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Induction and Validation of Cellular Senescence in Primary Human Cells
Published on: June 20, 2018
Cellular Senescence Triggered by Food and Environmental Genotoxins
Bernd Kaina1, Maja T Tomicic1, Markus Christmann1
1Institute of Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Obere Zahlbacher Str. 67, D-55131 Mainz, Germany.
Abstract:
Cellular senescence (CSEN) is caused by a variety of factors that trigger complex molecular pathways. These include telomere shortening, oncogene activation and replicative stress, as well as DNA damage caused by genotoxic anticancer drugs and endogenous and exogenous genotoxins. Here, we review the induction of CSEN by exogenous genotoxic insults resulting from food and environmental exposures. The available data show that genotoxins/carcinogens in tobacco smoke and smokeless tobacco, in the environment, in food, beverages and life-style products induce CNS. The exposures include N-nitroso compounds, polycyclic aromatic hydrocarbons, heterocyclic aromatic amines, acrylamide, heavy metals, fine dust, mycotoxins, phytotoxins, and phycotoxins. Also, heme in red meat contributes to CSEN as it catalyzes the formation of genotoxic species in the colon. Induction of CSEN by external genotoxins/carcinogens is bound on the DNA damage response pathway (DDR), which relies on activation of the ATM/ATR-CHK2/CHK1-p53-p21 axis and the p53-independent p16/p14 axis, eliciting cyclin-dependent kinase inhibition and permanent cell cycle arrest. Other factors that can be involved are DREAM, MAPK, cGAS/Sting, and NF-κB. The accumulation of non-repaired DNA damage triggering CSEN following external genotoxic exposures may contribute significantly to the amelioration of senescent cells and organ failure with age in humans. Senescent cells drive, via the senescence-associated secretory phenotype (SASP), inflammation that is involved in many diseases, including cancer. Although most of the studies were performed with in vitro cell systems, the consequences of CSEN induction by genotoxic nutritional components and environmental exposures seem to be underestimated. Since CSEN correlates with aging, it is reasonable to conclude that exogenous genotoxic pollutants contribute significantly to the aging process through CSEN induction. In light of these findings, it is deduced that reducing genotoxin exposures and using "rejuvenation" supplements (senotherapeutics) are reasonable strategies to counteract cellular senescence and the aging process.
Insights
External genotoxins from food and the environment trigger cellular senescence (CSEN), a process linked to aging and organ failure. Reducing exposure to these toxins and using senotherapeutics may counteract aging.
Area of Science:
- Cellular and Molecular Biology
- Toxicology
- Gerontology
Background:
- Cellular senescence (CSEN) is a complex process triggered by various stressors, including DNA damage from genotoxins.
- Exogenous genotoxins from environmental and dietary sources are increasingly recognized as inducers of CSEN.
- CSEN is implicated in aging, organ failure, and age-related diseases through the senescence-associated secretory phenotype (SASP).
Purpose of the Study:
- To review the induction of cellular senescence by exogenous genotoxic insults from food and environmental exposures.
- To highlight the molecular pathways involved in CSEN induction by these external factors.
- To discuss the implications of CSEN for aging and organ function.
Main Methods:
- Literature review of studies investigating CSEN induction by exogenous genotoxins.
- Analysis of data on genotoxins present in tobacco, food, beverages, and lifestyle products.
- Examination of the molecular mechanisms, including DNA damage response (DDR) pathways.
Main Results:
- Genotoxins/carcinogens in tobacco smoke, environment, food, and lifestyle products induce CSEN.
- Identified genotoxins include N-nitroso compounds, PAHs, HACs, acrylamide, heavy metals, and mycotoxins.
- CSEN induction by genotoxins involves DDR pathways (ATM/ATR-CHK2/CHK1-p53-p21, p53-independent p16/p14) and other signaling cascades.
Conclusions:
- Exogenous genotoxins significantly contribute to CSEN induction, potentially exacerbating aging and organ failure.
- The role of CSEN induced by dietary and environmental genotoxins is likely underestimated.
- Reducing genotoxin exposure and utilizing senotherapeutics are proposed strategies to mitigate CSEN and aging.
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