Objective: To investigate thiol/disulfide homeostasis in patients with stable angina pectoris.Materials and Methods: The study population consisted of 85 stable angina pectoris patients and 31 healthy volunteers. To compare the thiol/disulfide values of the patients and controls, the newly developed analysis method was used by Erel and Neselioglu. Disulfide/total thiol, free thiol/total thiol and disulfide/free thiol values were calculated for both groups.Results: Disulfide, free thiol and total thiol values obtained in the study were; 18.00 µmol/L, 365.08 µmol/L, 401.10 µmol/L for the patient group and 9.67 µmol/L for the control group, 372.51 µmol/L, 391.85 µmol/L for the control group. It is the first time thiol/disulphide homeostasis in plasma was examined by new developed method in stable angina pectoris patients with this study. Disulfide, disulfide/free thiol and disulfide/total thiol values were significantly higher in the patient group compared to the control group. free thiol/total thiol levels were significantly lower in patients (p<0.001).Conclusion: Thiol and disulfide values can be seen at high levels in patients with stable angina pectoris, so thiol/disulfide homeostasis may be an indicator for this disease.

Nanoplastics (NPs; ≤1 µm) have been detected in human placenta, blood, lung, atherosclerotic plaque, testis, semen, olfactory bulb, and brain, shifting the field from environmental description toward mechanistic interrogation of barrier crossing. This review synthesises current evidence on NP translocation across the intestinal epithelium, the blood–brain barrier (BBB) and the placental syncytiotrophoblast. We distinguish four evidence categories throughout the review: detection, association, mechanism, and causality. We also apply model-system labels (in silico, in vitro, ex vivo, animal, and human) to every mechanistic claim, so that the strength of each statement can be read off directly. Most current studies use pristine polystyrene nanoplastics at concentrations 3–6 orders of magnitude above plausible human exposure, so the mechanistic conclusions below are hypothesis-generating for human disease rather than definitive. We propose a working conceptual framework—corona-driven barrier selectivity (CDBS)—in which the particle–corona–surface complex, rather than the bare polymer, is hypothesised to dictate which receptor and transport machinery (TfR1, LRP1, FcRn, P-gp/BCRP, caveolae) each barrier engages. CDBS is offered as a hypothesis-stage organising tool requiring experimental validation, not as an established mechanism. We outline reported transport modes, including clathrin- and caveolin-mediated endocytosis, paracellular leakage via ROS-induced tight-junction disassembly, receptor-mediated transcytosis, and the candidate olfactory route. We emphasise that pristine polystyrene-bead doses commonly exceed plausible human exposure by 3–6 orders of magnitude, that detection methods underestimate sub-micrometre particles, and that causal links between NPs and human disease remain hypothesis-generating. A research agenda built on weathered reference materials, microphysiological systems, and integrative human biomarker science is proposed.

Laurocerasus officinalis , a valuable medicinal plant, has rich flavonoid and anthocyanin content, providing benefits for various diseases. It also has ethnopharmacological uses such as diuretics and antidiabetics. Phenolic compounds exhibit their anticarcinogenic effects directly by repairing DNA damage and reducing chromosomal abnormalities. This study aims to investigate genotoxicity/antigenotoxicity and cytotoxicity/anticytotoxicity of L. officinalis extract in human peripheral lymphocytes by the methods of chromosomal aberration (CA), cytokinesis‐block micronucleus (CBMN) test, and mitotic index value. The doses of L. officinalis extract were determined as 125, 250, 500, and 1,000 μg/mL for the genotoxicity test, and mitomycin C (MMC) was added to induce DNA damage for the investigation of antigenotoxicity. In both applications (24 and 48 h), all doses, positive control (MMC) and negative control (sterile dH ₂ O), were used. In CA and CBMN tests for genotoxicity, no significant differences existed between all doses and the solvent control group ( p > 0.05). In antigenotoxic activity, doses added with MMC were significantly lower than positive control ( p < 0.05). For both the 24‐hour and 48‐hour periods, the percentage of abnormal cells and the CAs per cell ratio were significantly lower at all L. officinalis extract concentrations compared to the positive control. Additionally, as the treatment concentration increased, the CA ratio showed a decreasing trend. These differences were strongly dose‐dependent compared to the positive control ( r = −0.799). In all concentrations in the CBMN test, the frequencies were significantly lower than the positive control, and the higher the L. officinalis extract concentrations, the lower the micronuclei (MN). There was a strong dose‐dependent relationship in MN formation compared to positive control ( r = −0.925). Therefore, L. officinalis extract has no genotoxic effect on human lymphocytes and also has antigenotoxic and protective effect to the damage of MMC. In the mitotic index result, the L. officinalis extract was cytotoxic at only one dose (125 μg/mL) but anticytotoxic at all other doses against MMC exposure. In conclusion, consuming L. officinalis medicinally benefits and may protect against exposure to genotoxic agents.