Ambient air pollution has become a common problem worldwide. Exposure to pollutant particles causes many health conditions, having a particular impact on pulmonary and cardiovascular disease. Increased understanding of the pathological processes related to these conditions may facilitate the prevention of the adverse impact of air pollution on our physical health. Evidence from in vitro, in vivo, and clinical studies has consistently shown that exposure to particulate matter could induce the inflammatory responses such as IL-6, TNF-α, IL-1β, as well as enhancing the oxidative stress. These result in vascular injury, adhesion molecule release, platelet activation, and thrombin generation, ultimately leading to a prothrombotic state. In this review, evidence on the effects of particulate matter on inflammation, oxidative stress, adhesion molecules, and coagulation pathways in enhancing the risk of thrombosis is comprehensively summarized and discussed. The currently available outcomes of interventional studies at a cellular level and clinical reports are also presented and discussed.

Human health hazards caused by bisphenol A (BPA), a precursor for epoxy resins and polycarbonate-based plastics, are well documented and are closely associated with mitochondrial impairment and oxidative imbalance. This study aimed to assess the therapeutic efficacy of N-acetylcysteine (NAC) on renal deterioration caused by long-term BPA exposure and examine the signaling transduction pathway involved. Male Wistar rats were given vehicle or BPA orally for 12 weeks then the BPA-treated group was subdivided to receive vehicle or NAC concurrently with BPA for a further 4 weeks, while the vehicle-treated normal control group continued to receive vehicle through to the end of experiment. Proteinuria, azotemia, glomerular filtration reduction and histopathological abnormalities caused by chronic BPA exposure were significantly reduced following NAC therapy. NAC also diminished nitric oxide and lipid peroxidation but enhanced renal glutathione levels, and counteracted BPA-induced mitochondrial swelling, increased mitochondrial reactive oxygen species production, and the loss of mitochondrial membrane potential. The benefit of NAC was related to the modulation of signaling proteins in the AMPK-SIRT3-SOD2 axis. The present study shows the potential of NAC to restore mitochondrial integrity and oxidative balance after long-term BPA exposure, and suggests that NAC therapy is an effective approach to tackle renal deterioration in this condition.

Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin’s lymphoma, characterized by its aggressive nature and heterogeneity. Despite significant advances in understanding DLBCL pathogenesis, there is still a need to elucidate the intricate mechanisms involved in disease progression and identify novel therapeutic targets. Extracellular vesicles (EVs), including exosomes and microvesicles, have emerged as crucial mediators of intercellular communication in various physiological and pathological processes, including cancer. In recent years, evidence has suggested that EVs play a vital role in DLBCL biology by facilitating the exchange of genetic material, especially miRNAs, and proteins and lipids between tumor cells, immune cells, and the tumor microenvironment. We summarize and discuss the biological functions of EVs in DLBCL and their effects on the tumor microenvironment, highlighting their influence on DLBCL pathobiology, immune evasion, angiogenesis, and drug resistance. We also investigated EVs’ diagnostic and prognostic potential as circulating biomarkers in DLBCL, emphasizing their utility in the non-invasive monitoring of the disease status and treatment response. Understanding the complex interplay between EVs and DLBCL may open up new avenues for personalized medicine, improve patient stratification, and facilitate the development of innovative therapeutic interventions in this devastating hematological malignancy.