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The aim of this review was to evaluate if micronucleus assay in oral exfoliated cells is a suitable tool for biomonitoring children exposed to environmental pollutants. Through the electronic databases PubMed/Medline, Scopus, and Web of Science, all published studies until April 2021 that examined the relationship between exposure to environmental pollutants and micronucleus frequency in oral cells were searched. All relevant articles using a combination of the following keywords-"children," "micronucleus," "oral cells," and "environmental pollution"-were considered. A total of 20 papers met the criteria for inclusion in the systematic review. The results regarding the cytogenetic damage induced by environmental pollutants are conflicting. Some authors have demonstrated that environmental pollution induces mutagenesis in oral cells while others did not. Following the parameters of the Project for Effective Public Health Practices (EPHPP) and after extensive reading of all the articles included, a total of 12 articles had moderate and strong scores and 8 had a classification considered weak. Taken together, this review was able to demonstrate the association between micronucleus frequency and exposure to environmental pollutants in oral exfoliated cells of children.

Aim The aim of this review was to evaluate the scientific literature regarding the cytogenetic damage in oral exfoliated cells of adult patients submitted to panoramic X-ray. Materials and methods An extensive search of the literature was conducted on PubMed, Scopus and Web of Science databases for all studies published until April 2021 using combinations of the following keywords: "panoramic X-ray," "DNA damage," "genetic damage", "genotoxicity", "mutagenicity", cytotoxicity", "buccal cells", "oral mucosa", "tongue", "gingiva", "micronucleus assay", according to the PRISMA guidelines. All clinical studies in English language were included in the study. A total of 10 studies were identified. Results As expected, the results regarding the cytogenetic damage induced by panoramic X-ray are conflicting. Some authors have demonstrated that panoramic X-ray induces mutagenesis in oral cells, whereas others did not. After reviewing the 10 studies, two were classified as strong, four were considered moderate, and four were considered weak, according to the quality assessment components of the Effective Public Health Practice Project (EPHPP). Meta-analysis data revealed a negative response related to mutagenicity in oral cells by panoramic X-ray. Conclusion Taken together, this review failed to demonstrate the association between micronucleus frequency and panoramic X-ray.

Dimethoate ([O,O-dimethyl S-(N-methylcarbamoylmethyl) phosphorodithioate]) is an organophosphate insecticide and acaricide widely used for agricultural purposes. Genotoxicity refers to the ability of a chemical agent interact directly to DNA or act indirectly leading to DNA damage by affecting spindle apparatus or enzymes involved in DNA replication, thereby causing mutations. Taking into consideration the importance of genotoxicity induced by dimethoate, the purpose of this manuscript was to provide a mini review regarding genotoxicity induced by dimethoate as a result of oxidative stress. The present study was conducted on studies available in MEDLINE, PUBMED, EMBASE, and Google scholar for all kind of articles (all publications published until May, 2020) using the following key words: dimethoate, omethoate, DNA damage, genetic damage, oxidative stress, genotoxicity, mutation, and mutagenicity. The results showed that many studies were published in the scientific literature; the approach was clearly demonstrated in multiple tissues and organs, but few papers were designed in humans. In summary, new studies within the field are important for better understanding the pathobiological events of genotoxicity on human cells, particularly to explain what cells and/or tissues are more sensitive to genotoxic insult induced by dimethoate.

Crack-cocaine is a cocaine by-product widely consumed by general population in developing countries. The drug is low cost and is associated with more intense effects when compared to other illicit drugs. Genotoxicity, oxidative stress, and inflammatory response are considered crucial events in carcinogenesis, since they actively participate in the multistep process. The purpose of this paper was to provide a mini review regarding the relationship between carcinogenesis and genotoxicity, oxidative stress, and inflammation induced by crack-cocaine. The present study was conducted on search of the scientific literature from the published studies available in PubMed, MEDLINE, Scopus, and Google Scholar for all kind of articles (all publications to November 2020) using the following key words: crack-cocaine, DNA damage, genotoxicity, cellular death, cytotoxicity, mutation, oxidative stress, inflammation, and mutagenicity. The results showed that published papers available were almost all in vivo test system being conducted in humans or rodents. Crack-cocaine was able to induce genotoxicity and oxidative stress in mammalian cells. However, the role of inflammatory response after exposure to crack-cocaine was not conclusive so far. In summary, this study is consistent with the notion that crack-cocaine is a chemical carcinogen as a result of genotoxicity and oxidative stress induced in mammalian and non-mammalian cells.

Ionic liquids (ILs) have been proposed as more efficient and sustainable solvents to replace volatile organic solvents (VOSs). However, the drawbacks associated with their use are still limiting the regular application of bioactive compounds obtained from the processes they mediate as food ingredients. It is true that the number of ILs approved by the Food and Drug Administration for food applications is still low and mainly focused on the ones from the quaternary ammonium family. However, this trend is changing, judging from the evidence that industries are surpassing overgeneralization about ILs (on price and toxicity) and starting to consider the potential and performance of ILs as solvents. Despite the examples of industries applying ILs in their processes, the use of bioactive compounds obtained from IL-based processes as ingredients in food formulations is still a big challenge. The positive influence of carotenoids on diseases associated or originating from the inflammatory scenario including, among others, obesity, is not new. Moreover, it is also well known that the poorest population worldwide does not have the recommended intake of carotenoids, especially those pro-vitaminic A. In an attempt to help answer this issue, dietary supplements containing adequate doses of natural carotenoids are expected to be the solution, or at least, part of the solution for a healthier life, but also, to reduce hunger. Thus, complete studies evaluating the toxicological potential and the real viability of adding these bioactive compounds in food formulations proving (or not!) their safety to consumers and handlers are highly demanded. This work proposes to investigate the potential of carotenoids extracted from Bactris gasipaes feedstocks mediated by an ethanolic solution of an imidazolium-based IL. Thus, male Wistar rats were randomized in six different groups, supplemented or not by carotenoids extracted by IL or VOS, and fed by control- and/or high-fat-diets (HFD). The adipose tissue-liver axis was studied as a model to investigate the influence of the carotenoids on the levels of inflammation and oxidative stress markers. The main results showed that animals supplemented with carotenoids extracted with IL displayed improvements in serum parameters, besides lower metabolic efficiency, and antioxidant response on the liver, even when fed with HFD. However, animals supplemented with carotenoids extracted by VOS showed higher levels of pro-inflammatory markers and huge oxidative stress on the liver. published

Background/aim The aim of the present study was to investigate the biological effects of subacute crack cocaine exposure in rat liver. Material and methods A total of 32 rats were distributed into four groups (n=8): Experimental group 1 (G1) and Experimental group 2 (G2): rats received 18 mg/kg of body weight (b.w) of crack cocaine for 5 days, once a day, group G2 remained 72 h without exposure after the experimental period (5 days)(abstinence); Experimental group 3 (G3): rats received 36 mg/kg of body weight (b.w) of crack cocaine for 5 days, once a day; Control Group (CTRL): rats received only the vehicle (DMSO) administered by the intraperitoneal (i.p) route for 5 days, once a day. Results All groups exposed to crack cocaine had an increase in the number of micronucleated hepatocytes and binucleated cells only in the highest tested dose (36 mg/kg). Karyolysis had an increase in the 18 mg/kg dose, in the abstinence group (G2), and 36 mg/kg group (G3); whereas pyknotic nuclei had an increase in the G2 group. The group exposed to 18 mg/kg of crack cocaine also showed high 8 OHdG expression. The p-NF-κB p65 protein decreased in the groups exposed to crack cocaine at doses of 18 and 36 mg/kg, as well as in the abstinence group. MyD88 was also found decreased in the group exposed to crack cocaine at 18 mg/kg. Conclusion Crack cocaine inhibited toll like signaling pathway whilst being associated with genomic instability in rat liver cells.

The negative aspects of unhealthy eating on obesity and hepatic health are well described. The axis between the adipose tissue and the liver participates in most of the damage caused to this tissue regarding obesogenic diets (OD). At the same time that the effects of consuming simple carbohydrates and saturated fatty acids are known, the effects of the cessation of its intake are scarce. Withdrawing from OD is thought to improve health; despite some studies had shown improvement in hepatic conditions in the long-term, short-term studies were not found. Therefore, we aimed to determine how OD intake and withdrawal would influence visceral and hepatic fat accumulation and inflammation. To this end, male 60-days-old Wistar rats received standard chow (n = 16) or a high-sugar/high-fat diet (HSHF) for 30 days (n = 32), a cohort of the HSHF-fed animals was then kept 48 h on standard chow (n = 16). In opposition to the generally reported, the results indicate that hepatic inflammation preceded hepatic steatosis. Additionally, inflammatory markers on the liver positively correlated visceral adipokines and visceral fat accumulation mediated them in a deposit-dependent manner. At the same time, a 48-h withdrawal was capable of reverting most of the risen inflammatory mediators, although MyD88 and TNFα persisted and serum non-HDL cholesterol was higher than control levels.

Background The aim of this study was to evaluate cytotoxic, mutagenic and genotoxic effects on buccal mucosa and peripheral blood cells from marijuana and tobacco smokers. Methods For this purpose, a total of 45 volunteers were distributed into four groups: CTRL group (control): individuals who did not smoke marijuana or tobacco (n = 11); Group M: Marijuana smokers (n = 13); Group T: Tobacco smokers (n = 13); Group M + T: Smokers of both marijuana and tobacco (n = 08). Results Smokers of both marijuana and tobacco led an increase of micronucleated cells on buccal mucosa when compared to control group. The occurrence of karyolysis showed significant changes in this group as well. The comet assay data revealed genetic damage in peripheral blood cells for all groups of smokers. Conclusion In summary, our results showed that marijuana and /or tobacco are able to induce genetic damage and cytotoxicity in oral and peripheral blood cells.

The aim of this study was to investigate histopathological and inflammatory response in liver and kidney of rats after crack exposure. For this purpose, a total of 32 male Wistar rats were distributed into four groups: (G1) and (G2): received 18 mg/kg of body weight (b.w) of crack cocaine, but Group G2 remained 72 h without exposure after the experimental period (5 days). Experimental group 3 (G3): received 36 mg/kg of body weight (b.w) of crack cocaine. Control Group (CTRL): received only the vehicle (DMSO) administered by intraperitoneal (i.p) route for 5 days. The results showed that crack cocaine induced histopathological changes in liver and kidney. Immunohistochemistry data revealed that G2 group showed a higher immunoexpression of Ki-67 in hepatic and renal tissues. Regarding inflammation, the results showed that all groups exposed to crack cocaine decreased the expression of TNF-α, IL-6, and IL-10 in liver and kidney. In summary, our results showed that the subacute doses of crack cocaine used in this study had cytotoxic, and immunosuppressive effects in liver and kidney of rats, especially at 36 mg/kg dose. Since cellular death and inflammation participates in the multi-step process of chemical carcinogenesis, these data offer new insights into potential ways to understand the pathobiological mechanisms induced by crack cocaine in several tissues and organs.

Oral cancer is a very common tumor worldwide with high incidence and mortality. The treatment of oral cancer involves surgery, radio- and chemotherapy; however, high failure rates and toxicity are noticed. Thus, the search of new drugs aiming a more effective treatment is welcomed. Natural products present chemopreventive and anti-cancer effects. Resveratrol is a naturally occurring antioxidant that contains several health benefits, including anti-inflammatory and antiproliferative activities. This review discusses the different action mechanisms of resveratrol related in the in vitro and in vivo studies using models of oral cancer.

One promising skin substitutes in the wound healing are the bacterial cellulose membranes (BCM). These biomaterials present nanostructures composed of microfibrils capable of forming three-dimensional pores that allow cell. In association with these biopolymers, several treatments are used, such as enrichment by growth factors and/or the application of photobiomodulation (PBM). Therefore, the aim of this study was to investigate the viability, proliferation and cytotoxicity of a BCM (culturing of Komagataeibacter xylinus), with or without FGF-2 in association with PBM therapy. In the characterization of BCM we saw that the membrane does not show great variations in pH and with the scanning electron microscopy it was possible to observe that the BCM has a denser and a porous side that allows the adhesion of fibroblasts, confirmed by histological staining and DAPI/Phalloidin. In vitro evaluation showed that the immunofluorescence (CaAM/EthD-1) for live and dead cells presented, in the groups with combined treatment at long-term of PBM and FGF-2, a greater quantity of live cells than with these isolated treatments and/or at short-term. However, in the short-term of combined treatment PBM and FGF-2 supplementation, fibroblasts and macrophages were more viable by Alamar Blue, in direct and indirect contact respectively. The comet assay did not show cytotoxicity for DNA damage in fibroblasts indirect contact with membrane extract. The results highlight the potential of association of FGF-2 supplementation with the application of PBM for use with BCM, due to its promoted increased cell density at long-term and improved viability in fibroblasts and macrophages at short-term.

The aim of the letter to editor is to provide some comments regarding the manuscript of DehghanNezhad et al.(1) recently published in the Iranian Journal of Pathology titled “Micronucleus Assay of Buccal Mucosa Cells in Waterpipe (Hookah) Smokers: A Cytologic Study.” In this article, the authors were able to detect high frequencies of micronucleus in buccal mucosa cells of waterpipe smokers when compared to non-smokers.