Is genotoxicity a suitable biomarker for monitoring anabolic-androgenic steroids exposure in vivo? A systematic review and meta-analysis.

Steroids stand for a class of hormones (natural and synthetic) known to be helpful for a number of disorders. Despite the aforementioned beneficial effects of using these hormones, anabolic-androgenic steroids (AAS) are also widely abused in a non-therapeutic manner for muscle-building and strength-increasing properties that may lead to genotoxicity in different tissues. The present study aims to understand whether genotoxicity may be a suitable biomarker for AAS exposure in vivo in both experimental animal and human studies. All studies published in PubMed/Medline, Scopus, and Web of Science electronic databases that presented data on DNA damage caused by AAS were analyzed. A total of 15 articles were included in this study, and after thoroughly reviewing the studies, a total of 8 articles were classified as Strong, 6 were classified as Moderate, and only 1 was classified as Weak, totaling 14 studies being considered either Strong or Moderate. This classification makes it possible to consider the present findings as reliable. The meta-analysis data revealed a statistically significant difference in Wistar rat testis cells with AAS compared to control for tail length and % tail DNA (p < 0.001), so that the selected articles were considered homogeneous and the I2 of 0% indicated low heterogeneity. In summary, genotoxicity can be considered a suitable biomarker for monitoring AAS exposure as a result of DNA breakage and oxidative DNA damage.

Is micronucleus assay a suitable method for biomonitoring children exposed to X-ray? A systematic review with meta-analysis.

PURPOSE: The aim of this study was to evaluate if the micronucleus test using oral epithelial cells is a suitable biomarker for biomonitoring children exposed to X-ray. MATERIAL AND METHODS: A search was performed through the electronic databases PubMed/Medline, Scopus, and Web of Science, all studies published up to February 2022 that examined the relationship between exposure of children to radiographic examinations and micronucleus. RESULTS: A total of 17 full-text manuscripts were screened for eligibility. Only two studies found a difference in micronucleus labeling. On the other hand, all studies showed that X-ray was able to induce cellular death in oral mucosa cells. Following the parameters of the Effective Practices in Public Health Project (EPHPP), five manuscripts reached moderate and strong scores, and four studies were categorized as weak at final rating. In the meta-analysis, statistically significant difference was detected in micronucleated cells in children before and after radiographic examinations (SMD = 0.96, 95% CI, 0.07-1.84, p = .04), with τ2=1.09; χ2=53.37, and p < .001. CONCLUSION: Radiographic examinations in children can cause genotoxic and cytotoxic damage in the oral epithelium with a large effect size.

The use of micronucleus assay in oral mucosa cells as a suitable biomarker in children exposed to environmental mutagens: theoretical concepts, guidelines and future directions.

In the last decades, the micronucleus assay has been recognized as a suitable biomarker for monitoring populations exposed to many different occupational factors, lifestyle, environmental conditions, radiation exposure, and deleterious effects of pesticides. The objective of this work is to direct the design of future field studies in the assessment of the risk of children exposed to environmental mutagens, radiation, and pesticides. This review sought available information on the analysis of micronuclei in oral cells in children. A literature search for papers investigating DNA damage, genetic damage, oral cells, buccal cells, genotoxicity, mutagenicity and micronucleus was begun in 2000 and is scheduled to be concluded in May, 2022. Briefly, a search of PubMed, MEDLINE, and Google Scholar for a variety of articles was performed. The results showed that there are still few studies that addressed micronuclei of oral cells in children exposed to the most diverse environmental conditions. Only environmental pollution was associated with damage to the genome of oral cells in children. Therefore, researchers need to be calibrated in cell analysis, standardization of field study protocols and the development of new research in the evaluation of children using the micronucleus test as a tool in child biomonitoring.

Assessment of genotoxicity of glass ionomer cements: a systematic review.

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.

Is micronucleus assay in oral exfoliated cells a useful biomarker for biomonitoring populations exposed to pesticides? A systematic review with meta-analysis.

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.

No association between dopamine D2 receptor (DRD2) alleles and crack/cocaine dependence in Brazilians

INTRODUCTION: The causal mechanisms behind crack/cocaine use are still unknown, but genetic influences are suggested. OBJECTIVE: To investigate the relationship between the genetic polymorphism TaqI (rs1800497) in the dopamine D2 receptor (DRD2) gene and susceptibility to crack/cocaine dependence in a group of addicts to crack/cocaine and a non-addicted group. METHODS: The case group (n=515) was composed of crack/cocaine-dependent men and the control group (n=106) comprised men who were considered not dependent on crack/cocaine. The oral hygiene habits, decayed, missing, and filled teeth index, gingival index, and plaque index were evaluated. The reference single nucleotide polymorphism (rs1800497 C/T) of the DRD2 gene was genotyped by a real-time polymerase chain reaction technique. Student's t-tests for independent samples or the non-parametric Mann-Whitney test were used to compare groups regarding quantitative variables. RESULTS: The case group showed a mean time of 9.91±7.03 years of crack use, and 61.06±92.96 stones/week. The socio-demographic profile of the sample was White, single men, with basic education, blue-collar worker, smoker, and reporting alcohol use. There was a high frequency of gingival inflammation, plaque accumulation, and caries experience. For all genetic models tested, there was no significant difference in the genotypic frequency in rs1800497 of the DRD2 gene, between case and control groups (p>0.05). CONCLUSION: The genetic variant in the DRD2 did not increase the vulnerability to develop crack/cocaine dependence. The complex genetic nature of crack/cocaine dependence and a large variation of DRD2 allele frequencies, depending on the population group sampled, could be one explanation for the no association.

Is micronucleus assay in oral exfoliated cells a suitable tool for biomonitoring children exposed to environmental pollutants? A systematic review.

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.

Does Panoramic X-ray Induce Cytogenetic Damage to Oral Cells? A Systematic Review With Meta-analysis.

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.

Inhibition of Toll Like Signaling Pathway Is Associated With Genomic Instability in Rat Liver Exposed to Crack Cocaine.

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.

Genotoxicity, oxidative stress, and inflammatory response induced by crack-cocaine: relevance to carcinogenesis.

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.

Cytopathological Changes Induced by the Crack Use in Oral Mucosa.

AIMS: To evaluate cytological alterations, inflammation, and microbial charge of the oral mucosa epithelium in crack users in in terms of the amount and duration of use. METHODS: Two hundred thirty four crack users (case group) and 120 non-users (control group) participated in this study. Clinically healthy epithelial cells were collected from the posterior mouth floor, using the conventional exfoliative cytology. Some of the aspects evaluated were as follows: Papanicolaou classification, nuclear area (NA), cytoplasmic area (CA), nuclear/cytoplasmic area ratio (NA/CA), inflammation, microbial charge, keratinization, enucleated superficial cells, and binucleation. RESULTS: The average time of crack consumption was 9.8 years (±7.1) and the average quantity of use was 13.97 g/week (±18.5). The average NA values and NA/CA ratio were increased and CA values were decreased in the case group compared to those in the controls (p < 0.05). Papanicolaou class II, intense inflammation, and intense microbial charge were more prevalent in the case group than in the controls (p < 0.05). There was a significant association between high quantity of smoked crack rocks per week and increased CA values, absence of keratinization, and presence of enucleated superficial cells (p < 0.05). CONCLUSION: Crack use seemed to induce inflammatory alterations and early indicators of malignant transformation on the oral mucosa epithelium.