Effects of atmospheric pollutants on the Nrf2 survival pathway.
OBJECTIVE
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.


METHODS
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.


CONCLUSIONS
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.


CONCLUSIONS
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.


CONCLUSIONS
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.
Instituto de Investigaciones Biomédicas, Departamento de Medicina Genómica y Toxicología Ambiental, Universidad Nacional Autónoma de México, México D.F., 04510, Mexico.
Valentina
V
Rubio
Mahara
M
Valverde
Emilio
E
Rojas
D000393:Air Pollutants / Q000633:toxicity*; D002248:Carbon Monoxide / Q000633:toxicity; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism*; D009589:Nitrogen Oxides / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects; D010126:Ozone / Q000633:toxicity; D052638:Particulate Matter / Q000633:toxicity; D011084:Polycyclic Aromatic Hydrocarbons / Q000633:toxicity; D015398:Signal Transduction / Q000187:drug effects*; D055549:Volatile Organic Compounds / Q000633:toxicity
D000393:Air Pollutants; D047908:Intracellular Signaling Peptides and Proteins; D051267:NF-E2-Related Factor 2; D009589:Nitrogen Oxides; D052638:Particulate Matter; D011084:Polycyclic Aromatic Hydrocarbons; D055549:Volatile Organic Compounds; D010126:Ozone; D002248:Carbon Monoxide