-SP47. doi: 10.2131/jts.41.SP37.

Abstract

Air pollutants such as diesel exhaust particles (DEP) are thought to cause pulmonary diseases such as asthma as a result of oxidative stress. While DEP contain a large number of polycyclic aromatic hydrocarbons, we have focused on 9,10-phenanthrenequinone (9,10-PQ) and 1,2-naphthoquinone (1,2-NQ) because of their chemical properties based on their oxidative and chemical modification capabilities. We have found that 9,10-PQ interacts with electron donors such as NADPH (in the presence of enzymes) and dithiols, resulting in generation of excess reactive oxygen species (ROS) through redox cycling. We have also shown that 1,2-NQ is able to modify protein thiols, leading to protein adducts associated with activation of redox signal transduction pathways at lower concentrations and toxicity at higher concentrations. In this review, we briefly introduce our findings from the last two decades.

Publication types

  • Review

MeSH terms

  • Air Pollutants / toxicity*
  • Antioxidant Response Elements*
  • Asthma / etiology
  • NADP
  • Naphthoquinones
  • Oxidation-Reduction
  • Oxidative Stress
  • Phenanthrenes
  • Polycyclic Aromatic Hydrocarbons / isolation & purification
  • Polycyclic Aromatic Hydrocarbons / toxicity*
  • Reactive Oxygen Species / toxicity*
  • Signal Transduction
  • Sulfhydryl Compounds
  • Vehicle Emissions / analysis
  • Vehicle Emissions / toxicity

Substances

  • Air Pollutants
  • Naphthoquinones
  • Phenanthrenes
  • Polycyclic Aromatic Hydrocarbons
  • Reactive Oxygen Species
  • Sulfhydryl Compounds
  • Vehicle Emissions
  • 9,10-phenanthrenequinone
  • NADP
  • 1,2-naphthoquinone