Accumulated oxidative stress risk in HUVECs by chronic exposure to non-observable acute effect levels of PM2.5

Toxicol In Vitro. 2022 Aug:82:105376. doi: 10.1016/j.tiv.2022.105376. Epub 2022 May 10.

Abstract

Few studies have reported the accumulation of non-observable acute effect (NOAE) of PM2.5, especially exposure to the NOAE doses (NOAEDs) of PM2.5 in chronic way. To address this issue, HUVECs were cultured from the 1st to 30th generations (G1 to G30) and treated by the NOAED PM2.5 once every three passages. The generational changes of oxidative damage markers, inflammatory factors, and cell adhesion molecules (CAMs) were monitored in HUVECs at G6, G12, G18, G24, and G30, and proteomes at G18 and G30, respectively. The oxidative damages monotonically accumulated with exposure time elongation and PM2.5 dose increases. Similar to the oxidative trends, VCAM1 and ICAM1 significantly and dose-dependently increased at G30. However, many inflammatory factors altered with complex patterns to respond the NOAEDs' PM2.5. Proteomic results demonstrated most proteins expressed stably, and the generational proteome alterations were more apparent than the NOAEDs' PM2.5 induced ones. The PM2.5-related proteins varied much, but only few can cross the doses and generations. These observations suggested that the proteins changed holistically rather than individually. In summary, SOD1, SUMO2, and H3F3A may initiate HUVECs responses to PM2.5, and then broadcast and accumulate the NOAE via DNA repair, immune response, and glycolysis.

Keywords: HUVECs; Non-observable acute effect dose; Oxidative stress; PM(2.5); Proteomics.

MeSH terms

  • Air Pollutants* / toxicity
  • Oxidation-Reduction
  • Oxidative Stress
  • Particulate Matter* / toxicity
  • Proteomics

Substances

  • Air Pollutants
  • Particulate Matter