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Benzene is used worldwide as a major raw material in a number of industrial processes and also a potent airborne pollutant emitted from traffic exhaust fume. The present systematic review aimed to identify potential associations between genetic polymorphisms and occupational benzene-induced genotoxicity. For this purpose, a total of 22 selected studies were carefully analysed. Our results revealed a positive relation between gene polymorphism and genotoxicity in individuals exposed to benzene, since 17 studies (out of 22) observed positive relations between genotoxicity and polymorphisms in xenobiotics metabolizing genes influencing, therefore, individuals' susceptibility to genomic damage induced by benzene. In other words, individuals with some genotypes may show increase or decrease DNA damage and/or higher or lower DNA-repair potential. As for the quality assessment, 17 studies (out of 22) were categorized as Strong or Moderate and, therefore, we consider our findings to be trustworthy. Taken together, such findings are consistent with the notion that benzene induces genotoxicity in mammalian cells being strongly dependent on the genetic polymorphism. Certainly, such findings are important for clarifying the role of biomarkers related to genotoxicity in human biomonitoring studies. [ABSTRACT FROM AUTHOR]

In a world with a rising use of pesticides, these chemicals, although designed to effectively control pests, pose potential threats to the environment and non-target organisms, including humans. Thus, this systematic review aims to investigate a possible association between genetic polymorphisms and susceptibility and genotoxicity in individuals occupationally exposed to pesticides. This review was conducted following the 2020 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. A total of 14 carefully selected studies were thoroughly analyzed by two reviewers, who assigned scores based on previously set evaluation criteria. This study classified over half of the chosen studies as having moderate or strong quality, observing a correlation between certain genetic polymorphisms involved in xenobiotic metabolism and genotoxicity in workers exposed to pesticides. Results suggest that the genes associated with xenobiotic metabolism play a substantial role in determining individuals' susceptibility to genomic damage due to pesticide exposure, affecting both their peripheral blood and oral mucosa. This implies that individuals with specific genotypes may experience increased or decreased levels of DNA damage when exposed to these chemicals. [ABSTRACT FROM AUTHOR]

In order to detect genetic damage, different methods have been developed, such as micronuclei and comet assay. The comet assay presents some advantages when compared to the other aforementioned methods, including wide versatility, as any eukaryotic cell can be evaluated at an individual cellular level. In this context, the aim of this systematic review was designed to help further elucidate the following question: is the comet assay a suitable biomarker of in vivo oral carcinogenesis? The present systematic review was performed in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines. Full manuscripts from 18 studies were carefully selected in this setting. A total of 15 studies demonstrated positive findings for genotoxicity in peripheral blood or oral cells in patients with pre-malignant lesions or oral cancer. In the quality assessment of studies, 1 was classified as Strong, 5 were considered as Moderate, and 12 were classified as Weak. In summary, the comet assay can be a useful biomarker for oral carcinogenesis. However, further studies with more strict parameters are suggested (with less uncontrolled confounders) in order to increase findings reliability for diagnosis of oral potentially malignant lesions. [ABSTRACT FROM AUTHOR]

Background and objectives: Nowadays, hair dye products are widely used for aesthetic purposes, in which it generates chemical exposure to customers and, mainly, hairdressers. The aim of this systematic review was designed to elucidate the following question: are hair dye products able to induce DNA damage in hairdressers? Methods: Studies were included in our analyses if they met the following criteria: (1) studies measuring genetic damage in vivo; (2) studies published in English; (3) studies that provided data clearly presented in scientific standards. Results: Full manuscripts from 13 studies were carefully selected in this setting. Our results demonstrate that hair dye products may contain chemical agents able to induce DNA strand breaks or chromosome damage since the majority of studies demonstrated positive findings for genotoxicity. A total of 7 studies (out of 13) had strong or moderate rates in the quality assessment. The type of genotoxicity assay and sample selection criteria time influenced the outcome. Conclusion: In summary, our results reveal that hairdressers are occupationally exposed to genotoxic agents. Such findings are very important for protecting these professionals who are continuously exposed to chemicals for long periods. [ABSTRACT FROM AUTHOR]

The systematic review (SR) with meta-analysis aimed to infer if micronucleus assay using oral mucosal cells a useful biomarker for biomonitoring populations continuously exposed to pesticides (EP). The SR has been made in accordance with the PRISMA-P guidelines. The PICOS strategy has focused to answer the following question: "Does exposure to pesticides cause genetic damage in oral cells?" The literature search was made in the following scientific databases: Web of Science, PubMed/Medline, and Scopus. The approach was defined as follows: standardized mean difference (SMD) and 95% confidence intervals (CI). The quality assessment of manuscripts was obtained by the EPHPP (Effective Public Health Practice Project). The GRADE tool was chosen for assessing the quality of evidence. A total of 108 articles were selected in this setting. After screening abstracts and titles, 23 manuscripts were evaluated for eligibility. After reviewing the studies, two were considered weak and 22 were classified as moderate or strong. The meta-analysis data pointed out statistically significant differences in volunteers exposed to EP (SMD = 1.23, 95% CI, 0.69 to 1.77, p < 0.001), with a Tau2 = 1.44; Chi2 = 566.38, and p < 0.001, so that the selected manuscripts were considered heterogeneous and the I2 of 97% indicated high heterogeneity. Taken together, this review was able to validate the micronucleus assay in oral exfoliated cells as a useful biomarker in individuals continuously exposed to EP because the studies categorized as moderate and strong have demonstrated positive response related to mutagenesis. [ABSTRACT FROM AUTHOR]

To evaluate, through a systematic review, the assessment of genotoxicity of glass ionomer cements in vitro and in vivo. A systematic review was performed with the problem, intervention, control, and outcomes (PICOS) strategy, aiming to answer the following question: "Can glass ionomer cements induce genetic damage in vitro and in vivo?" A systematic search was performed in the following electronic databases: PubMed (including MedLine), Web of Science, and Scopus. The quality of included studies was assessed using the Effective Public Health Practice Project (EPHPP). After the authors performed the review of all articles, a total of 13 manuscripts met all the inclusion criteria in the systematic review. Following the parameters of the EPHPP, eight articles were classified as strong or moderate quality. The other ones (five studies) were weak. Taken together our results demonstrated that, six studies reported genotoxicity of the modified glass ionomer cements tested and two studies concluded that the effect of genotoxicity was time dependent. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate cytogenotoxicity in mammalian cells induced by ingestion of superficial water from SESS. For this purpose, surface water was collected from two points of SESS: São Vicente Channel (SVC) and Piaçaguera Channel (PIC). Four groups (n = 5) of adult male Wistar (8 weeks old) received for 5 days: (a) filtered tap water (water control), (b) tap water with 2.4% of NaCl (saline control), (c) estuarine water from PIC and (d) estuarine water from SVC. Results demonstrated that Ki67 immunoexpression was higher in hepatocytes exposed to both sampling site, while caspase-3 demonstrated downregulation in rat liver exposed to estuarine water. There was also significant increase in micronuclei frequency in bone marrow cells and hepatocytes, and DNA damage in blood and liver of rats exposed to estuarine water from SVC and PIC. In summary, studies with complex mixtures, such as contaminated estuarine water are important since this work confirmed by experiments using in vivo mammalian cells of rats that SESS water are genotoxic, mutagenic and cytotoxic, denoting concern for environmental health. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The aim of the study was to evaluate cyto- and genotoxic effects in populations living in subnormal clusters in Santos São Vicente estuary. For in vivo study, samples of buccal mucosa and peripheral blood cells were collected. Micronucleus assay and single-cell gel (comet) assay were performed. For in vitro study, Chinese ovary hamster (CHO) cells were exposed to contaminated water. The results showed that people living in the contaminated estuary have increased DNA damage in oral mucosa and peripheral blood cells, as detected in the micronucleus and comet assays respectively. In addition, estuarine water was able to promote cytotoxicity at the highest concentrations, as well as decrease the number of cells in the G1 phase. In summary, our results indicate that water from the Santos-São Vicente estuary is capable of inducing cytogenotoxicity in mammalian cells in vivo and in vitro. [ABSTRACT FROM AUTHOR]

The presence of cocaine and its metabolites and by-products has been identified in different aquatic matrices, making crack cocaine the target of recent studies. The aim of this study was to evaluate the sublethal effects of crack on the brown mussel Perna perna. Mussels were exposed to three concentrations of crack cocaine (0.5, 5.0, and 50.0 μg L−1) for 168 h. Gills, digestive glands, and hemolymph were extracted and analyzed after three different exposure times using a suite of biomarkers (EROD, DBF, GST, GPX, LPO, DNA damage, ChE, and lysosomal membrane stability [LMS]). After 48 and 96 h of exposure, EROD, DBF, GST, GPX activities and DNA strand breaks in the gills increased significantly after 48 and 96 h of exposure. Alterations in LMS were also observed in the mussels exposed to all crack concentrations after 96 and 168 h. Our results demonstrated that crack cocaine is metabolized by CYP-like and GST activities in the gills. GPX was not able to prevent primary genetic damage, and cytotoxic effects in the hemocytes were also observed in a dose- and time-dependent response. Our study shows that the introduction of illicit drugs into coastal ecosystems must be considered a threat to marine organisms. [ABSTRACT FROM AUTHOR]

The ionic liquid or melted salt 1-Butyl-3-methylimidazolium is an alternative process to extract natural pigments, such as carotenoids. Lycopene represents 80–90% of total of carotenoids presents in tomatoes and it has been widely studied due its potent antioxidant action. The aim of this study was to evaluate genotoxicity, mutagenicity and cytotoxicity of carotenoids extracted from ionic liquid using experimental model in vivo . For this purpose, a total of 20 male Wistar rats were distributed into four groups ( n = 5), as follows: control group ; received a corresponding amount of corn oil for 7 days by intragastric gavage ( i.g. ), ionic liquid group , received 10 mg kg −1 body weight for 7 days by gavage; 10 mg carotenoids group , received 10 mg kg −1 bw dissolved in corn oil for 7 days by gavage and 500 mg carotenoids group , received 500 mg kg −1 bw dissolved in corn oil for 7 days by gavage. Rat liver treated with ionic liquid exhibited moderate histopathological changes randomly distributed in the parenchyma, such as cytoplasmic eosinophilia, apoptotic bodies, inflammatory infiltrate and focal necrosis. DNA damage was found in peripheral blood and liver cells of rats treated with ionic liquid or carotenoids at 500 mg. An increase of micronucleated cells and 8-OhDG immunopositive cells were also detected in rats treated with carotenoids at 500 mg. In summary, our results demonstrate that recommended dose for human daily intake of carotenoids extracted by ionic liquid did not induce genotoxicity, mutagenicity and cytotoxicity in multiple organs of rats. [ABSTRACT FROM AUTHOR]

Context: Crack cocaine is an illicit drug derived from cocaine, in which use and abuse have increased around the world, especially in developing countries.Objectives: The aim of this study was to evaluate genomic damage in multiple organs of mice following acute exposure to crack cocaine. For this purpose, single cell gel (comet) assay in peripheral blood, liver, kidney, and brain cells was performed and micronucleus test for bone narrow and liver cells was also made in this setting.Material and methods: A total of 20 C57BL/10 male mice were distributed into four groups, as follows: 0, 4.5, 9, and 18 mg/kg b.w. of crack cocaine dissolved to 1% dimethyl sulfoxide by intraperitoneal (i.p.) route. All animals were sacrificed 24 h after i.p. injection.Results: The results showed that crack cocaine induced DNA damage in peripheral blood, and brain cells for higher doses used as depicted by single cell gel (comet) assay data. Analysis of kidney cells showed no genetic damage for all groups tested. The number of micronucleated cells did not increase after crack cocaine exposure in bone narrow or liver cells.Conclusion: In summary, crack cocaine is a genotoxic agent in peripheral blood, liver, and brain cells but not mutagenic in multiple organs of mice. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate if purple carrot extract is able to protect against the noxious activities induced by cadmium exposure in multiple organs of rats. For this purpose, histopathological analysis, genotoxicity and oxidative status were investigated in this setting. A total of twenty Wistar rats weighing 250 g on the average, and 8 weeks age were distributed into four groups ( n = 5), as follows: Control group (non-treated group, CTRL); Cadmium group (Cd) and Purple carrot extract groups at 400 mg/L or 800 mg/L. Histopathological analysis revealed that liver from animals treated with purple carrot extract improved tissue degeneration induced by cadmium intoxication. Genetic damage was reduced in blood and hepatocytes as depicted by comet and micronucleus assays in animals treated with purple carrot extract. SOD-CuZn and cytocrome C gene expression increased in groups treated with purple carrot extract. Purple carrot extract also reduced the 8OHdG levels in liver cells when compared to cadmium group. Taken together, our results demonstrate that purple carrot extract is able to protect against cadmium intoxication by means of reducing tissue regeneration, genotoxicity and oxidative stress in multiple organs of Wistar rats. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the health benefits associated with apple consumption following cadmium exposure. A total of 15 Wistar rats were distributed into three groups ( n = 5), as follows: control group (non-treated group, CTRL); cadmium group (Cd) and apple juice group (Cd + AJ). The results showed a decrease in the frequency micronucleated cells in bone marrow and hepatocytes in the group exposed to cadmium and treated with apple juice. Apple juice was also able to reduce the 8OHdG levels and to decrease genetic damage in liver and peripheral blood cells. Catalase (CAT) was decreased following apple juice intake. Taken together, our results demonstrate that apple juice seems to be able to prevent genotoxicity and oxidative stress induced by cadmium exposure in multiple organs of Wistar rats. [ABSTRACT FROM AUTHOR]

The Mimosa ( Mimosa caesalpiniifolia) is a plant native from South America; it is used in the traditional medicine systems for treating bacterial, fungal, parasitic and inflammatory conditions. The aim of this study was to evaluate the antigenotoxic and antioxidant activities induced by mimosa ( M. caesalpiniifolia) in multiple rodent organs subjected to intoxication with cadmium chloride. A total of 40 Wistar rats (8 weeks old, 250 g) were distributed into eight groups ( n = 5), as follows: Control group (non-treated group, CTRL); Cadmium exposed group (Cd); cadmium exposure and treated with extract at 62.5 mg/kg/day; cadmium exposure and treated with extract at 125 mg/kg/day; cadmium exposure and treated with extract at 250 mg/kg/day; cadmium exposure and treated with ethyl acetate fraction at 62.5 mg/kg/day. For evaluating the toxicogenetic potential of mimosa, two groups were included in the study being treated with extract at 250 mg/kg/day and acetate fraction of mimosa at 62 mg/kg/day, only. Extract of mimosa at concentrations of 62.5 and 125 mg decreased DNA damage in animals intoxicated with cadmium when compared to cadmium group. In a similar manner, treatment with ethyl acetate fraction of mimosa at 62.5 mg concentration in animals previously exposed to cadmium reduced genetic damage in peripheral blood cells. In a similar manner, the treatment with ethyl acetate fraction reduced DNA damage in liver cells. Oxidative DNA damage was reduced to animals exposed to cadmium and treated with 125 mg of extract as well as those intoxicated to cadmium and treated with 62.5 of acetate fraction of mimosa. Taken together, our results indicate that mimosa prevents genotoxicity induced by cadmium exposure in liver and peripheral blood cells of rats as a result of antioxidant activity. [ABSTRACT FROM AUTHOR]

Background and objectives: The aim of this study was to evaluate genotoxicity and mutagenicity in peripheral blood and buccal mucosal cells in mucopolysaccharidosis (MPS) I, II or VI patients. Methods: A total of 12 patients with MPS type I, II and VI attended at the Institute of Genetics and Inborn Errors of Metabolism treated with enzyme replacement therapy (ERT) and 10 healthy control volunteers were included in this study. Mechanically exfoliated cells from cheek mucosa (left and right side) were used to micronucleus test and single cell gel (comet) assay in peripheral blood cells. Results: The results of this study detected the presence of genetic damage in peripheral blood for all individuals with MPS treated with ERT, regardless of type of MPS as depicted by tail moment results. In addition, an increased number of micronucleated cells were found in buccal cells of MPS type II patients. It was also observed an increase of other nuclear alterations closely related to cytotoxicity as depicted by the frequency of pyknosis, karyolysis and karyorrhexis in buccal mucosa cells of MPS VI patients ( p < 0.05). Conclusion: Taken together, such results demonstrate that metabolic alterations induced by the enzymatic deficiency characteristic of MPS associated with ERT therapy can induce genotoxicity and mutagenicity in peripheral blood and buccal mucosa cells, respectively. This effect appears to be more pronounced to MPS II. [ABSTRACT FROM AUTHOR]

We read the recent paper accepted for publication in I Environmental Science and Pollution Research i titled "Monitoring human genotoxicity risk associated to urban and industrial Buenos Aires air pollution exposure" by de Los A Gutiérrez et al. ([3]) with much interest. In view of the lack of DNA specificity of the Giemsa stain, the MN identification is very technical and hard due to the presence of some structures in the cytoplasm of oral cells that are similar to micronucleus, such as kerato-kyalin granules or bacteria. 1:CAS:528:DC%2BC1MXhvVagsrjI 6 Nersesyan A, Kundi M, Atefie K, Schulte-Hermann R, Knasmüller S. Effect of staining procedures on the results of micronucleus assays with exfoliated oral mucosa cells. [Extracted from the article]

Formocresol, paramonochlorophenol, and calcium hydroxide are widely used in dentistry because of their antibacterial activities in root canal disinfection. However, the results of genotoxicity studies using these materials are inconsistent in literature. The goal of this study was to examine the genotoxic potential of formocresol, paramonochlorophenol, and calcium hydroxide using mouse lymphoma cells and human fibroblasts cells in vitro by the comet assay. Data were assessed by Kruskal-Wallis nonparametric test. The results showed that all compounds tested did not cause DNA damage for the tail moment or tail intensity parameters. These findings suggest that formocresol, paramonochlorophenol, and calcium hydroxide do not promote DNA damage in mammalian cells and that the comet assay is a suitable tool to investigate genotoxicity. [Copyright &y& Elsevier]

Centropomus undecimalis fish inhabit the highly contaminated Santos-São Vicente Estuarine System (SESS) and could be a good biomonitor of contaminants. This study aimed to investigate the cytogenotoxic potential of superficial water from SESS using C. undecimalis as a biomonitoring model and to validate the use of farmed fish as controls. Using biochemical (DNA damage and Lipid Peroxidation - LPO), cellular (erythrocyte nuclear abnormality – ENA) and tissue (8-OHdG immunoexpression) biomarkers, our results showed fish from SEES had higher LPO concentration in gills and higher frequency of reniform, lobed and total ENA in erythrocytes when compared with control farmed fish. Thus, SESS surface water are cytogenotoxic for blood and gills cells of fishes. C. undecimalis has shown to be a good biomonitor model and farmed fish can be used as control only if livers were not the target organs of study since the dietary food from farmed fish causes steatosis. • Centropomus undecimalis are shown to be a good biomonitor model. • Biochemical and cellular biomarkers have been more sensitive than tissue biomarker. • Surface water from SESS were cytogenotoxic for fish cells. • Farmed fish can be used as control only if livers were not the target organs. [ABSTRACT FROM AUTHOR]

Formaldehyde is a chemical compound capable of preserving cells and tissue morphology, being extensively used worldwide in industrial and medical processes. However, due to the many biological effects that take place after an individual is chronically exposed to formaldehyde, this compound poses a greater cancer risk for workers under its occupational exposure, even at lower concentrations. Thus, the present systematic review aimed to understand whether there may be a positive relation between polymorphism (in terms of individual susceptibility) and genotoxicity in individuals occupationally exposed to formaldehyde. For this purpose, a total of eight selected studies were carefully analyzed by two reviewers, who attributed scores to each study according to the used analysis parameters. First, all studies investigated either pathologists under formaldehyde exposure or anatomical laboratory pathology workers. In addition, the majority of studies were categorized as moderate or strong in the quality assessment. The results revealed a positive association between some polymorphism and genotoxicity in individuals exposed to formaldehyde, since more than half of the studies observed positive relations between genotoxicity and polymorphisms in xenobiotics metabolizing genes. We understand such parameters influence individuals’ susceptibility to genomic damage induced by formaldehyde in peripheral blood. In conclusion, individuals with certain genotypes may show higher or lower DNA damage and/or lower or higher DNA repair potential. [ABSTRACT FROM AUTHOR]