CHANGES IN REDOX HOMEOSTASIS IN LUNG TISSUE UNDER CONDITIONS OF DMН-INDUCED COLON ADENOCARCINOMA
DOI:
https://doi.org/10.32782/2226-2008-2024-5-2Keywords:
induced carcinogenesis, antioxidant system, redox balance, lungsAbstract
The study is dedicated to the experimental assessment of the parameters of the redox system in the lung tissue of rats under conditions of modelled cancerogenesis. Materials and methods. The experiment involved 110 adult male outbred white rats. Colon adenocarcinoma in situ was modelled by the weekly administration of N,N-dimethylhydrazine hydrochloride for 30 weeks. Results. The most pronounced changes in redox reactions in the lung tissue of the experimental animals were observed starting from stage 4 of the study. Accordingly, the level of POM370 exceeded the control group results by 1.7 times (stage 4) and 2.8 times (stage 7). The activity of Cat in the lung tissue significantly decreased throughout all observation stages by 1.1 times at stage 1 and 2.0 times at stage 7. It should be noted that the activity of SOD in the lung tissue of the experimental animals increased at stages 1–3. However, starting from stage 4, this indicator significantly decreased. During stages 1–3, the concentration of CP in the lung tissue was almost identical to that of the control group. From stage 4 onwards, this indicator significantly increased, exceeding the control group values by 1.5 times (stage 4) and 2.8 times (stage 7). Analysis of non-enzymatic biological markers of the antioxidant system revealed that the GSH content in the lung tissue during stages 1–3 was virtually identical to the control group. Starting from stage 4, this indicator significantly decreased at all subsequent stages of carcinogenesis. A similar pattern was observed in the mediators of the glutathione system of antioxidant defense. At the final stage of observation, the GPx level was 1.5 times lower, and the GP level was 1.5 times lower compared to the control values. Conclusions. The development of the chronic neoplastic intoxication syndrome, due to the excessive formation of toxic metabolites, creates significant strain on the antioxidant system and leads to a decrease in the activity of antioxidant enzymes as well as a substantial reduction in the concentration of non-enzymatic antioxidant mediators.
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