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In vitro, the gaseous phase of cigarette smoke is known to induce both isomerization and degradation of dietary carotenoids, such as β-carotene and lycopene. However, the effects of cigarette smoke on the composition of circulating lycopene in vivo are not well understood. In this study, we examined the lycopene profiles of plasma from non-smokers and smokers. No oxidative intermediates of lycopene that have been observed previously in vitro were detected in the plasma, but evidence of isomerization of the carotenoid was seen. Four geometric forms of lycopene were detected in the plasma of both smokers and non-smokers, namely the (5), (9), (13) and (all-) forms. The relative amounts of these isomers differed between the two cohorts and there was a significant difference ( < 0.05) between smokers and non-smokers for the ratio of total-Z:all- lycopene, and in the relative amounts of (13) and (all-)-lycopene. The ratio of (all-):(13)-lycopene was 0.84:1.00 in smokers compared to 1.04:1.00 in non-smokers. In smokers, the (13)-isomer was generated in preference to the more thermodynamically stable (5) and (9)-isomers. This mirrors the scenario seen in vitro, in which the formation of (13)-lycopene was the main isomer that accompanied the depletion of (all-) lycopene, when exposed to cigarette smoke. The results suggest that the relative amount of (13)-lycopene could be used as an indicator of oxidative damage to lycopene in vivo.
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http://dx.doi.org/10.3390/antiox6030069 | DOI Listing |
Redox Biol
August 2025
Department of Medicine, School of Medicine, Universidad Autónoma de Madrid, Madrid, Spain; Instituto Investigación Sanitaria-Princesa IIS-IP, Madrid, Spain; Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Instituto de Salud Carlos III, Madrid, Spain. Electronic
Tobacco smoke is the main risk factor for the development of chronic obstructive pulmonary disease (COPD). Despite current therapies alleviate symptoms there are limitations in the efficacy of treatments to curb its cardiovascular morbidities, particularly vascular dysfunction and the development of pulmonary hypertension. Our previous studies demonstrate that cigarette smoke directly contributes to pulmonary arterial dysfunction.
View Article and Find Full Text PDFSTAR Protoc
September 2025
UCLA Children's Discovery and Innovation Institute, Mattel Children's Hospital, Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; UCLA Environmental and Molecular Toxicology Interdepartmental Program, University of California, Los Angeles, Los Angeles, CA
Exposure systems to study the effects of environmental exposures can be costly to purchase and difficult to use. Here, we present an accessible and cost-effective approach to building an exposure chamber in the lab. We describe steps for constructing the exposure system and writing the code to run it and simple instructions for experiments using the system.
View Article and Find Full Text PDFNicotine Tob Res
September 2025
College of Public Health, University of Nebraska Medical Center, Omaha, NE, United States.
Introduction: Nicotine pouches (NPs) are an emerging nicotine delivery system. Understanding nicotine and toxicant exposure among NP users compared with users of other tobacco products and non-users is critical for informing public health strategies.
Methods: Data (n = 4527) were drawn from the Population Assessment of Tobacco and Health Study Wave 7 (2022-2023).
J Pathol
September 2025
Sidney Kimmel Comprehensive Cancer Center and Department of Oncology, Johns Hopkins University, Baltimore, MD, USA.
Triple-negative breast cancer (TNBC) lacks expression of estrogen receptor (ER), progesterone receptor (PR), and HER2, and remains one of the most aggressive and therapeutically challenging breast cancer subtypes, marked by early relapse, metastasis, and limited targeted treatment options. In a recent study published in The Journal of Pathology, Kuo et al provide compelling evidence that nicotine exposure, whether from tobacco smoke or e-cigarette vapor, drives TNBC progression by promoting stem-like and metastatic phenotypes. Integrating clinical datasets, patient tissues, cell lines, and in vivo models, the authors demonstrate that nicotine enhances tumor aggressiveness via coordinated upregulation of CHRNA9 and IGF1R.
View Article and Find Full Text PDFGen Physiol Biophys
September 2025
Pneumology Department, Zigong First People's Hospital, Zigong, China.
Chronic obstructive pulmonary disease (COPD) is characterized by airway remodeling and inflammation. Cigarette smoke extract (CSE) induces apoptosis, inflammation, and oxidative stress in COPD. Tripterygium glycosides (TG) are an active compound found in the root extracts of Tripterygium wilfordii Hook F (TWHF) that possesses anti-inflammatory and immunosuppressive effects.
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