Benign Prostatic Hyperplasia (BPH) and Prostate Cancer (PC) are very common pathologies among aging men. Both disorders involve aberrant cell division and differentiation within the prostate gland. However, the direct link between these two disorders still remains controversial. A plethora of works have demonstrated that inflammation is a major causative factor in both pathologies. Another key factor involved in PC development is DNA methylation and hydroxymethylation. A broad spectrum of parameters, including epigenetic DNA modifications and 8-oxo-7,8-dihydro-2'-deoxyguanosine, was analyzed by two-dimensional ultraperformance liquid chromatography with tandem mass spectrometry in tissues of BPH, PC, and marginal one, as well as in leukocytes of the patients and the control group. In the same material, the expression of TETs and TDG genes was measured using RT-qPCR. Additionally, vitamin C was quantified in the blood plasma and within cells (leukocytes and prostate tissues). Unique patterns of DNA modifications and intracellular vitamin C (iVC) in BPH and PC tissues, as well as in leukocytes, were found in comparison with control samples. The majority of the alterations were more pronounced in leukocytes than in the prostate tissues. Characteristic DNA methylation/hydroxymethylation and iVC profiles have been observed in both PC and BPH, suggesting potential shared molecular pathways between the two conditions. As a fraction of leukocytes may be recruited to the pathological tissues and can migrate back into the circulation/blood, the observed alterations in leukocytes may reflect dynamic changes associated with the PC development, suggesting their potential utility as early markers of prostate cancer development.

Biological therapies for Crohn’s disease (CD), including infliximab, adalimumab, and vedolizumab, show variable efficacy. While some predictive biomarkers exist, data on regulatory immune cells are limited. This study examined whether baseline levels of circulating T and B cell subsets can predict response to these treatments. We recruited 43 adults with conventional treatment-resistant active CD (CDAI > 330) and 16 healthy controls. Blood samples were analysed by flow cytometry at baseline (week 0) and after induction therapy (week 12 or 14, depending on the received drug) to measure T and B cell subsets and correlate them with disease activity. CD patients at baseline showed a significantly reduced frequency of memory B cells, CD5⁺CD1d⁺ B cells, plasmablasts, and transitional B cells. Additionally, significant negative correlations were identified between transitional B cells and calprotectin/platelets, and between CD5⁺CD1d⁺ B cells and calprotectin. All CD patients responded clinically to biologic therapy. In those treated with infliximab or adalimumab, mature naïve B cells decreased, with a trend toward increased CD24^hiCD27⁺ B cells. Adalimumab responders showed a trend toward higher CD161 expression on Tregs, while vedolizumab-treated patients had a slight increase in plasmablasts. Biologic therapies in CD revealed treatment-specific immune correlations: infliximab/adalimumab responses involved B and T cell changes linked to inflammation, while VDZ response correlated with CD4⁺ and CD5⁺CD1d⁺ B cells. Our study suggests that infliximab/adalimumab induction therapy in CD expands circulating CD24^hiCD27⁺ B cells and reduces mature naïve B cells, while vedolizumab increases plasmablasts. These B-cell changes may reflect distinct mechanisms and serve as potential response biomarkers.

DNA methylation (5-mdC) and its oxidative derivatives reflect interactions between environmental exposures and genome regulation, yet their short-term responsiveness to occupational factors remains insufficiently characterized. This exploratory pilot study evaluated whether a standard workweek is associated with measurable changes in urinary epigenetic and oxidative DNA modification profiles across distinct occupational settings. A cohort representing three exposure scenarios—cyanoacrylate-based cosmetic services, toluene diisocyanate (TDI) exposure, and polyurethane (PUR) foam processing—was examined using a paired pre-/post-exposure design. Urinary levels of 5-methyl-2′-deoxycytidine (5-mdC), 5-hydroxymethylcytosine (5-hmCyt), 5-hydroxymethyl-2′-deoxycytidine (5-hmdC), 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), 5-hydroxymethyl-2′-deoxyuridine (5-hmdU), and 5-hydroxymethyluracil (5-hmUra) were quantified, and an epigenetic turnover ratio (5-hmdC/5-mdC) was derived. Although none of the observed shifts achieved formal statistical significance after False Discovery Rate (FDR) adjustment (p_FDR > 0.05), exposure-specific, directionally consistent non-significant trends were noted across cohorts. The isocyanate-exposed group demonstrated coordinated reductions in 5-mdC and 5-hmdC accompanied by an increase in 5-hmdU. The PUR-processing group exhibited the most pronounced response, including a marked elevation in 5-hmdU and an increased turnover ratio. In contrast, the beauty sector showed minimal median shifts but substantial inter-individual variability. These preliminary findings suggest that urinary epigenetic and oxidative DNA markers might reflect short-term, exposure-related biological trends, warranting further evaluation.

Background: DNA methylation changes are recognized as a key hallmark of biological aging. We analyzed the products of active DNA demethylation pathways in DNA isolated from leukocytes and the urine of healthy volunteers aged between 1.5 and 71 years. Results: A statistically significant inverse correlation between age and the analyzed modifications in urine was found for 5-hydroxymethyluracil, 5-hydroxymethylcytosine, 5-(hydroxymethyl)-2′-deoxycytidine, 5-methyl-2′-deoxycytidine, 5-carboxycytosine and 5-formylcytosine. The highest correlation coefficient was observed for 5-hydroxymethyluracil ( r = − 0.66). Interestingly, statistically significant inverse correlations were observed for 5-(hydroxymethyl)-2′-deoxycytidine and 5-methyl-2′-deoxycytidine in DNA. Conclusions: Changes in epigenetic modifications with age are more pronounced in urine than in cellular DNA. However, DNA modifications are limited to a single tissue (leukocytes), whereas modifications detected in urine reflect processes occurring at the level of the entire organism.