The Road to Malignant Cell Transformation after Particulate Matter Exposure: From Oxidative Stress to Genotoxicity.
Miguel Santibáñez-AndradeEricka Marel Quezada-MaldonadoAndrea Rivera-PinedaYolanda Irasema ChirinoClaudia M García-CuellarYesennia Sánchez-PérezPublished in: International journal of molecular sciences (2023)
In cells, oxidative stress is an imbalance between the production/accumulation of oxidants and the ability of the antioxidant system to detoxify these reactive products. Reactive oxygen species (ROS), cause multiple cellular damages through their interaction with biomolecules such as lipids, proteins, and DNA. Genotoxic damage caused by oxidative stress has become relevant since it can lead to mutation and play a central role in malignant transformation. The evidence describes chronic oxidative stress as an important factor implicated in all stages of the multistep carcinogenic process: initiation, promotion, and progression. In recent years, ambient air pollution by particulate matter (PM) has been cataloged as a cancer risk factor, increasing the incidence of different types of tumors. Epidemiological and toxicological evidence shows how PM-induced oxidative stress could mediate multiple events oriented to carcinogenesis, such as proliferative signaling, evasion of growth suppressors, resistance to cell death, induction of angiogenesis, and activation of invasion/metastasis pathways. In this review, we summarize the findings regarding the involvement of oxidative and genotoxic mechanisms generated by PM in malignant cell transformation. We also discuss the importance of new approaches oriented to studying the development of tumors associated with PM with more accuracy, pursuing the goal of weighing the impact of oxidative stress and genotoxicity as one of the main mechanisms associated with its carcinogenic potential.
Keyphrases
- particulate matter
- oxidative stress
- air pollution
- induced apoptosis
- dna damage
- cell death
- diabetic rats
- reactive oxygen species
- ischemia reperfusion injury
- lung function
- risk factors
- single cell
- cell cycle arrest
- endothelial cells
- polycyclic aromatic hydrocarbons
- stem cells
- signaling pathway
- hydrogen peroxide
- endoplasmic reticulum stress
- vascular endothelial growth factor
- squamous cell carcinoma
- mesenchymal stem cells
- young adults
- squamous cell
- nitric oxide
- pi k akt
- fatty acid