The increasing awareness of the potential health risks associated with microplastics’ (MPs) and nanoplastics’ (NPs) presence in the environment has led to a significant rise in research focused on these particles over the past few years. This review focuses on the research on MPs’/NPs’ presence and spread, pathways of exposure, toxicological effects on human health and legal framework related to MP/NP challenges. Several research projects have aimed to assess their potential harm to human health, focusing on different systems and organs. After exposure (independent of the pathway), these hazards reach the blood stream and concentrate in different organs. Further, they are responsible for harmful changes, having an immediate effect (pain, inflammation, or hormone imbalance) or lead to a long-term disease (e.g., infertility, chronic obstructive pulmonary disease, or cancer). Toxicological effects have been noticed at high concentrations of MPs, specifically polystyrene, the most widespread typical MP, but only short-term effects have been mostly studied. Significant quantities of consumed MPs have been discovered to have diverse detrimental effects, posing a threat to human welfare. The exact concentrations of microplastics that are inhaled and swallowed and then build up in the human body are still not known. Further investigation is necessary to evaluate the impact of MP/NP contamination at minimal concentrations and for prolonged durations.

Telomeres are part of chromatin structures containing repeated DNA sequences, which function as protective caps at the ends of chromosomes and prevent DNA degradation and recombination, thus ensuring the integrity of the genome. While telomere length (TL) can be genetically inherited, TL shortening has been associated with ageing and multiple xenobiotics and bioactive substances. TL has been characterised as a reliable biomarker for the predisposition to developing chronic pathologies and their progression. This narrative review aims to provide arguments in favour of including TL measurements in a complex prognostic and diagnostic panel of chronic pathologies and the importance of assessing the effect of different pharmacologically active molecules on the biology of telomeres. Medicines used in the management of cardiovascular diseases, diabetes, schizophrenia, hormone replacement therapy at menopause, danazol, melatonin, and probiotics have been studied for their positive protective effects against TL shortening. All these classes of drugs are analysed in the present review, with a particular focus on the molecular mechanisms involved.

This study proposed a high-performance thin-layer chromatography (HPTLC) screening method to detect phosphodiesterase 5 (PDE-5) inhibitors as possible adulterant agents in various dietary supplements. Chromatographic analysis was performed on silica gel 60F254 plates using a mixture of ethyl acetate:toluene:methanol:ammonia in a volume ratio of 50:30:20:0.5 as a mobile phase. The system provided compact spots and symmetrical peaks of sildenafil and tadalafil with retardation factor values of 0.55 and 0.90, respectively. The analysis of products purchased from the internet or specialized stores demonstrated the presence of sildenafil, tadalafil, or both compounds in 73.3% of products, highlighting inadequacies and inconsistencies in the labeling, as all dietary supplements were declared to be natural. The results were confirmed using ultra-high-performance liquid chromatography coupled with a positive electrospray ionization high-resolution tandem mass spectrometry (UHPLC-HRMS-MS) method. Furthermore, in some samples, vardenafil and various analogs of PDE-5 inhibitors were detected using a non-target HRMS-MS approach. The results of the quantitative analysis revealed similar findings between the two methods, with adulterant quantities found to be similar to or higher than those in approved medicinal products. This study demonstrated that the HPTLC method is a suitable and economical method for screening PDE-5 inhibitors as adulterants in dietary supplements intended for sexual activity enhancement.

Nicotine and cotinine are very polar basic molecules, which makes it difficult to analyze them by reversed-phase liquid chromatography (RPLC), especially in biological samples. Additives with an ionic character have been traditionally used in RPLC as silanol suppressors. The aim of our study was to investigate the potential of selected ionic liquids in improving chromatographic performance in comparison with common additives. The experimental design was conducted using the following ionic liquids as the mobile phase modifiers: 1-butyl-3-methylimidazolium tetrafluoroborate, BMIM[BF₄] and 1-butyl-3-methylimidazolium hexafluorophosphate BMIM[PF₆], with a C18 chromatographic column. The separation of these alkaloids on silica-based RPLC stationary phases was successfully conducted by the addition of BMIM[BF₄] in an acetonitrile:phosphate-buffer-based mobile phase in a pH range of 2.3–5.2. The presented chromatographic method can be used as alternative for monitoring studies or pharmacokinetic application necessary for the evaluation of tobacco smoke exposure.

The role of cigarette smoking as an aggravating factor of systemic oxidative stress in patients with mental disorders has not been extensively investigated, although significantly higher rates of smoking are recorded in these subjects in comparison with the general population. In the present study, we tested the hypothesis that smoking might be an exacerbator of systemic oxidative stress, being directly correlated with the degree of exposure to tobacco smoke. We analyzed, in 76 adult subjects from a public health care unit, the relationships between serum cotinine levels as a marker of tobacco smoke exposure, and three biomarkers of oxidative stress: the serum glutathione (GSH), the advanced oxidation protein products (AOPPs), and the total serum antioxidant status (FRAP). The results indicate that the degree of tobacco smoke exposure was inversely associated with GSH levels in both passive and active smokers, suggesting that smoke particulate components’ toxicity is associated with a systemic GSH depletion. Paradoxically, the lowest AOPP levels which were positively associated with GSH, were recorded in active smoking patients whereas in passive smokers individual values of AOPPs decreased along with the increase in GSH levels. Our data suggest that an enhanced inhalation of particulate constituents of cigarette smoke could induce critical changes in systemic redox homeostasis and GSH can no longer exert its antioxidant role.