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Oxidative Stress, Inflammatory Biomarkers and Toxicity in Mouse Lung and Liver after Inhalation Exposure to 100% Biodiesel or Petroleum Diesel Emissions
Citation:
Shvedova, A., N. Yanamala, A. Murray, E. Kisin, T. Khaliullin, M. Hatfield, A. Tkach, Todd Krantz, D. Nash, C. King, Ian Gilmour, AND S. Gavett. Oxidative Stress, Inflammatory Biomarkers and Toxicity in Mouse Lung and Liver after Inhalation Exposure to 100% Biodiesel or Petroleum Diesel Emissions. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, 76(15):907-21, (2013).
Impact/Purpose:
The purpose was to evaluate the adverse effects in mice after inhalation exposure to neat (100%) biodiesel (B100) emissions compared to petroleum diesel emissions (D100). The data indicate that oxidative stress and inflammation were greater after exposure to biodiesel than after exposure to diesel exhaust.
Description:
BACKGROUND: Over the past decade, biodiesel (BD) has become a first alternative energy source that is economically viable and meets requirements of the Clean Air Act. Due to lower mass emissions and reduced hazardous compounds compared to diesel combustion emissions (CE), BD exposure is proposed to cause fewer adverse health effects. However, considering the broad use of BD and its blends in different industries, this assertion needs to be supported and validated by mechanistic and toxicological data. OBJECTIVE: The main goal is to evaluate the adverse effects in mice after inhalation exposure to neat (100%) biodiesel (B100) CE compared to petroleum diesel (D100). METHODS: BALB/cJ mice were exposed by inhalation of CE from B100 and D100 to target concentrations of 0, 50, 150 and 500 ug/m3 (4hr/day, 5d/wk, for 4 weeks). Homogenates of lung and liver obtained at 2h post inhalation exposure were investigated for biomarkers of inflammation, oxidative stress and tissue damage. RESULTS: Biomarkers of tissue damage and inflammation were significantly elevated in mice exposed to B100. Additionally, B100 CE caused a significant accumulation of oxidatively modified proteins, an increase in 4-hydroxynonenal, oxidation of protein thiols, and depletion of antioxidant - gluthatione. The cytokines which play an important role in modulating inflammatory responses also exhibited key differences between B100 and D100 CE exposures. CONCLUSION: The results indicate that tissue damage, oxidative stress, inflammation and cytokine response were more pronounced in mice exposed to BD CE. Further studies are required to understand what combustion products in BD CE accelerate oxidative and inflammatory responses.