Chemoprotective effect of arbutin on azoxymethane-induced aberrant crypt foci in rat colon via modulation of PCNA/Bax protein.

Arbutin is utilized in traditional remedies to cure numerous syndromes because of its anti-microbial, antioxidant, and anti-inflammatory properties. This study aimed to evaluate chemopreventive effects of arbutin on azoxymethane (AOM)-induced colon aberrant crypt foci (ACF) in rats. Five groups of rats were used: normal control group (rats injected hypodermically with sterile phosphate-buffered saline once per week for two weeks) and groups 2-5, which were subcutaneously inoculated with 15 mg/kg AOM once a week for two weeks. AOM control and 5-fluorouracil (5-FU) control groups were fed 10% Tween orally daily for 8 weeks using a feeding tube. The treated groups were fed 30 and 60 mg/kg arbutin every day for 2 months. ACF from the AOM control group had aberrant nuclei in addition to multilayered cells and an absence of goblet cells. The negative control group displayed spherical cells and nuclei in basal positions. Histological examination revealed a reduced number of AFC cells from colon tissues of the 5-FU reference group. Arbutin-fed animals showed down-regulation of proliferating cell nuclear antigen (PCNA) and up-regulation of Bax protein compared to AOM control. Rats fed with arbutin displayed a significant increase of superoxide dismutase (SOD) and catalase (CAT) activities in colon tissue homogenates compared to the AOM control group. In conclusion, arbutin showed therapeutic effects against colorectal cancer, explained by its ability to significantly decrease ACF, down-regulate PCNA protein, and up-regulate Bax protein. In addition, arbutin significantly increased SOD and CAT, and decreased malondialdehyde (MDA) levels, which might be due to its anti-proliferative and antioxidant properties.

A rapid and improved method for the determination of ethyl carbamate in foodstuffs of different matrices.

This work deals with the rapid and simple determination of the probable carcinogen ethyl carbamate (EC), which is naturally present in fermented food products. An undemanding, robust, and rapid pre-column derivatization utilizing a 9-xanthydrol reagent has been developed. The resulting derivative was subsequently analysed by reversed-phase high-performance liquid chromatography coupled with fluorescence detection. As a result of the thorough optimisation of the chromatographic conditions, the run was completed in just 5 minutes, considerably speeding up the usual time of EC separation (30-60 min). Thanks to the fast separation, satisfactory yields (around 90%), negligible matrix effects, no interfering peaks, very low detection limit, and simple sample pre-treatment (for the very first time, the derivatization was performed in the presence of light and without any extraction step), the proposed method represents a significant improvement of the EC determination protocol used so far. After method validation, a total of fifty food samples were subjected to analysis without any additional sample pre-treatment despite their diverse matrix. Due to its robustness, simplicity, and low time, cost, and manual demands, this method is suitable for rapid screening of EC in both final food products and during their production.

Carcinogenicity of asbestos-free talc and talcum powder: A systematic review of the epidemiological evidence after the 2006 monograph of the International Agency for Research on Cancer.

BACKGROUND: in 2006, the International Agency for Research on Cancer (IARC) concluded that the evidence of carcinogenicity for asbestos-free talc was inadequate (group 3), whereas perineal use of talcum powder was classified as possibly carcinogenic (group 2B). OBJECTIVES: to assess whether later studies provide more solid information on the carcinogenic risk from asbestos-free talc and talcum powder and a better characterization of exposure. DESIGN: systematic review. METHODS: cohort studies of talc miners and millers exposed to asbestos-free talc, as well as cohort and case-control studies reporting cancer risk in talc powder consumers published from 2006 onwards were identified through PubMed and reference lists. Pooled analyses were included, but not reviews and meta-analyses. In the case of repeatedly reported studies, the article with the longest follow-up or the largest number of observed cases was selected for data abstraction. Notice was taken of studies which were both reported individually and included in pooled analyses. RESULTS: publications meeting inclusion criteria were: 2 cohort studies on talc miners and millers, 10 cohort studies on talcum powder users (4 of which estimated ovarian cancer risk), and 14 case-control studies (13 on ovarian and 1 on endometrial cancer) on the risk from talcum powder use. No excess cancer mortality has been reported among asbestos-free talc miners and millers. Case-control studies consistently led to estimates of ovarian cancer excesses associated with the use of perineal talcum powder (odds ratios up to 1.5). Most studies quantifying exposure also provided evidence of a dose-response relationship. Individual cohort studies estimated hazard ratios (HR) just above 1. In an analysis of pooled cohorts for a total of 3,112 cases, the HR for women with patent reproductive tract was 1.13 (95%CI 1.01-1.26) with a correlation between HR and frequency of use (p for trend 0.03). In all cohort studies, the perineal use of talcum powder was measured only once in the early phases of follow-up, thus producing an inaccurate measure of cumulative exposure. Results of epidemiological studies regarding cancer risk in other organs are limited and inconsistent. CONCLUSIONS: epidemiological studies updated or published after IARC 2006 evaluation indicate that: no increase in cancer risk is apparent among miners and millers of asbestos-free talc; risk for ovarian cancer increases following the perineal use of commercial talcum powder. A correlation between indicators of quantity of use and cancer risk is suggested by a number of studies. The composition of talcum powders considered in such studies is not known.

Talc and human cancer: a systematic review of the experimental animal and mechanistic evidence.

The potential carcinogenicity of talc has been evaluated in many studies in humans and experimental animals published in the scientific literature over the last several decades, with a number of these studies reporting no associations between talc exposure and any type of cancer. In order to fully understand the current state of the science regarding the potential for talc to induce human cancers, we conducted a comprehensive and systematic review of the available experimental animal and mechanistic evidence (in conjunction with a systematic review of the epidemiology evidence in a companion analysis) to evaluate whether it supports talc as being carcinogenic to humans. We considered study quality and its impact on the interpretation of results and evaluated all types of cancer and all exposure routes. We also evaluated the evidence on the potential for talc to migrate in the body to potential tumor sites. We identified seven experimental animal carcinogenicity studies and 11 mechanistic studies of talc to systematically review. We found that several of the experimental animal carcinogenicity studies of talc have limitations that preclude their sensitivity to detect increases in tumor incidence. Regardless, the studies cover multiple exposure routes, species, and exposure durations, and none indicate that talc is a carcinogen in experimental animals except in rats under conditions of extremely high exposure that likely resulted in lung particle overload, a nonspecific effect of high exposures to poorly soluble particles, and not from any carcinogenic properties of talc. Lung particle overload leading to lung tumor formation has only been observed in rats and not in any other species, including humans. The mechanistic studies indicate that talc is not genotoxic or mutagenic, but can induce some effects that could be events on a possible pathway to carcinogenicity, mainly at high exposures or in in vitro studies with exposures of unclear relevance in vivo, but these effects are not consistent across studies and cell types. This systematic review of the experimental animal carcinogenicity and mechanistic evidence for talc indicates that an association between talc exposure and cancer is not expected in humans. Talc carcinogenicity is not plausible in any species except rats, and only when the exposure conditions are high enough to induce lung particle overload, which is not relevant to human exposures.

Investigating the carcinogenic and non-carcinogenic health hazards of heavy metal ions in Spinacia oleracea grown in agricultural soil treated with biochar and humic acid.

This study addressed the bioaccumulation and human health risk among the consumption of Spinacia oleracea grown in agricultural soil treated with humic acid (189-2310 ppm) and biochars (0.00-5.10%.wt). The biochars came from two local feedstocks of rice-husk (RH) and sugar-beet-pulp (SBP) pyrolyzed at temperatures 300 and 600 °C. Total concentrations of Cu, Cd, and Ni found in both the soil and biomass/biochar exceeded global safety thresholds. The bioaccumulation levels of HMs in spinach leaves varied, with Fe reaching the highest concentration at 765.27 mg kg-1 and Cd having the lowest concentration at 3.31 mg kg-1. Overall, the concentrations of Zn, Cd, Pb, and Ni in spinach leaves exceeded the safety threshold limits, so that its consumption is not recommended. The assessment of hazard quotient (HI) for the HMs indicated potential health hazards for humans (HI > 1) from consuming the edible parts of spinach. The biochar application rates of 4.35%wt and 0.00%.wt resulted in the highest (3.69) and lowest (3.15) HI values, respectively. The cumulative carcinogenic risk (TCR) ranged from 0.0085 to 0.0119, exceeding the cancer risk threshold. Introducing 5.10%wt biomass/biochar resulted in a 36% rise in TCR compared to the control. The utilization of humic acid alongside HMs-polluted biochars results in elevated levels of HMs bioaccumulation exceeding the allowable thresholds in crops (with a maximum increase of 49% at 2000 ppm humic acid in comparison to 189 ppm). Consequently, this raised the HI by 46% and the TCR by 22%. This study demonstrated that the utilization of HMs-polluted biochars could potentially pose supplementary health hazards. Moreover, it is evident that the utilization of HMs-polluted biochars in treating metal-contaminated soil does not effectively stabilize or reduce pollution.

Tumor Promoters and Opportunities for Molecular Cancer Prevention.

Environmental carcinogens increase cancer incidence via both mutagenic and non-mutagenic mechanisms. There are over 500 known or suspected carcinogens classified by the International Agency for Research on Cancer. Sequencing of both cancerous and histologically non-cancerous tissue has been instrumental in improving our understanding of how environmental carcinogens cause cancer. Understanding how and defining which environmental or lifestyle exposures drive cancer will support cancer prevention. Recent research is revisiting the mechanisms of early tumorigenesis, paving the way for an era of molecular cancer prevention. Significance: Recent data have improved our understanding of how carcinogens cause cancer, which may reveal novel opportunities for molecular cancer prevention.

Melatonin Inhibits Chemical Carcinogen-mediated Malignant Transformation of Urothelial Cells: In Vitro Evidence.

BACKGROUND/AIM: The efficacy of melatonin and its biological significance in human bladder cancer remain poorly understood. This study aimed to investigate the functional role of melatonin in urothelial carcinogenesis. MATERIALS AND METHODS: In human normal urothelial SVHUC cells with exposure to the chemical carcinogen 3-methylcholanthrene, we assessed the effects of melatonin on the neoplastic/malignant transformation. RESULTS: In the in vitro system with carcinogen challenge, melatonin significantly prevented the neoplastic transformation of SV-HUC-1 cells. In addition, melatonin treatment resulted in increased expression of SIRT1, Rb1, and E-cadherin, and decreased expression of N-cadherin and FGFR3 in SV-HUC-1 cells. Furthermore, publicly available datasets from GSE3167 revealed that the expression of melatonin receptor 1 and melatonin receptor 2 was significantly down-regulated in bladder urothelial carcinoma tissues, compared with adjacent normal urothelial tissues. CONCLUSION: These findings indicate that melatonin serves as a suppressor for urothelial tumorigenesis. To the best of our knowledge, this is the first preclinical study demonstrating the impact of melatonin on the development of urothelial cancer.

Understanding the heterocyclic aromatic amines: An overview and recent findings.

Heterocyclic aromatic amines (HAAs) constitute a group of highly toxic organic compounds strongly associated with the onset of various types of cancer. This paper aims to serve as a valuable resource for food scientists working towards a better understanding of these compounds including formation, minimizing strategies, analysis, and toxicity as well as addressing existing gaps in the literature. Despite extensive research conducted on these compounds since their discovery, several aspects remain inadequately understood, necessitating further investigation. These include their formation pathways, toxic mechanisms, effective mitigation strategies, and specific health effects on humans. Nonetheless, recent research has yielded promising results, contributing significantly to our understanding of HAAs by proposing new potential formation pathways and innovative strategies for their reduction.

Carcinogenic formaldehyde in U.S. residential buildings: Mass inventories, human health impacts, and associated healthcare costs.

Formaldehyde, a human carcinogen, is formulated into building materials in the U.S. and worldwide. We used literature information and mass balances to obtain order-of-magnitude estimates of formaldehyde inventories in U.S. residential buildings as well as associated exposures, excess morbidity, and healthcare costs along with other economic ramifications. Use of formaldehyde in building materials dates to the 1940s and continues today unabated, despite its international classification in 2004 as a human carcinogen. Global production of formaldehyde was about 32 million metric tons (MMT) in 2006. In the U.S., 5.7 ± 0.05 to 7.4 ± 0.125 MMT of formaldehyde were produced annually from 2006 to 2022, with 65 ± 5 % of this mass (3.7 ± 0.03 to 4.8 ± 0.08 MMT) entering building materials. For a typical U.S. residential building constructed in 2022, we determined an average total mass of formaldehyde containing chemicals of 48.2 ± 10.1 kg, equivalent to 207 ± 40 g of neat formaldehyde per housing unit. When extrapolated to the entire U.S. housing stock, this equates to 29,800 ± 5760 metric tons of neat formaldehyde. If the health threshold in indoor air of 0.1 mg/m3 is never surpassed in a residential building, safe venting of embedded formaldehyde would take years. Using reported indoor air exceedances, up to 645 ± 33 excess cancer cases may occur U.S. nationwide annually generating up to US$65 M in cancer treatment costs alone, not counting ~16,000 ± 1000 disability adjusted life-years. Other documents showed health effects of formaldehyde exist, but could not be quantified reliably, including sick building syndrome outcomes such as headache, asthma, and various respiratory illnesses. Opportunities to improve indoor air exposure assessments are discussed with special emphasis on monitoring of building wastewater. Safer alternatives to formaldehyde in building products exist and are recommended for future use.

Evaluation of polypropylene microporous membranes as extraction devices for determination of carcinogenic aromatic amines in smoker urine by GC-MS/MS.

Exposure to tobacco smoke is highly correlated to the incidence of different types of cancer due to various carcinogenic compounds present in such smoke. Aromatic amines, such as 1-naphthylamine (1-NA) and 2-naphthylamine (2-NA), are produced in tobacco burning and are linked to bladder cancer. Miniaturized solid phase extraction techniques, such as microporous membrane solid phase extraction (MMSPE), have shown potential for the extraction of aromatic compounds. In this study, a bioanalytical method for the determination of 1-NA and 2-NA in human urine was developed using polypropylene microporous membranes as a sorptive phase for MMSPE. Urine samples were hydrolyzed with HCl for 1 h at 80 °C, after which pH was adjusted to 10. Ultrasound-assisted MMSPE procedure was optimized by factorial design as follows. To each sample, 750 µL of methanol was added, and ultrasound-assisted MMSPE was conducted for 1 h with four devices containing seven 2 mm polypropylene membrane segments. After extraction, the segments were transferred to 400 µL of hexane, and desorption was conducted for 30 min. Extracts were submitted to a simple and fast microwave-assisted derivatization procedure, by the addition of 10 µL of PFPA and heating at 480 W for 3 min, followed by clean-up with phosphate buffer pH 8.0 and GC-MS/MS analysis. Adequate linearity was obtained for both analytes in a range from 25 to 500 µg L-1, while the multiple reaction monitoring approach provided satisfactory selectivity and specificity. Intra-day (n = 6) and inter-day (n = 5) precision and accuracy were satisfactory, below 15 % and between 85 and 115 %, respectively. Recovery rates found were 91.9 and 58.4 % for 1-NA and 2-NA, respectively, with adequate precision. 1-NA was found in first-hand smokers' urine samples in a concentration range from 20.98 to 89.09 µg in 24 h, while it could be detected in second-hand smoker's urine samples, and 2-NA detected in all first and second-hand smokers' urine samples. The proposed method expands the applicability of low cost MMSPE devices to aromatic amines and biological fluids.

A systematic review of the epidemiology evidence on talc and cancer.

Over the past several decades, there have been many epidemiology studies on talc and cancer published in the scientific literature, and several reviews and meta-analyses of talc and respiratory, female reproductive, and stomach cancers, specifically. To help provide a resource for the evaluation of talc as a potential human carcinogen, we applied a consistent set of examination methods and criteria for all epidemiology studies that examined the association between talc exposure (by various routes) and cancers (of various types). We identified 30 cohort, 35 case-control, and 12 pooled studies that evaluated occupational, medicinal, and personal-care product talc exposure and cancers of the respiratory system, the female reproductive tract, the gastrointestinal tract, the urinary system, the lymphohematopoietic system, the prostate, male genital organs, and the central nervous system, as well as skin, eye, bone, connective tissue, peritoneal, and breast cancers. We tabulated study characteristics, quality, and results in a systematic manner, and evaluated all cancer types for which studies of at least three unique populations were available in a narrative review. We focused on study quality aspects most likely to impact the interpretation of results. We found that only one study, of medicinal talc use, evaluated direct exposure measurements for any individuals, though some used semi-quantitative exposure metrics, and few studies adequately assessed potential confounders. The only consistent associations were with ovarian cancer in case-control studies and these associations were likely impacted by recall and potentially other biases. This systematic review indicates that epidemiology studies do not support a causal association between occupational, medicinal, or personal talc exposure and any cancer in humans.

Involvement of multiple epigenetic mechanisms by altered DNA methylation from the early stage of renal carcinogenesis before proliferative lesion formation upon repeated administration of ochratoxin A.

Ochratoxin A (OTA) is a rat renal carcinogen that induces karyomegaly and micronuclei in proximal tubular epithelial cells (PTECs). We previously performed comprehensive gene profiling of alterations in promoter-region methylation and gene expression in PTECs of rats treated with OTA for 13 weeks. The OTA-specific gene profile was obtained by excluding genes showing expression changes similar to those upon treatment with 3-chloro-1,2-propanediol, a renal carcinogen not inducing karyomegaly. In this study, we validated the candidate genes using methylated DNA enrichment PCR and real-time RT-PCR, and identified Gen1, Anxa3, Cdkn1a, and Osm as genes showing OTA-specific epigenetic changes. These genes and related molecules were subjected to gene expression and immunohistochemical analyses in the PTECs of rats treated with OTA, other renal carcinogens, or non-carcinogenic renal toxicants for 4 or 13 weeks. Cdkn1a upregulation and increase of p21WAF1/CIP1+ karyomegalic PTECs were observed with OTA, matching the findings associated with micronucleus-inducing carcinogens. This suggested that the increase of p21WAF1/CIP1+ karyomegalic PTECs is linked to micronucleus formation, which in turn accelerates chromosomal instability. The upregulation of Cdkn1a-related genes with OTA suggests the acquisition of a senescence-associated secretory phenotype, which promotes the establishment of a carcinogenic environment. Meanwhile, OTA specifically caused a decrease of GEN1+ PTECs reflecting Gen1 downregulation and an increase of ANXA3+ PTECs reflecting Anxa3 upregulation, as well as Osm upregulation. OTA may efficiently disrupt pathways for repairing the DNA double-strand breaks that it itself causes, via Gen1 downregulation, and enhance cell proliferation through the upregulation of Anxa3 and Osm. This may exacerbate the chromosomal instability from the early stage of OTA-induced renal carcinogenesis before proliferative lesions form. OTA may cause renal carcinogenesis involving multiple epigenetic mechanisms.

Polycyclic aromatic hydrocarbons in indoor mosques dust in Saudi Arabia: Levels, source apportionment, human health and carcinogenic risk assessment for congregators.

Mosques are important places for Muslims where they perform their prayers. The congregators are exposed to hazardous pollutants such as polycyclic aromatic hydrocarbons (PAHs) associated with dust. However, studies on PAHs exposure in religious places are scarce. Air-condition filter (ACF) dust can correspond to air quality to a certain extent, since dust particles derived from indoor and outdoor places stick to it. Therefore, the present study aimed to evaluate the 16 EPA PAHs in ACF dust from mosques to determine their levels, profiles, sources and risks. Average Σ16 PAHs concentrations were 1039, 1527, 2284 and 5208 ng/g in AC filter dust from mosques in residential (RM), suburban (SM), urban (UM) and car repair workshop (CRWM), respectively, and the differences were statistically significant (p < 0.001). Based on the molecular diagnostic PAH ratios, PAHs in mosques dust is emitted from local incomplete fuel combustion, as well as complete fossil fuels combustion sources (pyrogenic), petroleum spills, crude and fuel oil, traffic emissions, and other possible sources of industrial emissions in different functional areas. The incremental lifetime cancer risks (ILCRs) values for children and adults across the different types of mosques follow the order: CRWM > UM > SM > RM. ILCRs values for both children and adults were found in order: dermal contact > ingestion > inhalation. The cancer risk levels via ingestion for children were relatively higher than the adults. The values of cancer risk for children and adults via dermal contact and ingestion (except in RM) were categorized in the 'potentially high risk' category (> 10-4). The mean values of total cancer risks (CR) for children (5.74 × 10-3) and adults (5.07 × 10-3) in mosques also exceeded the accepted threat value (>10-4). Finally, it is recommended that regular and frequent monitoring of PAHs should be carried out in mosques to improve the quality and maintain the health of congregators around the globe.

Hazard identification of endocrine-disrupting carcinogens (EDCs) in relation to cancers in humans.

Endocrine disrupting chemicals or carcinogens have been known for decades for their endocrine signal disruption. Endocrine disrupting chemicals are a serious concern and they have been included in the top priority toxicants and persistent organic pollutants. Therefore, researchers have been working for a long time to understand their mechanisms of interaction in different human organs. Several reports are available about the carcinogen potential of these chemicals. The presented review is an endeavor to understand the hazard identification associated with endocrine disrupting carcinogens in relation to the human body. The paper discusses the major endocrine disrupting carcinogens and their potency for carcinogenesis. It discusses human exposure, route of entry, carcinogenicity and mechanisms. In addition, the paper discusses the research gaps and bottlenecks associated with the research. Moreover, it discusses the limitations associated with the analytical techniques for detection of endocrine disrupting carcinogens.

The carcinogenic PAHs in breads, amount, analytical method and mitigation strategy, a systematic review study.

Bread is one of the most consumed foods all over the world. Several contaminants are identified in bread. Polycyclic aromatic hydrocarbons (PAHs) is one of these contaminants. This systematic study evaluates the amount of four carcinogenic PAHs (PAH4) in various types of breads. To conduct this study, a comprehensive search was carried out using keywords of polycyclic aromatic hydrocarbons, PAHs, PAH4, and bread, with no time limitations. 17 articles were selected and fully evaluated. The observed range of PAH4 concentrations in bread varied from non-detected (ND) to 20.66 µg/kg. In the sample preparation process for analysis, an ultrasonic bath was predominantly utilized. Most chromatographic methods are able to measure PAHs in food, but the GC-MS method has been used more. To mitigate PAH levels in bread, it is suggested to incorporate antioxidants during the bread-making process. Furthermore, the type of bread, the type of fuel used to bake the bread, the temperature and the cooking time were some of the factors affecting the amount of PAH. Restricting these factors could significantly reduce PAH content. Regarding the risk assessment conducted in the manuscript, it was determined that industrial breads are usually considered safe. However, some traditional breads may pose risks in terms of their potential PAH content.

The Known and Unknown: Investigating the Carcinogenic Potential of Plastic Additives.

Microplastics are routinely ingested and inhaled by humans and other organisms. Despite the frequency of plastic exposure, little is known about its health consequences. Of particular concern are plastic additives─chemical compounds that are intentionally or unintentionally added to plastics to improve functionality or as residual components of plastic production. Additives are often loosely bound to the plastic polymer and may be released during plastic exposures. To better understand the health effects of plastic additives, we performed a comprehensive literature search to compile a list of 2,712 known plastic additives. Then, we performed an integrated toxicogenomic analysis of these additives, utilizing cancer classifications and carcinogenic expression pathways as a primary focus. Screening these substances across two chemical databases revealed two key observations: (1) over 150 plastic additives have known carcinogenicity and (2) the majority (∼90%) of plastic additives lack data on carcinogenic end points. Analyses of additive usage patterns pinpointed specific polymers, functions, and products in which carcinogenic additives reside. Based on published chemical-gene interactions, both carcinogenic additives and additives with unknown carcinogenicity impacted similar biological pathways. The predominant pathways involved DNA damage, apoptosis, the immune response, viral diseases, and cancer. This study underscores the urgent need for a systematic and comprehensive carcinogenicity assessment of plastic additives and regulatory responses to mitigate the potential health risks of plastic exposure.

Morphological Changes and Inflammation Preceded the Pathogenesis of 1,2-Dimethylhydrazine-Induced Colorectal Cancer.

OBJECTIVE: This study examined the morphological changes in the colonic mucosa and the presence of inflammation in rats induced with 1,2-dimethylhydrazine (DMH) 30 mg/kg BW over 9, 11, and 13 weeks without a latency period. METHODS: Hematoxylin and eosin staining was performed to assess the morphology and characteristic alteration of the epitheliocytes in the colon. Immunohistochemistry was employed to assess the expression of tumor necrosis factor (TNF)-α and cyclooxygenase-2 (COX-2). The difference in the severity of inflammation and COX-2 expression was examined using one-way analysis of variance. The correlation of COX-2 expression with the severity of inflammation was analyzed using Spearman's rank correlation test. RESULT: Until week 13, chronic inflammation and non-hyperplastic and hyperplastic aberrant crypt foci occurred. The severity of inflammation gradually shifted from high moderate to low moderate. TNF-α expression was high in all groups; however, COX-2 expression was gradually lower with longer duration of induction, which corresponded with the severity of inflammation. CONCLUSION: DMH induction until week 13 without a latency period caused chronic inflammation without the formation of adenoma or adenocarcinoma. A very strong correlation was established between COX-2 expression and inflammation.

Is there a link between talcum powder, oxidative stress, and ovarian cancer risk?

INTRODUCTION: The link between talcum powder use and cancer, particularly ovarian cancer, has been a topic of scientific research and legal debate for several years. Studies have suggested a potential association between long-term talcum powder use in the genital area and an increased risk of ovarian cancer. AREAS COVERED: The following report includes up-to-date evidence to support the potential link between talcum powder use and the risk of developing ovarian cancer. The International Agency for Research on Cancer, which is part of the World Health Organization, classified talc-based body powder as possibly carcinogenic to humans when used in the female genital area. However, other studies have not consistently supported this association, and thus more research is needed to establish a clear and definitive link between talcum powder use and cancer. Despite this, recent molecular-level data have linked talc to alterations in redox balance, gene mutations, and inflammatory responses. Specifically, we have identified a role for talc to induce the pro-oxidant state, inhibit apoptosis, and more importantly induced cellular transformation in normal ovarian cells. EXPERT OPINION: We presented unequivocal evidence to support our opinion that talc is not biologically inert and induces molecular changes that mimic the hallmarks of cancer.

Intelligent onsite dual-modal assay based on oxidase-like fluorescence carbon dots-driven competitive effect for ethyl carbamate detection.

Intelligent onsite accurate monitoring ethyl carbamate (EC, a group 2 A carcinogen) in environment is of great significance to safeguard environmental health and public safety. Herein, we reported an intelligent dual-modal point-of-care (POC) assay based on the bimetallic Mn and Ce co-doped oxidase-like fluorescence carbon dots (Ce&MnCDs) nanozyme-driven competitive effect. In brief, the oxidase-like activity of Ce&MnCDs was inhibited by thiocholine (TCh, originating from the hydrolysis of acetylcholinesterase (AChE) to acetylthiocholine (ATCh)), preventing the oxidation of o-phenylenediamine (OPD) to 2,3-diaminophenothiazine (DAP). However, with the aid of Br2 + NaOH, EC inactivated AChE to prevent TCh generation for re-launching the oxidase-like activity of Ce&MnCDs to trigger the oxidation of OPD into DAP, thereby outputting an EC concentration-dependent ratiometric fluorescence and colorimetric readouts by employing Ce&MnCDs and OPD as the optical signal reporters. Interestingly, these dual-modal optical signals could be transduced into the gray values that was linearly proportional to the residual levels of EC on a smartphone-based portable platform, with a detection limit down to 1.66 µg/mL, qualifying the requirements of analysis of EC residues in real samples. This opened up a new avenue for onsite assessment of the risk of residues of EC, safeguarding environmental health and public safety.

A sustainable, eco-friendly Tb/Eu-modified HOFs for ultrasensitive detection and efficient adsorption of carcinogens in complex water environments.

Developing a multifunctional material that can detect and remove carcinogens in water environments, simultaneously monitor their toxic metabolites in living organisms is significant for environmental remediation and human health. However, most research only focused on detection or adsorption carcinogens due to the difficulty of integrating multiple functions into one material, let alone monitoring their toxic metabolites. Here, a multifunctional Tb/Eu@TATB-HOF (1) is first developed to monitor two carcinogens, malachite green (MG) and its metabolites leucomalachite green (LMG), and simultaneously remove MG from the contaminated water. 1, as the dual-emission fluorescence sensor, can achieve ultrasensitive and highly visualized sensing for MG and LMG with different response modes. Even in actual samples, 1 still exhibits satisfactory sensing performances. As the adsorbent, 1 displays good recyclability and high adsorption capacity for MG. The sensing and adsorption mechanisms are explored through experiments and theoretical calculations. This work not only provides a novel insight for environmental remediation and human health through detection and removal of carcinogens, simultaneously monitoring their toxic metabolites, but first reveals the enormous potential of HOFs as multifunctional materials simultaneously for fluorescence sensing and adsorption.