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Maximal physical effort induces a disturbance in the body's energy homeostasis and causes oxidative stress. The aim of the study was to determine whether prooxidant–antioxidant balance disturbances and the secretion of adipokines regulating metabolism, induced by maximal intensity exercise, are dependent on body composition in young, healthy, non-obese individuals. We determined changes in the concentration of advanced protein oxidation products (AOPP), markers of oxidative damage to nucleic acids (DNA/RNA/ox), and lipid peroxidation (LPO); catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activity, as well as concentrations of visfatin, leptin, resistin, adiponectin, asprosin, and irisin in the blood before and after maximal intensity exercise in men with above-average muscle mass (NFAT-HLBM), above-average fat mass (HFAT-NLBM), and with average body composition (NFAT-NLBM). We corrected the post-exercise results for the percentage change in plasma volume. In all groups after exercise, there was an increase in LPO and resistin. In HFAT-NLBM, additionally, an increase in CAT and a decrease in SOD activity were noted, and in NFAT-NLBM, an increase in visfatin concentration was observed. In our study, the effect was demonstrated of a maximal effort on six (LPO, CAT, SOD, visfatin, resistin, and asprosin) of the twelve parameters investigated, while the effect of body composition on all parameters investigated was insignificant. Maximal intensity aerobic exercise induces secretion of resistin and damages lipids regardless of the exercising subjects' body composition. Large fat tissue content predisposes to exercise-induced disorders in the activity of antioxidant enzymes. We have also shown that it is necessary to consider changes in blood plasma volume in the assessment of post-exercise biochemical marker levels. [ABSTRACT FROM AUTHOR]

The presence of circulating tumor DNA (ctDNA) in patients with colorectal adenomas remains uncertain. Studies using tumor-agnostic approaches report ctDNA in 10-15% of patients, though with uncertainty as to whether the signal originates from the adenoma. To obtain an accurate estimate of the proportion of patients with ctDNA, a sensitive tumor-informed strategy is preferred, as it ensures the detected signal originates from the adenoma. Here, tumor-informed whole-genome sequencing-based ctDNA analysis (MRD-EDGE SNV ) was applied to two independent cohorts. Cohort 1, comprising 93 patients with stage III colorectal cancer (CRC) and 40 healthy individuals, was used to establish the signal threshold at 95% specificity. This threshold was then applied to Cohort 2, consisting of 22 patients with symptomatic and 20 with asymptomatic adenomas. In stage III, MRD-EDGE SNV had an area under the curve of 0.98. ctDNA was detected in 50% and 25% of patients with symptomatic and asymptomatic adenomas, respectively. The median adenoma plasma tumor fraction was 5.9 × 10 -5 . These finding not only demonstrate the feasibility of ctDNA detection in patients with colorectal adenomas, but also provides an estimate of the necessary sensitivity required to detect these lesions, paving the way for future ctDNA-based screening strategies., (© 2025 The Author(s). Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)