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Molecular and Cellular Mechanisms of Genotoxicity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (30 December 2025) | Viewed by 1959

Special Issue Editor


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Guest Editor
Institute of Toxicology, University Medical Center, 55131 Mainz, Germany
Interests: DNA repair; MGMT; tumour therapy; alkylating agents; apoptosis; anticancer drugs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Genetic toxicology is an important part of molecular toxicology that addresses the problems of toxicity to the DNA in cells.

Topics to be covered may include, but are not limited to, the following:

  • Emerging contaminants and genetic change;
  • Biochemical mechanism of genotoxicity;
  • Molecular mechanism of genotoxicity;
  • Genomic instability and carcinogenesis;
  • DNA damage and cancer;
  • Human health effects of genetic change;
  • Endocrine disruptors and the DNA;
  • Current approach in genotoxicity testing;
  • Genotoxicity and epigenetics;
  • Alternatives to laboratory animals in genotoxicity testing;
  • DNA damage and repair;
  • Genomic instability and gene expression analysis.

This Special Issue aims to provide new insights into the molecular and cellular mechanisms underlying genotoxicity and to indicate development perspectives. The paper presented in this issue will be of valuable interest to the scientific community in several research areas, including cell biology, physiopathology, toxicology, etc.

Prof. Dr. Bernd Kaina
Guest Editor

Manuscript Submission Information

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Keywords

  • DNA damage
  • gene instab
  • genetic instab
  • DNA methyl
  • genotoxic
  • gene mutation
  • DNA repair
  • genotoxicity
  • toxicogenetic
  • toxicogenomic

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Published Papers (1 paper)

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Review

28 pages, 2674 KB  
Review
Cellular Senescence Triggered by Food and Environmental Genotoxins
by Bernd Kaina, Maja T. Tomicic and Markus Christmann
Int. J. Mol. Sci. 2026, 27(5), 2389; https://doi.org/10.3390/ijms27052389 - 4 Mar 2026
Viewed by 1198
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Genotoxicity)
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