Obesity causes genetic instability, which plays a key-role in the etiology of cancer and aging. We investigated the impact of bariatric surgery (BS) on DNA repair, oxidative DNA damage, telomere lengths, alterations of antioxidant enzymes and, selected proteins which reflect inflammation. The study was realized with BS patients (n = 35). DNA damage, base oxidation, BER, and NER were measured before and 1 month and 6 months after surgery with the single-cell gel electrophoresis technique. SOD and GPx were quantified spectrophotometrically, malondealdehyde (MDA) was quantified by HPLC. Telomere lengths were determined with qPCR, and plasma proteome profiling was performed with high-resolution mass spectrophotometry. Six months after the operations, reduction of body weight by 27.5% was observed. DNA damage decreased after this period, this effect was paralleled by reduced formation of oxidized DNA bases, a decline in the MDA levels and of BER and NER, and an increase in the telomere lengths. The activities of antioxidant enzymes were not altered. Clear downregulation of certain proteins (CRP, SAA1) which reflect inflammation and cancer risks was observed. Our findings show that BS causes reduced oxidative damage of DNA bases, possibly as a consequence of reduction of inflammation and lipid peroxidation, and indicate that the surgery has beneficial long-term health effects.

Tetraploidisation plays a crucial role in evolution, development, stress adaptation, and disease, but its beneficial or pathological effects in different tissues remain unclear. This study aims to compare physiological and unphysiological tetraploidy in eight steps: 1) mechanisms of diploidy-to-tetraploidy transition, 2) induction and elimination of unphysiological tetraploidy, 3) tetraploid cell characteristics, 4) stress-induced unphysiological tetraploidy, 5) comparison of physiological vs. unphysiological tetraploidy, 6) consequences of unphysiological stress-induced tetraploidy, 7) nutritional or pharmacological prevention strategies of tetraploidisation, and 8) knowledge gaps and future perspectives. Unphysiological tetraploidy is an adaptive stress response at a given threshold, often involving mitotic slippage. If tetraploid cells evade elimination through apoptosis or immune surveillance, they may re-enter the cell cycle, causing genetic instability, micronuclei formation, aneuploidy, modification of the epigenome and the development of diseases. The potential contributions of unphysiological tetraploidy to neurodegenerative, cardiovascular and diabetes related diseases are summarized in schematic figures and contrasted with its role in cancer development. The mechanisms responsible for the transition from physiological to unphysiological tetraploidy and the tolerance to tetraploidisation in unphysiological tetraploidy are not fully understood. Understanding these mechanisms is of critical importance to allow the development of targeted nutritional and pharmacological prevention strategies and therapies.

The majority of the woodland area in Central Europe is composed of managed forests. Although the species diversity and composition, particularly in older forests, may be similar to those of natural or close-to-nature forests, intensive forestry and other human activities have adverse impacts on biodiversity. The present study focused on bryophyte diversity in managed lowland forests, as these have received less attention compared to other types of forests. Our research targeted the area located within the Borská nížina Lowland in south-western Slovakia. In total, 37 forest sampling plots (SPs) were selected, representing five different forest types, namely Quercus, Fraxinus, Robinia, Pinus, and mixed forests. Multivariate statistical analyses were conducted across these forest types to demonstrate variations in bryophyte species richness, composition, and functional traits. Overall, 60 species of bryophytes were identified, of which five were liverworts and 55 were mosses. Epiphytes were the most abundant substrate group in deciduous and mixed stands, while epigeic species prevailed in Pinus forests. Considering environmental factors, the bryophyte diversity was influenced mostly by the forest type and area size of SPs. Clear differences in species composition were observed when comparing coniferous and deciduous stands, as well as non-native Robinia forests and native tree stands. Overall, intensive forest management results in a high concentration of hemerophilous and nitrophilous species, along with the absence of rare and threatened mosses and liverworts. Nevertheless, by adhering to proper management methods, even managed forests can provide suitable habitats for various bryophytes.

Circulating cell-free DNA (cfDNA), particularly in blood, is emerging as a critical non-invasive biomarker for the prediction, diagnosis, and monitoring of human diseases. Additionally, cytoplasmic DNA has been implicated in promoting genetic aberrations, genome instability, and inflammation-factors that can contribute to the development of various diseases, including cancer. However, the heterogeneous nature of both intra- and extracellular DNA presents a significant challenge. This review synthesizes current evidence on the origin, composition, and fate of micronuclei (MN) and their derived DNA/chromatin, highlighting their potential as active participants in genomic instability and immune activation. We examine the molecular characteristics of MN, including their formation from acentric fragments, whole chromosomes, or double minutes, and their dynamic intracellular outcomes, such as reintegration, degradation, or extrusion. A major focus is placed on the consequences of micronuclear envelope rupture, including chromothripsis and cGAS-STING-mediated inflammation. We explore the emerging evidence for the extrusion of MN or MN-derived DNA via direct extrusion or packaging in extracellular vesicles, and discuss their implications for cfDNA composition, detection, and biomarker development. The review also underscores the relevance of MN in disease pathogenesis and senescence, and concludes by outlining critical knowledge gaps, particularly concerning the mechanisms of MN clearance, their tissue origin, and their survival and detectability in plasma. In conclusion, by elucidating the mechanistic link between MN biology and cfDNA, we propose that MN-derived DNA and chromatin may serve as informative indicators of genomic instability and disease progression, and offer valuable insights for future diagnostic and therapeutic strategies.