Oxidation of PUFAs in the diet has the potential to be genotoxic and hence carcinogenic. Such carcinogenic processes originate within stem cells of the colon. These cells appear to be predisposed to the carcinogenic process. In colon cells (CRL-1807) exposed to chemical reactions simulating exogenous and endogenous peroxidation reactions, we have observed that undifferentiated cells could mount an effective recombinational repair/TCR response to an endogenous peroxidative DNA damage insult, but not to an external exogenous peroxidative insult as one would encounter from a dietary source. This may suggest that defects in such specific DNA repair may play a role in tumour development in undifferentiated colonocytes exposed to a diet-derived lipid peroxides.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1179/135100007X162239 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Stress triggers gut dysbiosis via CRH-CRHR1-mitochondria pathway.
NPJ Biofilms Microbiomes
September 2024
Department of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Stress can lead to gut dysbiosis in brain-gut axis disordered diseases as irritable bowel syndrome (IBS), yet the mechanisms how stress transfer from the brain to the gut and disrupt gut microbiota remain elusive. Here we describe a stress-responsive brain-to-gut axis which impairs colonocytes' mitochondria to trigger gut dysbiosis. Patients with IBS exhibit significantly increased facultative anaerobes and decreased obligate anaerobes, related to increased serum corticotropin-releasing hormone (CRH) level and defected colonocytes' mitochondria ultrastructure.
View Article and Find Full Text PDFis a common cause of diarrhea and mortality, especially in immunosuppressed and hospitalized patients. is a toxin-mediated disease, but the host cell receptors for toxin B (TcdB) have only recently been revealed. Emerging data suggest TcdB interacts with receptor tyrosine kinases during infection.
View Article and Find Full Text PDFEpithelial-mesenchymal interaction protects normal colonocytes from 4-HNE-induced phenotypic transformation.
PLoS One
April 2024
Toxalim UMR1331 (Research Centre in Food Toxicology), Toulouse University, INRAE, ENVT, INP-Purpan, UPS, Toulouse, France.
Introduction: Recent studies have shown that epithelial-stromal interactions could play a role in the development of colorectal cancer. Here, we investigated the role of fibroblasts in the transformation of normal colonocytes induced by 4-HNE.
Methods: Normal Co colonocytes and nF fibroblasts from the same mouse colon were exposed, in monoculture (m) or coculture (c), to 4-HNE (5 μM) twice weekly for 3 weeks.
Impact of Reactive Sulfur Species on : Modulating Viability, Motility, and Biofilm Degradation Capacity.
Antioxidants (Basel)
February 2024
Department of Molecular Microbiology, Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 3525433, Israel.
Reactive sulfur species (RSS) like hydrogen sulfide (HS) and cysteine persulfide (Cys-SSH) emerged as key signaling molecules with diverse physiological roles in the body, depending on their concentration and the cellular environment. While it is known that HS and Cys-SSH are produced by both colonocytes and by the gut microbiota through sulfur metabolism, it remains unknown how these RSS affect amebiasis caused by , a parasitic protozoan that can be present in the human gastrointestinal tract. This study investigates HS and Cys-SSH's impact on physiology and explores potential therapeutic implications.
View Article and Find Full Text PDFInflammatory Bowel Disease-Associated Colorectal Cancer: Translational and Transformational Risks Posed by Exogenous Free Hemoglobin Alpha Chain, A By-Product of Extravasated Erythrocyte Macrophage Erythrophagocytosis.
Medicina (Kaunas)
July 2023
School of Medicine, Division of Biomedical Sciences, Meharry Medical College, Nashville, TN 37208, USA.
Colonic inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn's colitis (CC). Patients with IBD are at increased risk for colitis-associated colorectal cancer (CACRC) compared to the general population. CACRC is preceded by IBD, characterized by highly heterogenous, pharmacologically incurable, pertinacious, worsening, and immune-mediated inflammatory pathologies of the colon and rectum.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!