Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of free radical scavengers, micronutrient antioxidants, on antioxidant enzyme activities in cigarette smokers. We measured the intracellular superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and vitamin E and beta-carotene levels in the bronchoalveolar cells of 14 smokers before and after 6 weeks of supplementation with vitamins E and C and beta-carotene. Eight nonsmokers served as control subjects. CAT and GPx activities were higher in BAL cells from smokers compared with nonsmokers (20.5 +/- 2.3 vs 9.6 +/- 1.3 U/10(6) cells; p = 0.027; 0.90 +/- 0.10 vs 0.46 +/- 0.12 U/10(6) cells; p = 0.049, respectively), while there was no difference in SOD activity between the two groups. Likewise, vitamin E and beta-carotene concentrations were markedly higher in smokers' lung lavage cells (403.3 +/- 81.0 in smokers vs 16.6 +/- 5.3 ng/10(6) cells in nonsmokers, and 1.23 +/- 0.21 in smokers vs 0.15 +/- 0.04 ng/10(6) cells in nonsmokers, respectively). The serum levels of vitamin E and C and beta-carotene increased by 2.0-, 1.6-, and 8.9-fold in smokers after supplementation, which were similar to nonsmokers. Similarly, BAL cell vitamin E increased from 403.3 +/- 81.0 to 477.4 +/- 97.7 ng/10(6) cells and beta-carotene increased from 1.23 +/- 0.21 to 4.32 +/- 0.45 ng/10(6) cells (p < 0.05). Despite increased concentrations of vitamins in serum as well as beta-carotene levels in BAL cells, there was no significant down regulation in SOD, CAT, or GPx activities in the lung lavage cells. These data suggest that augmentation of micronutrient antioxidants in smokers and nonsmokers does not appear to have an effect on antioxidant enzyme activities, suggesting a differential regulation of these defenses.
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PMID:Adaptation of lung antioxidants to cigarette smoking in humans. 887 45

The outbreak of vaping-related acute lung injury in the United States, named EVALI (e-cigarette or vaping product use associated acute lung injury), has reignited concerns about the health effects of vaping. Initial case reports of vaping-related lung injury date back to 2012, but the ongoing outbreak of EVALI began in the summer of 2019 and has been implicated in 2,807 cases and 68 deaths as of this writing. Review of the scientific literature revealed 216 patient cases that spanned 41 reports of parenchymal lung injury attributed to vaping. In this review, we detail the clinical, radiographic, and pathologic patterns of lung injury that are attributable to vaping and provide an overview of the scientific literature to date on the effects of vaping on respiratory health. Tetrahydrocannabinol was the most commonly vaped substance, and vitamin E acetate was found in BAL specimens from many affected individuals. However, no specific component or contaminant has been identified conclusively to date as the cause for the injury. Patients present with cough, dyspnea, constitutional symptoms, and GI symptoms. Radiologic and histopathologic findings demonstrate a spectrum of nonspecific acute injury patterns. A high index of suspicion combined with a good history are the keys to an accurate diagnosis. Treatment is supportive; the mortality rate is low, and most patients recover. Corticosteroids have been used with apparent success in patients with severe disease, but more rigorous studies are needed to clarify their role in the treatment of vaping-related lung injury.
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PMID:Vaping-Related Acute Parenchymal Lung Injury: A Systematic Review. 3244 59

Electronic-cigarette, or vaping, product use-associated lung injury (EVALI) is a syndrome of acute respiratory failure characterized by monocytic and neutrophilic alveolar inflammation. Epidemiological and clinical evidence suggests a role of vitamin E acetate (VEA) in the development of EVALI, yet it remains unclear whether VEA has direct pulmonary toxicity. To test the hypotheses that aerosolized VEA causes lung injury in mice and directly injures human alveolar epithelial cells, we exposed adult mice and primary human alveolar epithelial type II (AT II) cells to an aerosol of VEA generated by a device designed for vaping oils. Outcome measures in mice included lung edema, BAL analysis, histology, and inflammatory cytokines; in vitro outcomes included cell death, cytokine release, cellular uptake of VEA, and gene-expression analysis. Comparison exposures in both models included the popular nicotine-containing JUUL aerosol. We discovered that VEA caused dose-dependent increases in lung water and BAL protein compared with control and JUUL-exposed mice in association with increased BAL neutrophils, oil-laden macrophages, multinucleated giant cells, and inflammatory cytokines. VEA aerosol was also toxic to AT II cells, causing increased cell death and the release of monocyte and neutrophil chemokines. VEA was directly absorbed by AT II cells, resulting in the differential gene expression of several inflammatory biological pathways. Given the epidemiological and clinical characteristics of the EVALI outbreak, these results suggest that VEA plays an important causal role.
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PMID:Dose-Dependent Pulmonary Toxicity of Aerosolized Vitamin E Acetate. 3282 37