A comprehensive study of the removal of selected biologically active compounds (pharmaceuticals and pesticides) from different water types was conducted using bare TiO₂ nanoparticles and TiO₂/polyaniline (TP-50, TP-100, and TP-150) nanocomposite powders. In order to investigate how molecular structure of the substrate influences the rate of its removal, we compared degradation efficiency of the initial substrates and degree of mineralization for the active components of pharmaceuticals (propranolol, and amitriptyline) and pesticides (sulcotrione, and clomazone) in double distilled (DDW) and environmental waters. The results indicate that the efficiency of photocatalytic degradation of propranolol and amitriptyline was higher in environmental waters: rivers (Danube, Tisa, and Begej) and lakes (Moharač, and Sot) in comparison with DDW. On the contrary, degradation efficacy of sulcotrione and clomazone was lower in environmental waters. Further, of the all catalysts applied, bare TiO₂ and TP-100 were found to be most effective in the mineralization of propranolol and amitriptyline, respectively, while TP-150 appeared to be the most efficient in terms of sulcotrione and clomazone mineralization. Also, there was no significant toxicity observed after the irradiation of pharmaceuticals or pesticides solutions using appropriate catalysts on rat hepatoma (H-4-II-E), mouse neuroblastoma (Neuro-2a), human colon adenocarcinoma (HT-29), and human fetal lung (MRC-5) cell lines. Subsequently, detection and identification of the formed intermediates in the case of sulcotrione photocatalytic degradation using bare TiO₂ and TP-150 showed slightly different pathways of degradation. Furthermore, tentative pathways of sulcotrione photocatalytic degradation were proposed and discussed.

Lung cancer is the most common cancer in China and second worldwide, of which the incidence of lung adenocarcinoma is rising. As an independent factor, air pollution has drawn the attention of the public. An increasing body of studies has focused on the effect of PM₂.₅ on lung adenocarcinoma; however, the mechanism remains unclear. We collected the PM₂.₅ in two megacities, Beijing (BPM) and Shijiazhuang (SPM), located in the capital of China, and compared the different components and sources of PM₂.₅ in the two cities. Vehicle emissions are the primary sources of BPM, whereas SPM is industrial emissions. We found that chronic exposure to PM₂.₅ promotes the tumorigenesis and metastasis of lung adenocarcinoma in patient-derived xenograft (PDX) models, as well as the migration and invasion of lung adenocarcinoma cell lines. SPM has more severe effects in vivo and in vitro. The underlying mechanisms are related to the stem cell properties of cancer cells, the epithelial-mesenchymal transition (EMT) process, and the corresponding miRNAs. It is hopeful to provide a theoretical basis for improving air pollution in China, especially in the capital area, and is of the significance of long-term survival of lung cancer patients.

PM2.5 pollution is an important and urgent problem in China that can increase mortality and hospital admissions. Traffic-originated PM2.5 organic component (tPo) mainly contains polycyclic aromatic hydrocarbons (PAHs). Research has shown that PAHs can promote invasion, metastasis, and cancer stem cell properties in lung adenocarcinoma cells, but the exact toxicological mechanism is unknown. In the present study, we investigated the effect of lncRNAs on the progression of lung adenocarcinoma induced by tPo and the underlying mechanisms mediated by lncRNA-signaling pathway interactions. We found that chronic tPo treatment upregulated the expression of loc107985872, which further promoted cell invasion and migration, EMT and cancer stem cell properties via notch1 pathway in lung adenocarcinoma cells. Meanwhile, activation of the notch1 signaling pathway through loc107985872 might be associated with abnormally high expression of its upstream proteins, such as ADAM17, PSEN1 and DLL1. Moreover, tPo exposure induced EMT and the acquisition of cancer stem cell-like properties via the notch1 signaling pathway in vivo. In summary, loc107985872 upregulated by tPo promoted lung adenocarcinoma progression via the notch1 signaling pathway.

In this work we have investigated in details the process of degradation of the 4-amino-6-chlorobenzene-1,3-disulfonamide (ABSA), stable hydrolysis product of frequently used pharmaceutical hydrochlorothiazide (HCTZ), as one of the most ubiquitous contaminants in the sewage water. The study encompassed investigation of degradation by hydrolysis, photolysis, and photocatalysis employing commercially available TiO₂ Degussa P25 catalyst. The process of direct photolysis and photocatalytic degradation were investigated under different type of lights. Detailed insights into the reactive properties of HCTZ and ABSA have been obtained by density functional theory calculations and molecular dynamics simulations. Specifically, preference of HCTZ towards hydrolysis was confirmed experimentally and explained using computational study. Results obtained in this study indicate very limited efficiency of hydrolytic and photolytic degradation in the case of ABSA, while photocatalytic degradation demonstrated great potential. Namely, after 240 min of photocatalytic degradation, 65% of ABSA was mineralizated in water/TiO₂ suspension under SSI, while the nitrogen was predominantly present as NH4+. Reaction intermediates were studied and a number of them were detected using LC-ESI-MS/MS. This study also involves toxicity assessment of HCTZ, ABSA, and their mixtures formed during the degradation processes towards mammalian cell lines (rat hepatoma, H-4-II-E, human colon adenocarcinoma, HT-29, and human fetal lung, MRC-5). Toxicity assessments showed that intermediates formed during the process of photocatalysis exerted only mild cell growth effects in selected cell lines, while direct photolysis did not affect cell growth.

Coronavirus disease 2019 (COVID-19) continues as a global pandemic. Patients with lung cancer infected with COVID-19 may develop severe disease or die. Treating such patients severely burdens overwhelmed healthcare systems. Here, we identified potential pathological mechanisms shared between patients with COVID-19 and lung adenocarcinoma (LUAD). Co-expressed, differentially expressed genes (DEGs) in patients with COVID-19 and LUAD were identified and used to construct a protein–protein interaction (PPI) network and to perform enrichment analysis. We used the NetworkAnalyst platform to establish a co-regulatory of the co-expressed DEGs, and we used Spearman’s correlation to evaluate the significance of associations of hub genes with immune infiltration and immune checkpoints. Analysis of three datasets identified 112 shared DEGs, which were used to construct a protein-PPI network. Subsequent enrichment analysis revealed co-expressed genes related to biological process (BP), molecular function (MF), and cellular component (CC) as well as to pathways, specific organs, cells, and diseases. Ten co-expressed hub genes were employed to construct a gene-miRNA, transcription factor (TF)-gene, and TF-miRNA network. Hub genes were significantly associated with immune infiltration and immune checkpoints. Finally, methylation level of hub genes in LUAD was obtained via UALCAN database. The present multi-dimensional study reveals commonality in specific gene expression by patients with COVID-19 and LUAD. These findings provide insights into developing strategies for optimising the management and treatment of patients with LUAD with COVID-19.

Among all the pharmaceutical drugs that contaminate the environment, antibiotics occupy an important place due to their high consumption rates in both veterinary and human medicine. The present study examined the ability of Pseudomonas putida to grow on the antibiotic wastewater, currently expanding in Tunisia, containing amoxicillin and cefadroxil. P. putida was very efficient to grow quickly in pharmaceutical wastewater (PW) and in reducing the total dissolved solids to 80.1 %. Cytotoxicity of PW, before and after biodegradation with P. putida mt-2, was evaluated in vitro, using the MTT assay, against four human tumor cell lines such as A549 (lung cell carcinoma), HCT15 (colon cell carcinoma), MCF7 (breast adenocarcinoma), and U373 (glioma cell carcinoma). The PW reduced all human cell lines viability in a dose-dependent manner. This activity was very remarkable against U373 cell line. For this reason, we have tested the genotoxicity of PW using comet assay for quantification of DNA fragmentation. In fact, PW has statistically significant (p < 0.001) influence on DNA. Indeed, the percentage of genotoxicity was 66.87 and 87.5 %, after 24 and 48 h of treatment, respectively. However, cytotoxicity and genotoxicity decreased strongly when tested the PW obtained after incubation with P. putida mt-2. Our results indicate that P. putida is a promising and improved alternative to treating industrial-scale effluent compared to current chemical treatment procedures used by the industrials.

Capsaicin (CPS, 8-methyl-N-vanillyl-trans-6-nonenamide), a pungent alkaloid from chili peppers, has contradictory effects in both experimental and human carcinogenesis. Thus, we evaluated the modifying effects of chronic CPS during the promotion and progression stages of rat colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH). Male Wistar rats were given four subcutaneous injections of DMH (40 mg/body weight (b.w.)) twice a week, for 2 weeks. After DMH-induced tumor initiation, the animals were treated with CPS at 5 or 50 mg/kg b.w. by gavage for 24 weeks (three times a week). High-dose CPS reduced both cell proliferation in adjacent “normal-appearing” colonic crypts and the total number of preneoplastic aberrant crypt foci (ACF) but did not change the number of dysplastic ACF or ACF multiplicity. Although the proportion of adenomas was increased, and tubular adenocarcinomas decreased in high-dose CPS, both CPS interventions exerted no effects on total tumor incidence, volume, multiplicity, cell proliferation (Ki-67), and apoptosis (caspase-3). In accordance, high-dose CPS treatment had discrete effects on gene expression in colon tumors, as only 3/94 (3.19%) genes were significantly modified (downregulation of Cebpd and Fasl, and upregulation of Jag1). The findings of the present study show that CPS does not impact on the promotion/progression stages of rat colon carcinogenesis. Therefore, CPS at a high-dose intervention showed to be a safe food ingredient.

Cleome amblyocarpa Barr. and Murb is a medicinal plant widespread in North Africa and widely used in Tunisia to treat diabetes and colic. The non-volatile (polyphenols, flavonoids, tannins, and flavonols) and volatile compounds (GC-MS) of C. amblyocarpa leaves and stems have been studied. The antioxidant, antimicrobial, analgesic, and cytotoxic activities of hydroalcoholic extracts of C. amblyocarpa leaves and stems were also investigated. The major volatile components were β-caryophyllene (46.9%), eugenol (25.6%), ethyl 3-methylpentanoate (16.2%), 7-epi-silphiperfol-5-ene (11.0%), and α-copaene (7.0%). The antioxidant activity has been evaluated using various in vitro assays, such as DPPH free radical scavenging activity, iron-chelating capability, and ability to inhibit lipid peroxidation (TBARS). The antibacterial and antifungal effectiveness of leaves and stems parts of Cleome amblyocarpa were investigated by means of the disc diffusion and microdilution techniques. The in vitro cytotoxicity of the hydroalcoholic extract of C. amblyocarpa on A549 and H1299 lung adenocarcinoma cells was determined using the crystal violet assay. The acute toxicity of the extracts on Swiss albino mice at the doses of 3000, 1500, and 500 mg/kg body weight was evaluated. The analgesic effect of leaves and stems extract was also determined by means of the acetic acid induced writhing test. The results indicated that the leaves have higher phenols, and flavonoids contents and potential antioxidant, antimicrobial, and anticancer activities in comparison to stem. In addition, the aerial part of C. amblyocarpa did not cause signs of toxicity or death in animals at doses up to 3000 mg/kg and have a significant analgesic activity.

Arsenic in fine air particulate matter (PM₂.₅) has been identified as an important factor responsible for the morbidity of lung cancer, which has increased sharply in many regions of China. Some reports in China have shown that arsenic in the air exceeds the ambient air quality standard value, while long-term airborne arsenic concentrations in central China and human exposure via inhalation of PM–bound arsenic (inhalable airborne PM) have not been well characterized. In this study, 579 outdoor air PM₂.₅ samples from Wuhan, a typical city in central China, were collected from 2015 to 2017, and arsenic was measured by inductively coupled plasma-mass spectrometry. Personal exposure to PM-bound arsenic via inhalation and urinary arsenic concentration were also measured. The concentrations of arsenic in PM₂.₅ were in the range of 0.42–61.6 ng/m³ (mean 8.48 ng/m³). The average concentration of arsenic in 2015 (10.7 ng/m³) was higher than that in 2016 (6.81 ng/m³) and 2017 (8.18 ng/m³), exceeded the standard value. The arsenic concentrations in spring and winter were higher than those in summer and autumn. No significant differences (p > 0.05) were found among different sites. The daily intake of arsenic inhalation based on PM₁₀ samples collected by personal samplers (median, 10.8 ng/m³) was estimated. Urban residents inhaled higher levels of PM-bound arsenic than rural residents. Daily intake of arsenic via inhalation accounted for a negligible part (< 1%) of the total daily intake of arsenic (calculated based on excreted urinary arsenic); however, potential associations between the adverse effects (e.g., lung adenocarcinoma) and inhaled PM-bound arsenic require more attention, particularly for those who experience in long-term exposure. This study is the first report of a 3-year temporal trend of airborne PM₂.₅-bound arsenic in central China.

Co-exposure to carboxylic acid functionalized multi-walled carbon nanotubes (F-MWCNTs) and polycyclic aromatic hydrocarbons (PAHs) such as benzo a pyrene (BaP) in ambient air have been reported. Adsorption of BaP to F-MWCNTs can influence combined toxicity. Studying individual toxicity of F-MWCNTs and BaP might give unrealistic data. Limited information is available on the combined toxicity of F-MWCNTs and BaP in human cells. The objective of the present work is to evaluate the toxicity of F-MWCNTs and BaP individually and combined in human lung adenocarcinoma (A549 cells). The in vitro toxicity is evaluated through cell viability, the production of reactive oxygen species (ROS), apoptosis, and the production of 8-OHdG assays. Adsorption of BaP to F-MWCNTs was confirmed using a spectrophotometer. The results indicated that the F-MWCNTs and BaP reduce cell viability individually and produce ROS, apoptosis, and 8-OHdG in exposed cells. Stress oxidative is found to be a mechanism of cytotoxicity for both F-MWCNTs and BaP. Combined exposure to F-MWCNTs and BaP decreases cytotoxicity compared to individual exposure, but the difference is not statistically significant in all toxicity assays; hence, the two-factorial analysis indicated an additive toxic interaction. Adsorption of BaP to F-MWCNTs could mitigate the bioavailability and toxicity of BaP in biological systems. Considering the mixture toxicity of MWCNTs and BaP is required for risk assessment of ambient air contaminants.