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Tobacco smoking is a risk factor for cancers of the liver and gastrointestinal (GI) tract, but the causal agents responsible for these cancers are uncertain. 2-Amino-9H-pyrido[2,3-b]indole (AαC) is an abundant heterocyclic aromatic amine present in tobacco smoke. AαC is a liver carcinogen and both a transgene mutagen and inducer of aberrant crypt foci in the colon of mice. We hypothesize that AαC may contribute to DNA damage and tumorigenesis in these organs of smokers. The potential of AαC to induce DNA adduct formation in liver, organs of the GI tract, lung, and urinary bladder, which are target organs of cancer in smokers, was examined using the C57BL/6 mouse as an animal model. AαC (400 or 800 ppm) and 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) (300 ppm), a liver and colon carcinogen in C57BL/6 mice, were given in the diet for up to 12 weeks. Liquid chromatography/mass spectrometry was employed to measure DNA adducts. The major DNA adducts of both carcinogens were identified as deoxyguanosine-C8 adducts. The levels of formation of AαC- and MeIQ-DNA adducts were similar in liver and extrahepatic tissues when adjusted for dose. The highest levels of adducts occurred in liver, followed by urinary bladder, and then in cecum and colon; lower DNA adduct levels were formed in the lung and pancreas following 12 weeks of feeding. The high levels of AαC adduct formed in liver, GI tract, and bladder of C57BL/6 mice reinforce the notion that AαC may contribute to DNA damage and cancer of these organs in smokers.
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http://dx.doi.org/10.1093/toxsci/kft077 | DOI Listing |
Chem Res Toxicol
December 2024
University of Missouri, Department of Chemistry, 125 Chemistry Building, Columbia, Missouri 65211, United States.
Apurinic/apyrimidinic endonuclease 1 (APE1) is a central enzyme in the base excision repair (BER) pathway. APE1 catalyzes incision of the phosphodiester linkage on the 5'-side of apurinic/apyrimidinic (AP) sites during the repair of damaged nucleobases in cellular DNA. Inhibition of this enzyme can potentiate the action of DNA-damaging chemotherapeutic agents.
View Article and Find Full Text PDFGenetics
December 2024
Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Acetaldehyde is the primary metabolite of alcohol and is present in many environmental sources including tobacco smoke. Acetaldehyde is genotoxic, whereby it can form DNA adducts and lead to mutagenesis. Individuals with defects in acetaldehyde clearance pathways have increased susceptibility to alcohol-associated cancers.
View Article and Find Full Text PDFActa Biomater
December 2024
School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, 510006, People's Republic of China. Electronic address:
Drug resistance and off-target toxicity of cisplatin (CDDP) pose significant challenges in effectively treating non-small cell lung cancer (NSCLC). Recently, chemodynamic therapy (CDT), an emerging reactive oxygen species (ROS)-mediated tumor-specific therapeutic modality, has shown great potential in sensitizing multidrug resistance tumor cells. Herein, a glutathione (GSH)-responsive Pt(IV) prodrug-based oxidative stress nanoamplifier (CuBSO@Pt) was developed for effective chemo/chemodynamic therapy to reverse CDDP resistance in NSCLC.
View Article and Find Full Text PDFGut Microbiome (Camb)
November 2024
Department of Hospital Medicine, University of Cincinnati Medical Center, Cincinnati, OH, USA.
, subspecies (Sgg) is a gram-positive bacterium associated with infective endocarditis and colorectal cancer (CRC). Sgg has features that allow the bacterium to thrive in the colorectal tumor microenvironment and further progress the development of CRC to facilitate its survival. Sgg contains 3 pili that facilitate colonic cell adhesion and translocation through phase variation.
View Article and Find Full Text PDFPhotochem Photobiol Sci
December 2024
Instituto Universitario Mixto de Tecnología Química (UPV-CSIC), Universitat Politècnica de València, Consejo Superior de Investigaciones Científicas, Avda de los Naranjos s/n, 46022, Valencia, Spain.
Photophysical and photochemical studies were carried out to examine the photoreactivity of etheno adducts, 1,N-ethenoadenine (εdA) and 1,N-ethenoguanine (εdG), in the presence of two well-known photosensitizers acting by Type I and/or Type II mechanisms such as 4-carboxybenzophenone (CBP) and rose Bengal (RB), respectively. Steady-state photolysis experiments combined with HPLC and mass spectroscopy measurements lead to photoproducts that correspond to the repaired nucleosides. To determine the mechanism of this photooxidation processes, phosphorescence spectroscopy, direct detection of singlet oxygen luminescence and laser flash photolysis were carried out.
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