Environmental pollution is a complex issue because of the diversity of anthropogenic agents, both chemical and physical, that have been detected and catalogued. The consequences to biota from exposure to genotoxic agents present an additional problem because of the potential for these agents to produce adverse change at the cellular and organismal levels. Past studies in genetic toxicology at the Oak Ridge National Laboratory have focused on structural damage to the DNA of environmental species that may occur after exposure to genotoxic agents and the use of this information to document exposure and to monitor remediation. In an effort to predict effects at the population, community, and ecosystem levels, current studies in genetic ecotoxicology are attempting to characterize the biologic mechanisms at the gene level that regulate and limit the response of an individual organism to genotoxic factors in their environment.
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http://dx.doi.org/10.1289/ehp.94102s1213 | DOI Listing |
Environ Toxicol Pharmacol
January 2025
Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239; Department of Molecular and Medical Genetics, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, Oregon 97239.
Aflatoxicosis is a life-threatening nephrotoxic condition arising from eating foods highly contaminated with aflatoxin-producing molds. Additionally, chronic aflatoxin exposures are linked to enhanced hepatocellular carcinomas. Using recent advances in mass spectrometry for the detection of aflatoxin B (AFB) DNA adducts, we present data which show generation of these adducts in the kidney, albeit at ≈100-fold lower levels than in the liver of the same animal.
View Article and Find Full Text PDFTob Induc Dis
January 2025
Institute of Medical Science, University of Toronto, Toronto, Canada.
Introduction: There is substantial interest in the association of vaping e-cigarettes with the risk of cancer. We analyzed this risk in different populations by updating the Kings College London (KCL) review to include the period between July 2021 and December 2023.
Methods: We searched six databases and included peer-reviewed human, animal, and cell/ original studies examining the association between e-cigarettes and cancer risk, but we excluded qualitative studies.
Indian J Occup Environ Med
December 2024
Viral Research and Diagnostic Laboratory (VRDL), Government Medical College, Patiala, Punjab, India.
Pesticides induce oxidative DNA damage and genotoxic effects such as DNA single-strand breaks (SSBs), double-strand breaks (DSBs), DNA adducts, chromosomal aberrations, and enhanced sister chromatid exchanges. Such DNA damage can be repaired by DNA repair mechanisms. In humans, single nucleotide polymorphisms (SNPs) are present in DNA repair genes involved in base excision repair (BER) (, and nucleotide excision repair (NER) (, , , and ), and double-strand break repair (DSBR) ( and ).
View Article and Find Full Text PDFSci Rep
January 2025
Department of Earth, Environment and Life Sciences, University of Genoa, 16132, Genoa, Italy.
The World Health Organization has confirmed that asbestos fibres are carcinogenic, claiming that asbestos-related diseases should be eradicated worldwide. Actinolite, amosite, anthophyllite, chrysotile, crocidolite, and tremolite are regulated asbestiform mineral phases. However, in nature, asbestos minerals occur either in a fibrous and asbestiform (original morphology characterized by high length-to-width ratio and provided of high tensile strength and flexibility) or fibrous but not asbestiform appearance.
View Article and Find Full Text PDFCell Death Discov
January 2025
Laboratory of Genome Stress Signaling, National Cancer Center Research Institute, Chuo-ku, Tokyo, 104-0045, Japan.
DNA replication stress (RS), a prevalent feature of various malignancies, arises from both genetic mutations and genotoxic exposure. Elevated RS levels increase the vulnerability of cancer cells to ataxia telangiectasia and Rad3-related kinase inhibitors (ATRis). Here, we screened for DNA damage response inhibitors that enhance ATRi-induced cytotoxicity using SWI/SNF complex-deficient cells and identified a potent synergy between ATRi and poly(ADP-ribose) polymerase inhibitor (PARPi), particularly in SMARCA4-deficient cells.
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