Environmental toxicity, oxidative stress and apoptosis: ménage à trois

Our plain-English summary of Environmental toxicity, oxidative stress and apoptosis: ménage à trois, by R. Franco, R. Sánchez-Olea, E.M. Reyes-Reyes, et al (Mutation Research, 2009).

The study

• Authors: R. Franco, R. Sánchez-Olea, E.M. Reyes-Reyes, M.I. Panayiotidis
• Journal: Mutation Research
• Published: 2009;674(1-2):3-22
• Type of article: Review
• Cited by: 365 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Apoptosis is an evolutionary conserved homeostatic process involved in distinct physiological processes including organ and tissue morphogenesis, development and senescence. Its deregulation is also known to participate in the etiology of several human diseases including cancer, neurodegenerative and autoimmune disorders. Environmental stressors (cytotoxic agents, pollutants or toxicants) are well known to induce apoptotic cell death and to contribute to a variety of pathological conditions. Oxidative stress seems to be the central element in the regulation of the apoptotic pathways triggered by environmental stressors. In this work, we review the established mechanisms by which oxidative stress and environmental stressors regulate the apoptotic machinery with the aim to underscore the relevance of apoptosis as a component in environmental toxicity and human disease progression.

In plain English

This article was a short review (a "minireview"), not a new study. The authors gathered earlier research on how environmental stressors trigger apoptosis (programmed cell death) and on the role of oxidative stress. The stressors covered were metals, particulate matter, cigarette smoke, carbon monoxide, asbestos, pesticides, dioxins, polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs) and radiation. Asbestos had one short section. Summarizing other researchers' work, the authors wrote that asbestos has been shown to cause oxidative stress and DNA damage, and apoptosis in mesothelial and lung epithelial cells. They wrote that iron-derived reactive species have been suggested to drive this, and that amphibole fibers contain more iron than chrysotile. They also reported that crocidolite has been shown to deplete the cell antioxidant glutathione, and that iron chelators and antioxidants prevent asbestos-induced DNA damage and apoptosis. The authors concluded that redox signaling is one of the central mechanisms by which many environmental stressors trigger apoptosis. They acknowledged that research on mechanisms is lacking for many hazardous contaminants, and that space limits kept many stressors out of the review.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Minireview (literature review) of published research; no new data
• Who was studied: No study population. The review summarized published research on cells and organisms exposed to environmental stressors. For asbestos it mentions mesothelial and lung epithelial cells.
• Exposure: Environmental stressors: metals (antimony, arsenic, beryllium, cadmium, chromium, cobalt, copper, lead, mercury, nickel, vanadium), particulate matter and smoke, carbon monoxide, asbestos (amphiboles, chrysotile, crocidolite named), pesticides, dioxins, PCBs and PAHs, ionizing radiation and ultraviolet radiation
• Main results:
  • The review stated, citing earlier studies, that asbestos has been shown to cause oxidative stress and DNA damage (double-strand breaks)
  • The review stated that several research groups have shown asbestos causes apoptosis in mesothelial and lung epithelial cells
  • The review noted that iron-derived reactive species have been suggested to mediate asbestos-induced apoptosis, and that amphibole fibers have a higher iron content than chrysotile asbestos
  • The review reported that crocidolite has been shown to deplete the cell's glutathione (an antioxidant)
  • The review reported that iron chelators and antioxidants prevent asbestos-induced DNA damage and apoptosis
  • The review reported that asbestos has been shown to release cytochrome c inside cells, which activates caspase 9 (part of the mitochondrial cell-death pathway)
  • The review reported that chrysotile asbestos activates the Fas death-receptor pathway
  • The review reported that several studies have shown p53-dependent transcription plays a role in asbestos-induced DNA damage and apoptosis
• The authors' conclusion: The authors concluded that the summarized data show redox signaling is one of the central mechanisms by which many environmental stressors trigger or modulate apoptosis
• Limitations the authors state:
  • The authors stated that research on how many hazardous environmental contaminants cause cell death is very limited
  • The authors stated that many environmental stressors were left out of the review because of space limits

Topics

Medical terms in this study, explained in our Lexicon: Oxidative Stress, Apoptosis, Etiology, Disease Progression.

Related studies

• Phagocytosis of crocidolite asbestos induces oxidative stress, DNA damage, and apoptosis in mesothelial cells — W. Liu, J.D. Ernst, et al. (2000)
• Cisplatin and resveratrol induce apoptosis and autophagy following oxidative stress in malignant mesothelioma cells — Y.J. Lee, G.J. Lee, et al. (2016)
• Potential role of ferritin heavy chain in oxidative stress and apoptosis in human mesothelial and mesothelioma cells: implications for asbestos-induced oncogenesis — W. Aung, S. Hasegawa, et al. (2007)
• Oxidative stress-mediated cytotoxicity and apoptosis induction by TiO2 nanofibers in HeLa cells — K.M. Ramkumar, C. Manjula, et al. (2012)
• The protective role of antioxidants in the defence against ROS/RNS-mediated environmental pollution — B. Poljšak, R. Fink (2014)
• Oxidative and cytotoxic stress induced by inorganic granular and fibrous particles — S. Helmig, D. Walter, et al. (2018)

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