Component Of Cigarette Smoke Research Articles

The impact of cigarette smoke as a risk factor for hypertension in pregnancy

Introduction: Hypertension in pregnancy is one of the severe complications and is the leading cause of maternal and perinatal morbidity and mortality. Risk factors for hypertension in pregnancy include various aspects, including exposure to cigarette smoke, which has a detrimental impact on the mother and fetus. This study aims to analyze the impact of exposure to cigarette smoke as a risk factor for hypertension in pregnancy. Methods: The design of observational analytical research with a cross-sectional design uses point-time, observation, or data collection methods to examine the relationship dynamics between impact risk factors. The dependent variable of this study is the prevalence of hypertension in pregnant women. The number of samples was 128 people using the purposive sampling technique. Results: The results of the study showed that pregnant women who were exposed to cigarette smoke, both active and passive, had a higher risk of developing hypertension compared to mothers who were not exposed. Harmful components in cigarette smoke, such as nicotine and carbon monoxide, play a role in raising blood pressure through vasoconstriction mechanisms and oxidative stress, which aggravate the workload of the heart and circulatory system. Conclusions: These findings show the need for prevention and education efforts to reduce exposure to cigarette smoke in pregnant women, to reduce the incidence of hypertension in pregnancy, and improve the health of mothers and babies. With this information, it is hoped that health workers and the public can be more aware of the dangers of cigarette smoke during pregnancy and strive for a smoke-free environment for pregnant women.

Molecular impact of nicotine and smoking exposure on the developing and adult mouse brain.

Maternal smoking during pregnancy (MSDP) is associated with significant cognitive and behavioral effects on offspring. While neurodevelopmental outcomes have been studied for prenatal exposure to nicotine, the main psychoactive component of cigarette smoke, its contribution to MSDP effects has never been explored. Comparing the effects of these substances on molecular signaling in the prenatal and adult brain may provide insights into nicotinic and broader tobacco consequences that are developmental-stage specific or age-independent. Pregnant mice were administered nicotine or exposed to chronic cigarette smoke, and RNA-sequencing was performed on frontal cortices of postnatal day 0 pups born to these mice, as well as on frontal cortices and blood of the adult dams. We identified 1,010 and 4,165 differentially expressed genes (DEGs) in nicotine and smoking-exposed pup brains, respectively (FDR<0.05, Ns = 19 nicotine-exposed vs 23 vehicle-exposed; 46 smoking-exposed vs 49 controls). Prenatal nicotine exposure (PNE) alone was related to dopaminergic synapses and long-term synaptic depression, whereas MSDP was associated with the SNARE complex and vesicle transport. Both substances affected SMN-Sm protein complexes and postsynaptic endosomes. Analyses at the transcript, exon, and exon-exon junction levels supported gene level results and revealed additional smoking-affected processes. No DEGs at FDR<0.05 were found in adult mouse brain for any substance (12 nicotine-administered vs 11 vehicle-administered; 12 smoking-exposed vs 12 controls), nor in adult blood (12 smoking-exposed vs 12 controls), and only 3% and 6.41% of the DEGs in smoking-exposed pup brain replicated in smoking-exposed blood and human prenatal brain, respectively. Together, these results demonstrate variable but overlapping molecular effects of PNE and MSDP on the developing brain, and attenuated effects of both smoking and nicotine on adult versus fetal brain.

Prediction of typical gas components in cigarette smoke based on transformer

Abstract Harm reduction of cigarette products has become one of the primary objectives of the entire tobacco industry. The prediction of typical gas components (TGC) and dynamic adjustment of process parameters are crucial for cigarette coke reduction and harm reduction. In this study, a deep learning (DL)-assisted TGC prediction framework is proposed to predict CO and NI simultaneously. Firstly, a large number of experimental and simulation parameters of cigarette process are collected as the data base for subsequent model construction. Then, the feature importance analysis of the process parameters was carried out by combining the mechanism of the combustion process through the mutual information method. Finally, DL models based on Multilayer Perceptron, One-Dimension Convolutional Neural Network and Transformer (TF) was developed as data-driven surrogate models to establish the mapping relationship between process parameters and TGC. The results show that TF model generalizes best and can predict TGC quickly and accurately with R2 over 0.99. This work will provide a valuable predictive and decision-making tool for cigarette harm reduction.

The double-edged nature of nicotine: toxicities and therapeutic potentials.

Nicotine is the primary addictive component of cigarette smoke and is associated with various smoking-related diseases. However, recent research has revealed its broader cognitive-enhancing and anti-inflammatory properties, suggesting its potential therapeutic applications in several conditions. This review aims to examine the double-edged nature of nicotine, encompassing its positive and negative effects. We provide a concise overview of the physiochemical properties and pharmacology of nicotine, including insights into nicotine receptors. Therefore, the article is divided into two main sections: toxicity and therapeutic potential. We comprehensively explored nicotine-related diseases, focusing on specific signaling pathways and the underlying mechanisms that contribute to its effects. Furthermore, we addressed the current research challenges and future development perspectives. This review aims to inspire future researchers to explore the full medical potential of nicotine, which holds significant promise for the clinical management of specific diseases.

Development of an IoT-Integrated Cigarette Smoke Detection System Using MiCS-5524 Sensor

Cigarette smoke is one of the primary causes of indoor air pollution, leading to various adverse health impacts. To address this issue, this research aims to design of a cigarette smoke detection device using the MiCS-5524 sensor integrated with the Internet of Things (IoT). This device can detect the level of cigarette smoke in indoor spaces and provide alerts through an LCD, a buzzer, and the Blynk application. Furthermore, the device can activate an exhaust fan to remove cigarette smoke from the room. The device employs the NodeMCU ESP8266 microcontroller as the central control unit for system operation and internet communication. The MiCS-5524 sensor was chosen for its high sensitivity to carbon monoxide (CO), a major component of cigarette smoke. Test results demonstrate that the device functions effectively and accurately in detecting cigarette smoke and responding to indoor air conditions. It is anticipated that this device will contribute to improving indoor air quality and human health.

Problems in diagnosing pre-COPD (case report)

Cigarette smoke is a key risk factor for developing COPD (GOLD, 2024). One of the factors responsible for tissue damage and bronchial remodeling in the early stages of the disease is patients’ hypersensitivity to nicotine and components of cigarette smoke. Because of early life adversity combined with environmental and genetic interactions, pulmonary function measures alone may not be appropriate for the early recognition and diagnosis of COPD. It seems necessary to identify biomarkers of the risk of developing pre-COPD to identify the early stage of the disease. In the article we describe the clinical case of patient M., 21 years old, a smoker with a history of respiratory symptoms, who has signs of chronic obstructive pathology with the formation of bronchial hypersensitivity and persistent obstruction that does not reach the threshold for COPD, which reflects a common clinical problem. Сertainly, the formation of the concept of pre-COPD and the development of clinical and instrumental diagnostic criteria are necessary. Previously, we developed and tested a prick-prick test method with nicotine. We propose to use skin testing with a nicotine solution as one of the diagnostic biomarkers to identify hypersensitivity at the first stage of tissue damage.

Cellulose acetate filter rods tuned by surface engineering modification for typical smoke components adsorption

Abstract A series of filter rods (FRs) with sodium alginate (SA) modification were prepared by a simple one-pot pre-treatment surface modification method for the retention of typical smoke components. The influences of SA on the physico-chemical properties and adsorption behaviors (or retention characteristics) toward FRs were investigated in detail. Based on the results of XRD, BET, and SEM, it can be inferred that SA modification has no influences on compositions and textural properties of FRs. However, surface modification of FR by SA can greatly improve the hydrophilicity of FR, which is crucial for water retention. In situ diffuse Fourier-transform infrared spectroscopy results demonstrate that FR modified by 2 g·L−1 SA presents superior adsorption character for acetone. The differences in the adsorption or retention of water and acetone are ascribed to surface enriched functional groups tuned by surface engineering modification. By contrast, the modification of SA had no obvious effect on the adsorption of CO at room temperature. By contrast, at high temperature, low modification concentration is conducive to the CO2 and CO adsorption. It presents a good perspective for the rational design of new filter materials to reduce the release of harmful components in cigarette smoke.

Article Review: Effect of Electronic Cigarette on Fertility in Male

Numerous researches have shown that blood plasma, sperm parameters, or a host of other fertility-related characteristics are adversely affected by the components of cigarette smoking. However, it's unclear how smoking really affects fertility in men. Depending on the well-established scientific observation that smoking enhances the amount of radical oxide organisms, which in turn causes oxidative stress (OS), smoking has an influence on the sperm variables. Men are affected by OS as it damages seminal characteristics including survival that appearance as well as inhibits sperm functioning. Still, not every research has reached identical findings. This research evaluates the influence of tobacco use via non-smoking methods on male infertility on clarifies the contentious relationship among smoking on fertility in men. Additionally, it explores the therapeutic consequences of the evidence—which includes recently discovered genomic or regulatory data—that tie smoking to male infertility.

Surface active functional groups enhanced PET non‐woven fabric for the filtering of harmful substances in smoke

AbstractHarmful components in cigarette smoke, such as nicotine, tar, and organic particulate matter, are the primary culprits behind lung diseases. While conventional filter materials based on cellulose, carbon, and molecular sieves exhibit commendable filtration capabilities, their high cost restricts their widespread applications. Based on this, the authors aim to prepare PET‐based filter materials with good adsorption properties through a simple surface functionalisation strategy. The adsorption performance of the PET‐based non‐woven fabric was enhanced by the introduction of sodium alginate (SA). The gas adsorption experiments results reveal that SA‐modified PET (SA‐PET) exhibits significantly improved filtration efficiency for nicotine, tar, and total particulate matter—increasing by 27.1%, 26.2%, and 21.3%, respectively. Moreover, SA‐PET exhibits more odour control ability than traditional activated carbon‐based filter materials. These results prove that surface‐functionalised SA‐PET has better filtration performance for harmful substances in smoke and provides a new strategy for the design of high‐performance filtration materials.

Role of circPSEN1 in carbon black and cadmium co-exposure induced autophagy-dependent ferroptosis in respiratory epithelial cells

Carbon black and cadmium (Cd) are important components of atmospheric particulate matter and cigarette smoke that are closely associated with the occurrence and development of lung diseases. Carbon black, particularly carbon black nanoparticles (CBNPs), can easily adsorbs metals and cause severe lung damage and even cell death. Therefore, this study aimed to explore the mechanisms underlying the combined toxicity of CBNPs and Cd. We found that the combined exposure to CBNPs and Cd promoted significantly greater autophagosome formation and ferroptosis (increased malonaldehyde (MDA), reactive oxygen species (ROS), and divalent iron ions (Fe2+) levels and altered ferroptosis-related proteins) compared with single exposure in both 16HBE cells (human bronchial epithelioid cells) and mouse lung tissues. The levels of ferroptosis proteins, transferrin receptor protein 1 (TFRC) and glutathione peroxidase 4 (GPX4), were restored by CBNPs-Cd exposure following treatment with a 3-MA inhibitor. Additionally, under CBNPs-Cd exposure, circPSEN1 overexpression inhibited increases in the autophagy proteins microtubule-associated protein 1 light chain 3 (LC3II/I) and sequestosome-1 (P62). Moreover, increases in TFRC and Fe2+, and decreases in GPX4were inhibited. Knockdown of circPSEN1 reversed these effects. circPSEN1 interacts with autophagy-related gene 5 (ATG5) protein and upregulates nuclear receptor coactivator 4 (NCOA4), the co-interacting protein of ATG5, thereby degrading ferritin heavy chain 1 (FTH1) and increasing Fe2+ in 16HBE cells. These results indicated that the combined exposure to CBNPs and Cd promoted the binding of circPSEN1 to ATG5, thereby increasing autophagosome synthesis and ATG5-NCOA4-FTH1 axis activation, ultimately inducing autophagy-dependent ferroptosis in 16HBE cells and mouse lung tissues. This study provides novel insights into the toxic effects of CBNPs and Cd in mixed pollutants.

Could cigarette smoke be associated with metaplastic type of meibomian gland dysfunction?

Madam, The meibomian glands are located in the tarsal plates of the eyelids. The diseases involving these glands belong to a broad classification. However, the metaplastic diseases of the meibomian gland are the focus of this letter.1 We intend to propose the possible role of cigarette smoke as an active agent in developing metaplastic type of meibomian gland dysfunction (MGD). A meibomian gland is made up of multiple acini that are arranged around a long central duct. Owing to its vigorous function of producing meibum and maintaining tear film stability, the gland requires a constant turnover and differentiation of cells. Consequently, during this intricate cascade of continuous production and differentiation of cells, even a slight deviation from normality can lead to drastic pathological effects.2 We presume that oxidative stress can produce such a pathologic deviation. One of the most common causes of increased oxidative stress in cells is exposure to cigarette smoke. It has also been experimentally established that cigarette smoke is a well-known inducer of metaplastic changes; especially known to cause squamous metaplasia in the bronchial epithelium.3 Therefore, exposure to cigarette smoke may also be a culprit when the meibomian orifice, owing to its superficial location on the eyelid, is exposed to the components of cigarette smoke. Cigarette smoke contains carbon particles and other toxic compounds that begin the cascade of inflammation and during the attempts of phagocytic elimination of these toxic compounds, inflammatory damage to DNA and proteins can occur.4 The aspect of protein damage and hyperkeratinization in response to increased oxidative stress has already been studied and implicated in the pathogenesis of MGD.2 Furthermore, it has been demonstrated that EGF (Epidermal Growth Factor) is produced in epithelial cells in response to smoke and that further increases the possibility of metaplastic as well as hyperplastic changes.5 Therefore, we suggest that there exists a strong relation between exposure to cigarette smoke and the development of metaplastic meibomian gland dysfunction. Further studies in this regard might help in prevention, as well as newer diagnostic approaches towards MGD especially in populations exposed to cigarette smoke on a regular basis.

Cadmium toxicity and autophagy: a review.

Cadmium (Cd) is an important environmental pollutant that poses a threat to human health and represents a critical component of air pollutants, food sources, and cigarette smoke. Cd is a known carcinogen and has toxic effects on the environment and various organs in humans. Heavy metals within an organism are difficult to biodegrade, and those that enter the respiratory tract are difficult to remove. Autophagy is a key mechanism for counteracting extracellular (microorganisms and foreign bodies) or intracellular (damaged organelles and proteins that cannot be degraded by the proteasome) stress and represents a self-protective mechanism for eukaryotes against heavy metal toxicity. Autophagy maintains cellular homeostasis by isolating and gathering information about foreign chemicals associated with other molecular events. However, autophagy may trigger cell death under certain pathological conditions, including cancer. Autophagy dysfunction is one of the main mechanisms underlying Cd-induced cytotoxicity. In this review, the toxic effects of Cd-induced autophagy on different human organ systems were evaluated, with a focus on hepatotoxicity, nephrotoxicity, respiratory toxicity, and neurotoxicity. This review also highlighted the classical molecular pathways of Cd-induced autophagy, including the ROS-dependent signaling pathways, endoplasmic reticulum (ER) stress pathway, Mammalian target of rapamycin (mTOR) pathway, Beclin-1 and Bcl-2 family, and recently identified molecules associated with Cd. Moreover, research directions for Cd toxicity regarding autophagic function were proposed. This review presents the latest theories to comprehensively reveal autophagy behavior in response to Cd toxicity and proposes novel potential autophagy-targeted prevention and treatment strategies for Cd toxicity and Cd-associated diseases in humans.

Expression of AHR-regulated and PD-L1-regulated microRNAs in squamous cell lung cancer

Introduction. Despite modern advances in research into the risk of development, immunological control and treatment options for lung cancer (LC), it is the leading cause of death from cancer. Tobacco smoking remains the predominant risk factor for the development of lung cancer, especially one of its aggressive subtypes, squamous cell lung cancer (SCLC). Benzo[a]pyrene, a component of cigarette smoke, promotes the activation of the aryl-hydrocarbon receptor (AhR). AhR regulates the expression of many oncogenes, including PD-L1, the positive status of which is an indication for immunotherapy, one of the main treatment strategies for SCLC. However, to improve the effectiveness of treatment of SCLC, further search for new diagnostic, prognostic and therapeutic markers is necessary. MicroRNAs (miRs), which are highly stable and present in biological fluids, can act as such markers.Objective. Search for microRNAs that could potentially serve as diagnostic markers or therapeutic targets for SCLC. For this purpose, microRNAs were selected whose promoter regions contain AhR binding sites or whose target is PD-L1.Materials and methods. A biocollection of tumor and conditionally normal lung tissue samples (n = 40) was collected at the thoracic department of the Novosibirsk Clinical Oncology Dispensary. The relative levels of selected miRNAs were examined using real-time reverse transcription-PCR (RT-PCR) technique.Results. The levels of miR-342 and miR-181a in SCLC tissues were reduced by 3 times relative to conditionally normal tissue. The expression of miR-181a and miR-155 is associated with tumor size (lower levels in tumors larger than 3 cm) and the presence of metastases in the lymph nodes (3- and 2-fold lower levels in cases with metastases). The level of miR-146a decreased by 3 times in patients with metastatic lesions of lymph nodes. A significant relationship between the levels of miR-93, miR-181a and miR-155 and the expression status of PD-L1 was also found.Conclusions. The expression profile of miR-146a, miR-93, miR-181a and miR-155 differs in SCLC patients depending on PD-L1 status and the presence or absence of lymph node metastases.

Gene architecture is a determinant of the transcriptional response to bulky DNA damages.

Bulky DNA damages block transcription and compromise genome integrity and function. The cellular response to these damages includes global transcription shutdown. Still, active transcription is necessary for transcription-coupled repair and for induction of damage-response genes. To uncover common features of a general bulky DNA damage response, and to identify response-related transcripts that are expressed despite damage, we performed a systematic RNA-seq study comparing the transcriptional response to three independent damage-inducing agents: UV, the chemotherapy cisplatin, and benzo[a]pyrene, a component of cigarette smoke. Reduction in gene expression after damage was associated with higher damage rates, longer gene length, and low GC content. We identified genes with relatively higher expression after all three damage treatments, including NR4A2, a potential novel damage-response transcription factor. Up-regulated genes exhibit higher exon content that is associated with preferential repair, which could enable rapid damage removal and transcription restoration. The attenuated response to BPDE highlights that not all bulky damages elicit the same response. These findings frame gene architecture as a major determinant of the transcriptional response that is hardwired into the human genome.

Surface plasma modification of cellulose acetate fiber filter for the adsorption of typical components in smoke components.

Surface modification of cellulose acetate filter rods with low temperature plasma was performed to explore the retention and adsorption effect of modified filter rods on typical components (CO, H2O, benzene, and formaldehyde) in cigarette smoke. The surface structure and composition of the cellulose acetate filter rods were modified by changing the plasma treatment time. The modified filter rods were characterized by N2 physical adsorption (BET), scanning electron microscopy (SEM), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), contact angle of H2O, Fourier transform infrared spectroscopy (FTIR) and in situ DRIFTS. Various functional groups were found on the surface of filter rods with the introduction of plasma modification, which exhibited strong retention performance for water vapor in cigarette smoke at room temperature and significantly enhanced adsorption for harmful substances (CO, benzene, and formaldehyde) in cigarette smoke.

Nicotine Diminishes Alpha2-Adrenergic Receptor-Dependent Protection Against Oxidative Stress in H9c2 Cardiomyocytes.

Nicotine is a major component of cigarette smoke with various detrimental cardiovascular effects, including increased oxidative stress in the heart. Agonism of α2-adrenergic receptors (ARs), such as with dexmedetomidine, has been documented to exert cardioprotective effects against oxidative stress and related apoptosis and necroptosis. α2-ARs are membrane-residing G protein-coupled receptors (GPCRs) that primarily activate Gi/o proteins. They are also subjected to GPCR-kinase (GRK)-2-dependent desensitization, which entails phosphorylation of the agonist-activated receptor by GRK2 to induce its decoupling from G proteins, thus terminating α2AR-mediated G protein signaling. In the present study, we sought to examine the effects of nicotine on α2AR signaling and effects in H9c2 cardiomyocytes exposed to H2O2 to induce oxidative cellular damage. As expected, treatment of H9c2 cardiomyocytes with H2O2 significantly decreased cell viability and increased oxidative stress, as assessed by reactive oxygen species (ROS)-associated fluorescence levels (DCF assay) and superoxide dismutase activity. Both H2O2 effects were partly rescued by α2AR activation with brimonidine in control cardiomyocytes but not in cells pretreated with nicotine for 24 hours, in which brimonidine was unable to reduce H2O2-induced cell death and oxidative stress. This was due to severe α2AR desensitization, manifested as very low Gi protein activation by brimonidine, and accompanied by GRK2 upregulation in nicotine-treated cardiomyocytes. Finally, pharmacological inhibition of adenylyl cyclase (AC) blocked H2O2-dependent oxidative damage in nicotine-pretreated H9c2 cardiomyocytes, indicating that α2AR activation protects against oxidative injury via its classic coupling to Gai-mediated AC inhibition. Nicotine can negate the cardioprotective effects of α2AR agonists against oxidative injury, which may have important implications for patients treated with this class of drugs that are chronic tobacco smokers.

CIGARETTE SMOKE-INDUCED VITAMIN A DEFICIENCY CONTRIBUTES TO EMPHYSEMA PROGRESSION IN RATS

Emphysema and lung inflammation can be accelerated by a lack of vitamin A, an important nutrient. Vitamin A levels were shown to be lower in rats that were given benzopyrene, a component of cigarette smoke. Two separate groups of rats served as experimental subjects for the length of the study. The first group, known as the experimental group, was subjected to daily, unfiltered cigarette smoke exposure for fifteen sessions, while the second group, called the control group, was exposed just to outside air. An assessment was conducted to measure the levels of retinol and vitamin A in the blood, liver, and lungs six weeks after the investigation began. Vitamin A levels were found to be lower in the group of rats that were exposed to cigarette smoke. Additionally, amounts of pulmonary vitamin A were positively correlated with emphysema severity, indicating a negative connection. Hyperplasia of the tracheal epithelium and the development of hepatic vacuoles were also noted.

Carbon black nanoparticles and cadmium co-exposure aggravates bronchial epithelial cells inflammation via autophagy-lysosome pathway

Carbon black nanoparticles (CBNPs) and cadmium (Cd) are major components of various air pollutants and cigarette smoke. Autophagy and inflammation both play critical roles in understanding the toxicity of particles and their components, as well as maintaining body homeostasis. However, the effects and mechanisms of CBNPs and Cd (CBNPs-Cd) co-exposure on the human respiratory system remain unclear. In this study, a CBNPs-Cd exposure model was constructed to explore the respiratory toxicity and combined mechanism of these chemicals on the autophagy-lysosome pathway in the context of respiratory inflammation. Co-exposure of CBNPs and Cd significantly increased the number of autophagosomes and lysosomes in human bronchial epithelial cells (16HBE) and mouse lung tissues compared to the control group, as well as the groups exposed to CBNPs and Cd alone. Autophagic markers, LC3II and P62 proteins, were up-regulated in 16HBE cells and mouse lung tissues after CBNPs-Cd co-exposure. However, treatment with Cq inhibitor (an indicator of lysosomal acid environment) resulted in a substantial decreased co-localization fluorescence of LC3 and lysosomes in the CBNPs-Cd combination group compared with the CBNPs-Cd single and control groups. No difference in LAMP1 protein expression was observed among the exposed groups. Adding 3 MA alleviated inflammatory responses, while applying the Baf-A1 inhibitor aggravated inflammation both in vitro and in vivo following CBNPs-Cd co-exposure. Factorial analysis showed no interaction between CBNPs and Cd in their effects on 16HBE cells. We demonstrated that co-exposure to CBNPs-Cd increases the synthesis of autophagosomes and regulates the acidic environment of lysosomes, thereby inhibiting autophagy-lysosome fusion and enhancing the inflammatory response in both 16HBE cells and mouse lung. These findings provide evidence for a comprehensive understanding of the interaction between CBNPs and Cd in mixed pollutants, as well as for the prevention and control of occupational exposure to these two chemicals.

Expression of transient receptor potential channels on peripheral blood leukocytes of patients with chronic obstructive pulmonary disease

It is known that transient receptor potential (TRP) channels are receptors for reactive oxygen species and components of cigarette smoke, and therefore may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD).Aim: To investigate the expression of TRPV1, TRPV4, TRPM8 and TRPA1 channels on peripheral blood leukocytes of COPD patients and healthy individuals and to establish its possible relationships with inflammatory markers and lung function parameters.Methodology and Research Methods. 23 patients with COPD of varying severity and 17 individuals without bronchial obstruction were examined. The expression of TRP channels on monocytes, lymphocytes and granulocytes was determined by indirect flow cytometry. Plasma concentrations of cytokines were measured in a multiplex assay. Lung function parameters were assessed by spirometry.Results. Monocytes from COPD patients were characterized by increased expression of TRPV1 (98.8 (97.6; 99.6)% vs. 97.8 (96.3; 98.6)%, p = 0.03) and TRPA1 (99.2 (98.7; 99.8)% vs. 95.1 (94.2; 98.4)%, p = 0.003). In addition, COPD was associated with an increased ratio of TRPV4/TRPM8 expression on monocytes (0.66 (0.51, 0.90) vs. 0.27 (0.12, 0.70), p = 0.02) and granulocytes (0.97 (0.86; 0.92) vs. 0.29 (0.06; 0.89), p = 0.003). TRPV4 expression on monocytes showed correlation with CXCL10 level (ρ = 0.55, p = 0.01), and for TRPM8 inverse relationships were found with the concentrations of IL-6 (ρ = –0.56, p = 0.02) and IL-10 (ρ = –0.55, p = 0.02). We did not find any associations between the expression of TRP channels and lung function parameters.Conclusion. Increased expression of TRPV1 and TRPA1, as well as an increased TRPV4/TRPM8 ratio on peripheral blood monocytes of COPD patients may indicate the contribution of these receptors to the proinflammatory activation of the cells and indicate possible prospects of TRP channels pharmacological modulation for the purpose of the disease therapy.

Azadirachtin Attenuates Carcinogen Benzo(a) Pyrene-Induced DNA Damage, Cell Cycle Arrest, Apoptosis, Inflammatory, Metabolic, and Oxidative Stress in HepG2 Cells.

Azadirachtin (AZD), a limonoid from the versatile, tropical neem tree (Azadirachta indica), is well known for its many medicinal, and pharmacological effects. Its effects as an anti-oxidant, anti-inflammatory, and anti-cancer agent are well known. However, not many studies have explored the effects of AZD on toxicities induced by benzo(a)pyrene (B(a)P), a toxic component of cigarette smoke known to cause DNA damage and cell cycle arrest, leading to different kinds of cancer. In the present study, using HepG2 cells, we investigated the protective effects of Azadirachtin (AZD) against B(a)P-induced oxidative/nitrosative and metabolic stress and mitochondrial dysfunction. Treatment with 25 µM B(a)P for 24 h demonstrated an increased production of reactive oxygen species (ROS), followed by increased lipid peroxidation and DNA damage presumably, due to the increased metabolic activation of B(a)P by CYP 450 1A1/1A2 enzymes. We also observed intrinsic and extrinsic apoptosis, alterations in glutathione-dependent redox homeostasis, cell cycle arrest, and inflammation after B(a)P treatment. Cells treated with 25 µM AZD for 24 h showed decreased oxidative stress and apoptosis, partial protection from DNA damage, and an improvement in mitochondrial functions and bioenergetics. The improvement in antioxidant status, anti-inflammatory potential, and alterations in cell cycle regulatory markers qualify AZD as a potential therapeutic in combination with anti-cancer drugs.