Nanoparticle-rich diesel exhaust-induced liver damage via inhibited transactivation of peroxisome proliferator-activated receptor alpha

Abstract

Diesel exhaust emission contains a high amount of nano-sized particles and is considered to be systemically distributed in the body. However, few studies about the effects of nanoparticle rich-diesel exhaust (NR-DE) on liver have been reported. The present investigation focuses on the effects of NR-DE on livers in rats, especially concerning inflammation and lipid metabolism. Male F344 rats were exposed to fresh air or low (24 ± 7 µg/m ), medium (39 ± 4 µg/m ) and high (138 ± 20 µg/m ) concentrations of NR-DE for 1, 2, or 3 months (5 hours/day, 5 days/week). Exposure to both medium and high concentrations of NR-DE for one month increased plasma asparate aminotransferase and alanine aminotransferase activities, while only high concentrations increased plasma interleukin-6 and hepatic nuclear factor kappa B (NFκB), suggesting that activation of hepatic inflammatory signaling took place. Although these exposures elevated peroxisome proliferator-activated receptor (PPAR) α levels or its binding activity to the response element, neither activated PPARα-target genes such as β-oxidative enzymes nor inhibited NFκB elevation. Thus, NR-DE may contain some materials that inhibit PPARα activation in relation to lipid metabolism and inflammation. Taken together, NR-DE exposure at one month may cause inflammation; however, this finding may not be observed after a longer exposure period. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1985-1995, 2016.

Rooibos tea (<i>Aspalathus linearis</i>) extract protects against air particulate matter induced hepatic oxidative stress in Nrf2-independent manner

“…1B) activities respectively,when compared to control. The data also showed that pretreatment with aqueous rooibos extract significantly (p<0.001) caused a 1.55-and 1.42-fold decrease in serum AST and ALT activities when compared to DEP exposure only ( Fig.1A & B), Exposure of rats to nanoparticle rich-diesel exhaust has been reported to increase serum ALT and AST activities (Ito et al, 2016). The present study was in agreement with this earlier study.…”

TF-343 Alleviates Diesel Exhaust Particulate-Induced Lung Inflammation via Modulation of Nuclear Factor-κB Signaling

“…PM is a complex mixture of solid and/or liquid organic and inorganic substances suspended in the atmosphere and comprises many different types of particle depending on the emission source (e.g., natural or industrial), including diesel exhaust particles (DEP), residual oil fly ash, and urban air particles [1]. Epidemiological and toxicological studies have shown that exposure to PM can induce and exacerbate clinical manifestations of lung [2], liver [3], kidney [4], and heart [5] diseases. In particular, PM with an aerodynamic diameter < 2.5 μ m (i.e., PM2.5 or fine particles) can affect the human respiratory and circulatory systems, since small particles can travel deep into the respiratory tract, carrying toxic compounds into lung alveoli and blood vessels or capillaries [6, 7].…”

Establishment of an artificial particulate matter-induced lung disease model through analyzing pathological changes and transcriptomic profiles in mice

“…Firstly, in this study, we analyzed the PAHs and OC/EC ratios in APM and DEP. PAHs and OC/EC ratios are associated with the induction and exacerbation of lung diseases [8][9][10][11][12][13][14][15] . Our results showed that PAH levels were higher in APM than in DEP, and the OC/EC ratio was similar between DEP and APM (Fig.…”