Search Results (3)

Heated tobacco products (HTPs) are marketed as lower-risk alternatives to conventional cigarettes; however, their toxicological impacts remain insufficiently characterized. This study evaluated the effects of HTP emissions on gene expression and mitochondrial function in comparison with conventional cigarettes. Whole cigarette smoke condensates (WCSCs), comprising both gas and particulate phases, were prepared from three commercially available HTPs and from 3R4F reference cigarettes. Human lung epithelial BEAS-2B cells were exposed to WCSCs at 3 μg nicotine/mL for 24 h, followed by transcriptome profiling using RNA sequencing. Principal component analysis demonstrated that HTP-WCSCs induced weaker gene expression changes than 3R4F-WCSC, with only modest variation among HTPs. Gene set enrichment analysis revealed that both HTP- and 3R4F-WCSCs significantly downregulated oxidative phosphorylation (OXPHOS)–related pathways, indicating potential mitochondrial impairment. Functional assays confirmed that both exposures elevated mitochondrial reactive oxygen species (ROS), while mitochondrial morphology, ATP production, membrane potential, and cytosolic ROS were largely unaffected. Collectively, these results show that although HTP emissions elicit weaker transcriptomic perturbations than conventional cigarette emissions, both converge on mitochondrial targets by suppressing OXPHOS gene expression and increasing mitochondrial ROS. Mitochondrial dysfunction may therefore represent a common mechanism underlying tobacco product toxicity. Full article

Although cigarette smoking has been postulated to be a potential risk factor for Alzheimer’s disease (AD), the toxic mechanism is still unclear. Additionally, astrocytes have been identified as a potential target, given they play multiple roles in maintaining normal brain function. In this study, we explored the toxic mechanism of whole cigarette smoke condensates (WCSC) using murine astrocytes. Cell proliferation, the percentage of cells in the G2/M phase, and LDH concentrations in the cell supernatants were all reduced in WCSC-treated cells. In addition, oxidative stress was induced, together with shortening of processes, structural damage of organelles, disturbances in mitochondrial function, blockage of autophagic signals, accumulation of amyloid β precursor protein, and loss of chemotactic functions. Based on these results, we hypothesize that dysfunction of astrocytes may contribute to the occurrence of cigarette-smoking-induced AD. Full article

Pesticides have been considered as potential chemical mutagens; however, little is known about toxic and genotoxic effects during pesticide application in Zamora-Jacona, Michoacan State in Mexico. This study sought to determine DNA damage and cholinesterase activities inhibitions in 54 agricultural workers exposed to complex mixtures of pesticides vs. control group (26 individuals) using Comet assay in peripheral whole blood, micronucleus (MN) test in oral mucosa cells, Cytokinesis-blocked MN assay in lymphocytes (L-CBMNcyt) and measuring AChE and BChE activities in whole blood and plasma samples, respectively. Exposed subjects demonstrated significantly elevated levels of primary (Comet assay: tail intensity, tail length, tail moment, Olive tail moment) and permanent DNA damage (MN assay: in blood/buccal cells; frequencies of nuclear buds, binucleated cells, cells with condensed chromatin, karyorrhexis, pyknosis, and karyolysis). However, inhibition of cholinesterase activities (AChE and BChE) was not observed in the workers. Confounding factors including sex, age, BMI, working exposure period, protection level, smoking habit (cigarettes per day units), alcohol consumption (weekly), medication, were considered in the analysis. These combined techniques demonstrated usefulness in the health hazards risks pesticide exposure assessment and suggested the need for periodic monitoring together with the education and the training of occupational workers for the safe application of potentially harmful pesticides. Full article