Effects of atmospheric pollutants on the Nrf2 survival pathway
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Background, aim, and scope
Atmospheric pollution is a worldwide problem. Exposure to atmospheric pollutants causes toxic cellular effects. One of the mechanisms of toxicity by these pollutants is the promotion of oxidative stress. Several signaling pathways control cellular redox homeostasis. In this respect, nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial transcription factor in the cell’s response to oxidative stress.
In cellular animal models, exposure to atmospheric pollutants activates Nrf2, attenuating its toxic and even its carcinogenic effects. Therefore, we have reviewed the scientific literature in order to indicate that air pollutants, such as particulate matter, polycyclic aromatic hydrocarbons, and gaseous matter, are Nrf2 pathway inductors, triggering self-defense through the establishment of proinflammatory and antioxidant responses.
Results and discussion
Exposure to reactive molecules as atmospheric pollutants causes the activation of Nrf2 and the subsequent regulation of the expression of cytoprotective and detoxifying enzymes, as well as antioxidants. Moreover, induction of Nrf2 prior to exposure reduces the harmful effects of pollutants. The present article discusses the protective role of the Nrf2 pathway against different atmospheric pollutant insults.
Nrf2 regulates the expression of numerous cytoprotective genes that function to detoxify reactive species produced during atmospheric pollutant metabolic reactions. From the papers highlighted in this review, we conclude that Nrf2 has an important role in the defense against atmospheric pollutant-induced toxicity.
Further studies are needed to understand the signaling events that turn on the system in response to atmospheric pollutant stress. This could allow for the possibility of targeting the pathway for prevention benefits in the near future.
- Effects of atmospheric pollutants on the Nrf2 survival pathway
Environmental Science and Pollution Research
Volume 17, Issue 2 , pp 369-382
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