There Is No Smoke without Mitochondria.
Ontology highlight
ABSTRACT:
SUBMITTER: Han S
PROVIDER: S-EPMC6503615 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPeople who smoke with serious mental illness carry disproportionate costs from smoking, including poor health and premature death from tobacco-related illnesses. Hospitals in New Zealand are ostensibly smoke-free; however, some mental health wards have resisted implementing this policy.AimThis study explored smoking in acute metal health wards using data emerging from a large sociological study on modern acute psychiatric units.MethodsEighty-five in-depth, semi-structured interviews were conducted with staff and service users from four units. Data were analysed using a social constructionist problem representation approach.ResultsAlthough high-level smoke-free policies were mandatory, most participants disregarded these policies and smoking occurred in internal courtyards. Staff reasoned that acute admissions were not the time to quit smoking, citing the sceptres of distress and possibly violence; further, they found smoking challenging to combat. Inconsistent enforcement of smoke-free policies was common and problematic. Many service users also rejected smoke-free policies; they considered smoking facilitated social connections, alleviated boredom, and helped them feel calm in a distressing environment - some started or increased smoking following admission. A minority viewed smoking as a problem; a fire hazard, or pollutant. No one mentioned its health risks.ConclusionPsychiatric wards remain overlooked corners where hospital smoke-free policies are inconsistently applied or ignored. Well-meaning staff hold strong but anachronistic views about smoking. To neglect smoking cessation support for people with serious mental illness is discriminatory and perpetuates health and socioeconomic inequities. However, blanket applications of generic policy are unlikely to succeed. Solutions may include myth-busting education for service users and staff, local champions, and strong managerial support and leadership, with additional resourcing during transition phases. Smoke-free policies need consistent application with non-judgemental NRT and, potentially, other treatments. Smoking cessation would be supported by better designed facilities with more options for alleviating boredom, expressing autonomy, facilitating social connections, and reducing distress.
| S-EPMC8592473 | biostudies-literature
Project description:Mitochondrial functionality is crucial for the execution of physiologic functions of metabolically active cells in the respiratory tract including airway epithelial cells (AECs). Cigarette smoke is known to impair mitochondrial function in AECs. However, the potential contribution of mitochondrial dysfunction in AECs to airway infection and airway epithelial barrier dysfunction is unknown. In this study, we used an in vitro model based on AECs exposed to cigarette smoke extract (CSE) followed by an infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress as an indicator of mitochondrial stress were quantified upon CSE and Sp treatment. In addition, expression of proteins associated with mitophagy, mitochondrial content, and biogenesis as well as mitochondrial fission and fusion was quantified. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with indices of mitochondrial function. We observed that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp.
| S-EPMC9179351 | biostudies-literature
Project description:Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.
2022-05-27 | GSE197751 | GEO
Project description:Smoking habit is the most widely accepted environmental factor affecting the incidence and disease progression in the inflammatory bowel diseases. The contrasting effects in Crohn's disease (CD) and ulcerative colitis are unexplained. The purpose of this review is to summarise the existing data on the effects of smoking in CD on disease history, recurrence after surgery, effects on drug responses and to review available evidence that carriage of some of the known susceptibility genes may be disproportionate in smokers with CD. The review also highlights potential mechanisms involved and factors that might affect patients' smoking habits. The clinical and scientific implications of the data are discussed.
| S-EPMC5517176 | biostudies-other
Project description:ObjectiveObesity and cigarette smoking are leading preventable causes of mortality, with greater mortality risk when these disorders occur together. Comorbid obesity and cigarette smoking may affect the valuation of cigarettes. The present study examines the demand for cigarettes between obese and nonobese smokers.MethodParticipants (N = 187) from four in-laboratory studies completed the hypothetical cigarette purchase task. According to self-reported height and weight, participants were assigned to either the obese group (body mass index [BMI] ≥ 30) or to the nonobese group (BMI < 30).ResultsSignificant differences in demand intensity were observed between individuals with and without obesity, F(1, 168) = 9.284, p = .003, with individuals who smoke and are obese showing higher demand intensity (product purchasing when free). These differences in demand intensity between groups remained after adjusting for the number of cigarettes consumed per day. No differences were observed in elasticity of demand, F(1, 168) = 1.033, p = .311.ConclusionsThe results reported here suggest that individuals who smoke and are obese may value brief, intense, and immediate reinforcers more than individuals who smoke and are not obese. Further research may suggest reinforcer pathology as a basis for this result. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
| S-EPMC9972959 | biostudies-literature
Project description:Mitochondrial dysfunction is an underlying pathology in numerous diseases. Delivery of diagnostic and therapeutic cargo directly into mitochondria is a powerful approach to study and treat these diseases. The triphenylphosphonium (TPP+) moiety is the most widely used mitochondriotropic carrier. However, studies have shown that TPP+ is not inert; TPP+ conjugates uncouple mitochondrial oxidative phosphorylation. To date, all efforts toward addressing this problem have focused on modifying lipophilicity of TPP+-linker-cargo conjugates to alter mitochondrial uptake, albeit with limited success. We show that structural modifications to the TPP+ phenyl rings that decrease electron density on the phosphorus atom can abrogate uncoupling activity as compared to the parent TPP+ moiety and prevent dissipation of mitochondrial membrane potential. These alterations of the TPP+ structure do not negatively affect the delivery of cargo to mitochondria. Results here identify the 4-CF3-phenyl TPP+ moiety as an inert mitochondria-targeting carrier to safely target pharmacophores and probes to mitochondria.
| S-EPMC8293692 | biostudies-literature
Project description:Isolation of functional and intact mitochondria from solid tissue is crucial for studies that focus on the elucidation of normal mitochondrial physiology and/or mitochondrial dysfunction in conditions such as aging, diabetes, and cancer. There is growing recognition of the importance of mitochondria both as targets for drug development and as off-target mediators of drug side effects. Unfortunately, mitochondrial isolation from tissue is generally carried out using homogenizer-based methods that require extensive operator experience to obtain reproducible high-quality preparations. These methods limit dissemination, impede scale-up, and contribute to difficulties in reproducing experimental results over time and across laboratories. Here we describe semiautomated methods to disrupt tissue using kidney and muscle mitochondria preparations as exemplars. These methods use the Barocycler, the PCT Shredder, or both. The PCT Shredder is a mechanical grinder that quickly breaks up tissue without significant risk of overhomogenization. Mitochondria isolated using the PCT Shredder are shown to be comparable to controls. The Barocycler generates controlled pressure pulses that can be adjusted to lyse cells and release organelles. The mitochondria subjected to pressure cycling-mediated tissue disruption are shown to retain functionality, enabling combinations of the PCT Shredder and the Barocycler to be used to purify mitochondrial preparations.
| S-EPMC3172370 | biostudies-literature
Project description:The chemical nature and functional significance of mitochondrial flashes associated with fluctuations in mitochondrial membrane potential is unclear. Using a ratiometric pH probe insensitive to superoxide, we show that flashes reflect matrix alkalinization transients of ?0.4 pH units that persist in cells permeabilized in ion-free solutions and can be evoked by imposed mitochondrial depolarization. Ablation of the pro-fusion protein Optic atrophy 1 specifically abrogated pH flashes and reduced the propagation of matrix photoactivated GFP (paGFP). Ablation or invalidation of the pro-fission Dynamin-related protein 1 greatly enhanced flash propagation between contiguous mitochondria but marginally increased paGFP matrix diffusion, indicating that flashes propagate without matrix content exchange. The pH flashes were associated with synchronous depolarization and hyperpolarization events that promoted the membrane potential equilibration of juxtaposed mitochondria. We propose that flashes are energy conservation events triggered by the opening of a fusion pore between two contiguous mitochondria of different membrane potentials, propagating without matrix fusion to equilibrate the energetic state of connected mitochondria.
| S-EPMC3981180 | biostudies-literature
Project description:Cigarette smoking causes hypomethylation of the gene Aryl Hydrocarbon Receptor Repressor (AHRR), which regulates detoxification and oxidative stress-responses. We investigated whether AHRR DNA methylation is related to chronic obstructive pulmonary disease (COPD) and studied its function in airway epithelial cells (AECs). The association with COPD was assessed in blood from never and current smokers with/without COPD, and in AECs from ex-smoking non-COPD controls and GOLD stage II-IV COPD patients cultured with/without cigarette smoke extract (CSE). The effect of CRISPR/Cas9-induced AHRR knockout on proliferation, CSE-induced mitochondrial membrane potential and apoptosis/necrosis in human bronchial epithelial 16HBE cells was studied. In blood, DNA methylation of AHRR at cg05575921 and cg21161138 was lower in smoking COPD subjects than smoking controls. In vitro, AHRR DNA methylation at these CpG-sites was lower in COPD-derived than control-derived AECs only upon CSE exposure. Upon AHRR knockout, we found a lower proliferation rate at baseline, stronger CSE-induced decrease in mitochondrial membrane potential, and higher CSE-induced late apoptosis/necroptosis. Together, our results show lower DNA methylation of AHRR upon smoking in COPD patients compared to non-COPD controls. Our data suggest that higher airway epithelial AHRR expression may lead to impaired cigarette smoke-induced mitochondrial dysfunction and apoptosis/necroptosis, potentially promoting unprogrammed/immunogenic cell death.
| S-EPMC9656229 | biostudies-literature
Project description:BackgroundIt is known that environmental tobacco smoke (ETS) has adverse effects on pregnancy and birth outcomes. We aimed to assess the impact of ETS in pregnant women with and without asthma.MethodsA cohort study was conducted from August 2014 to June 2015 enrolling 1603 pregnant women during their 2nd trimester. Data on tobacco exposure were collected at first visit and women were followed through pregnancy till postpartum.ResultsOf the 1603 women, 231 reported passive smoking, 223 non-asthmatics and 8 asthmatics. Women exposed to ETS during pregnancy were more likely to have an infant admitted to the pediatric ward (10.8% vs. 6.5%, p = 0.026) and to have low one- and five-minute Apgar scores (1 min: 6.1% vs. 2.6%, p = 0.011; 5 min: 2.2% vs. 0.7%, p = 0.039). Complications of pregnancy were also elevated in women exposed to ETS (53.7% vs. 42.3%, p = 0.002). Asthma had no additional effect beyond the impact of ETS except for cesarean sections that were more frequent in women with asthma exposed to ETS.ConclusionsDue to the small number of women with asthma exposed to ETS, combined effects of asthma and ETS were only found for cesarean sections. Still counseling of pregnant women about adverse effects of ETS should consider women's asthma as an additional reason to avoid ETS.
| S-EPMC7240917 | biostudies-literature