DISRUPTION OF REDOX HOMEOSTASIS IN LUNG TISSUE IN A DMH-INDUCED COLON ADENOCARCINOMA MODEL

Abstract

Introduction. Disruption of redox homeostasis is one of the key factors contributing to the progression of malignant neoplasms, including colorectal adenocarcinoma. Changes in the oxidative-reductive balance can affect various organs, including the lungs, through systemic oxidative stress and related cellular damage mechanisms. Recent studies show that the development of neoplastic lesions is accompanied by an increase in reactive oxygen species (ROS) and disruption of antioxidant system functions. The aim of the study. This study aims to assess the impact of DMG-induced disruption of redox homeostasis on lung tissue, which is crucial for understanding the overall oxidative stress pattern in colorectal cancer. Research Methods. The study was conducted on 105 male rats, housed under standard vivarium conditions. The animals were divided into two groups: Group I – control group with 35 animals; Group II – experimental group, which received N,N-dimethylhydrazine dihydrochloride (70 rats) for 30 weeks. The oxidative stress level in lung tissue was assessed using the concentration of TBARS-active products, dienic and trienic conjugates, Schiff bases, ceruloplasmin, aldehyde- and ketone-derived neutral (OMP370) and basic (OMP430) compounds, as well as the activity of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and the level of reduced glutathione. Results and Discussion. This paper examines the complex relationship between oxidative stress and cancer development, highlighting its importance at various stages of carcinogenesis and tumor progression. The results show that oxidative stress can enhance the aggressive properties of cancer cells. The study demonstrated that DMG-induced colorectal adenocarcinoma leads to significant disruption of redox homeostasis in lung tissue, manifesting as an increase in reactive oxygen species and a decrease in antioxidant system activity. Such changes in the oxidative-reductive balance may increase the risk of oxidative cellular damage and contribute to the development of secondary pathologies in lung tissue. The findings are important for understanding the mechanisms of the systemic impact of colorectal cancer on the body and may serve as the basis for developing new antioxidant strategies in the comprehensive therapy of oncological diseases. Conclusions. The study results revealed that DMG-induced colorectal adenocarcinoma causes significant disruption of redox homeostasis in lung tissue. This is manifested by an increase in reactive oxygen species and a decrease in the activity of antioxidant enzymes. Such changes in the oxidative-reductive balance increase the risk of oxidative cell damage, which may contribute to the development of additional pathological processes in lung tissue.