Explore the vast range of titles available.

Natural compounds, including alkaloids, terpenes, and polyphenols, are increasingly recognized for their potential to modulate epigenetic mechanisms and influence cellular function, particularly in cancer. Studies have shown that diverse phytochemicals impact epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNA expression. Epigenetics is critical in cancer and can dysregulate crucial cellular processes, such as cell proliferation, apoptosis, and differentiation. In cancer, aberrant epigenetic patterns can silence tumor suppressor genes and activate oncogenes, contributing to uncontrolled cell growth and metastasis. Understanding the precise mechanisms by which these natural compounds interact with the epigenetic machinery holds significant promise for developing novel therapeutic strategies for cancer and other diseases. Future research, including basic studies and well-designed clinical trials, will be crucial in validating these findings and developing effective clinical applications of natural compounds.

The aim of this study was to evaluate the nature and mechanisms of interaction between HIV peptide/dendrimer complexes (dendriplex) and artificial lipid membranes, such as large unilayered vesicles (LUV) and lipid monolayers in the air–water interface. Dendriplexes were combined as one of three HIV-derived peptides (Gp160, P24 and Nef) and one of two cationic phosphorus dendrimers (CPD-G3 and CPD-G4). LUVs were formed of 1,2-dimyristoyl-sn-glycero-3-phosphatidylcholine (DMPC) or of a mixture of DMPC and dipalmitoyl-phosphatidylglycerol (DPPG). Interactions between dendriplexes and vesicles were characterized by dynamic light scattering (DLS), fluorescence anisotropy, differential scanning calorimetry (DSC) and Langmuir–Blodgett methods. The morphology of formed systems was examined by transmission electron microscopy (TEM). The results suggest that dendriplexes interact with both hydrophobic and hydrophilic regions of lipid bilayers. The interactions between dendriplexes and negatively charged lipids (DMPC–DPPG) were stronger than those between dendriplexes and liposomes composed of zwitterionic lipids (DMPC). The former were primarily of electrostatic nature due to the positive charge of dendriplexes and the negative charge of the membrane, whereas the latter can be attributed to disturbances in the hydrophobic domain of the membrane. Obtained results provide new information about mechanisms of interaction between lipid membranes and nanocomplexes formed with HIV-derived peptides and phosphorus dendrimers. These data could be important for the choosing the appropriate antigen delivery vehicle in the new vaccines against HIV infection.

Conventional cancer treatment is mainly based on the surgical removal of the tumor followed by radiotherapy and/or chemotherapy. When surgical removal is not possible, radiotherapy and, less often, chemotherapy is the only way to treat patients. However, despite significant progress in understanding the molecular mechanisms of carcinogenesis and developments in modern radiotherapy techniques, radiotherapy (alone or in combination) does not always guarantee treatment success. One of the main causes is the radioresistance of cancer cells. Increasing the radiosensitivity of cancer cells improves the processes leading to their elimination during radiotherapy and prolonging the survival of cancer patients. In order to enhance the effect of radiotherapy in the treatment of radioresistant neoplasms, radiosensitizers are used. In clinical practice, synthetic radiosensitizers are commonly applied, but scientists have recently focused on using natural products (phytocompounds) as adjuvants in radiotherapy. In this review article, we only discuss naturally occurring radiosensitizers currently in clinical trials (paclitaxel, curcumin, genistein, and papaverine) and those whose radiation sensitizing effects, such as resveratrol, have been repeatedly confirmed by many independent studies.

Air pollution is a major global health threat, responsible for over 8 million deaths in 2021, including 700,000 fatalities among children under the age of five. It is currently the second leading risk factor for mortality worldwide. Key pollutants, such as particulate matter (PM2.5, PM10), ozone, sulfur dioxide, nitrogen oxides, and carbon monoxide, have significant adverse effects on human health, contributing to respiratory and cardiovascular diseases, as well as neurodevelopmental and neurodegenerative disorders. Among these, particulate matter poses the most significant threat due to its highly complex mixture of organic and inorganic compounds with diverse sizes, compositions, and origins. Additionally, it can penetrate deeply into tissues and cross the blood–brain barrier, causing neurotoxicity which contributes to the development of neurodegenerative diseases. Although the link between air pollution and neurological disorders is well documented, the precise mechanisms and their sequence remain unclear. Beyond causing oxidative stress, inflammation, and excitotoxicity, studies suggest that air pollution induces epigenetic changes. These epigenetic alterations may affect the expression of genes involved in stress responses, neuroprotection, and synaptic plasticity. Understanding the relationship between neurological disorders and epigenetic changes induced by specific air pollutants could aid in the early detection and monitoring of central nervous system diseases.

This work is supported by a grant from the Faculty of Biology and Environmental Protection, University of Lodz (grant number: B1711000001504.02) and by National Science Centre, Poland (grant number 2017/25/N/NZ1/02849) and supported by subsidy for young scientists (Faculty of Biology and Environmental Protection, University of Lodz). Bionanopark Ltd. is a non-profit research institution providing employment for two of the authors [JG, JAB], whose facilities were used for part of the conducted studies. The funder provided support in the form of research materials, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

The effects of resveratrol on a cancer cell line derived from the nervous system, neuroblastoma and a cell line derived from hippocampal neurons under hydrogen peroxide-induced oxidative stress were evaluated and compared. Our studies indicate that resveratrol exerts different effects on tumour and normal cells. Interestingly, in the presence of an oxidising factor resveratrol can sensitise cancer cells and decrease their viability substantially. Under conditions of oxidative stress similar to those found in the tumour environment, resveratrol also intensified apoptosis in Neuro-2a cells. Our data indicate that resveratrol does not protect neuronal, hippocampal cells from oxidative damage.

Radiotherapy is among the most important methods for breast cancer treatment. However, this method’s effectiveness is limited by radioresistance. The aim of this study was to investigate whether the stilbene derivatives piceid, resveratrol, and piceatannol have a radiosensitising effect on breast cancer cells (MCF-7). The conducted research enabled us to determine which of the tested compounds has the greatest potential in sensitising cells to ionising radiation (IR). Among the stilbene derivatives, resveratrol significantly increased the effect of IR. Resveratrol and IR used in combination had a higher cytotoxic effect on MCF-7 cells than using piceatannol, piceid, or radiation alone. This was due to a significant decrease in the activity of antioxidant enzymes, which resulted in the accumulation of formed reactive oxygen species (ROS). The effect of resveratrol and IR enhanced the expression of apoptotic genes, such as Bax, p53, and caspase 8, leading to apoptosis.

Chlorpyrifos (CP) remains one of the most globally pervasive organophosphorus pesticides, and its toxicological profile continues to raise substantial public health and environmental concerns. While traditionally characterized by its potent acetylcholinesterase-inhibitory properties, accumulating evidence now shows that chlorpyrifos and its bioactive metabolite, chlorpyrifos-oxon (CPO), exert far broader toxic effects, including the induction of oxidative stress, enhancement of neuroinflammatory processes, and the triggering of persistent epigenetic alterations. In this review, we synthesize current findings to highlight the expanding spectrum of CP-induced toxicity, while also providing a multidisciplinary overview of chlorpyrifos characteristics, including its environmental fate, metabolism, and transformation pathways. The analysis encompasses not only classical neurotoxicity but also disruptions in neurodevelopment, endocrine signaling, gut microbiota composition, hepatic function, musculoskeletal integrity and carcinogenic pathways. By synthesizing results across human, animal, and environmental studies, this review offers a comprehensive overview of CP's multidimensional toxicity and highlights the urgent need for improved biomonitoring, regulatory harmonization, and global strategies to reduce exposure.