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TDK conference 2023Michelberger, Vincent - year 5 University of Veterinary Medicine Budapest, Department of Microbiology and Infectious Diseases Supervisor: Éva Szücs-Somlyó The p53 protein family is pivotal in preventing tumoral cell transformations by aiding DNA repair or inducing apoptosis in cases of irreparable damage. This mechanism activates not only for tumor prevention but also for various DNA damages, such as those caused by oxidative stress from inhalation of Zn or Cu oxides. These oxides can induce metal fume fever (MFF), an occupational ailment primarily affecting welders and metal workers, potentially leading to chronic asthma. Our study aimed to investigate the impact of ZnO fume inhalation on multiple genes from the p53-family associated with tumor suppression in mice, focusing on lung and the analysis of lymph node samples, to unravel their role in MFF's pathogenesis. During the experiments, animals were exposed to a sub-toxic amount of ZnO fume for 4 hours daily, consecutively for 3 days, with sample collection at 3- and 12-hours post-treatment. Significantly, our findings reveal unprecedentedly elevated levels of ATM gene expression at 12-hour sampling time points, along with heightened expression rates of various p53-family genes, including BRCA1&2, CHK1&2, CCNB1 & E2F1. This pioneering animal experiment offers novel insights into the cellular processes underlying early metal fume fever development. Notably, all these genes play crucial roles in DNA repair, cell cycle regulations, and cell proliferation, encompassing both mitosis and apoptosis pathways. Our examinations revealed possible double & single stranded DNA damage caused by inhalation of zink-oxide in mice which explain both the oxidative stress origin of the disease and the further immune reactions as well. Our results make a much deeper understanding of the MFF pathomechanism than any previous investigation before, however, further research is required for uncovering the complete process. List of lectures |