Agrochemicals are substances used to prevent, destroy, or mitigate any pest. Their indiscriminate use can cause serious problems in ecosystems, contaminating surface and groundwater and affecting surrounding biota. However, in the environment, various natural processes such as biological degradation and photodegradation can mitigate their persistence and, consequently, their ecotoxicological impact. In this regard, this study aimed to obtain relevant data on the cytotoxic effects produced by pesticides on bioindicator plants. As observed in the literature review, cellular inhibition, nuclear anomalies, and micronucleus index are some of the different impacts commonly known from pesticides. These chemical substances can cause cytogenetic alterations in a plant bioassay. Plant bioindicators such as Allium cepa L, Vicia faba L, Pisum sativum L, Lactuca sativa L, and Lens culinaris Med are very important and effective experimental models for identifying the cytogenotoxicity of pesticides. These have been available for many years. However, they are still used today for their effectiveness in detecting and monitoring chemical substances such as agrochemicals.

Senataxin is an evolutionarily conserved DNA/RNA helicase, whose dysfunctions are linked to neurodegeneration and cancer. A main activity of this protein is the removal of R-loops, which are nucleic acid structures capable to promote DNA damage and replication stress. Here we found that Senataxin deficiency causes the release of damaged DNA into extranuclear bodies, called micronuclei, triggering the massive recruitment of cGAS, the apical sensor of the innate immunity pathway, and the downstream stimulation of interferon genes. Such cGAS-positive micronuclei are characterized by defective membrane envelope and are particularly abundant in cycling cells lacking Senataxin, but not after exposure to a DNA breaking agent or in absence of the tumor suppressor BRCA1 protein, a partner of Senataxin in R-loop removal. Micronuclei with a discontinuous membrane are normally cleared by autophagy, a process that we show is impaired in Senataxin-deficient cells. The formation of Senataxin-dependent inflamed micronuclei is promoted by the persistence of nuclear R-loops stimulated by the DSIF transcription elongation complex and the engagement of EXO1 nuclease activity on nuclear DNA. Coherently, high levels of EXO1 result in poor prognosis in a subset of tumors lacking Senataxin expression. Hence, R-loop homeostasis impairment, together with autophagy failure and unscheduled EXO1 activity, elicits innate immune response through micronuclei formation in cells lacking Senataxin.

Microplastics (MPs) are present in ambient air in a respirable size fraction; however, their potential impact on human health via inhalation routes is not well documented. In the present study, methods for a lab-scale generation of MPs from regularly used and littered plastic articles were optimized. The toxicity of 11 different types of MPs, both commercially purchased and in-lab prepared MPs, was investigated in lung epithelial cells using cell viability, immune and inflammatory response, and genotoxicity endpoints. The underlying mechanisms were identified by microarray analysis. Although laborious, the laboratory-scale methods generated a sufficient quantity of well characterized MPs for toxicity testing. Of the 11 MPs tested, the small sized polyethylene terephthalate (PETE) MPs prepared from disposable water bottles induced the maximum toxicity. Specifically, the smaller size PETE MPs induced a robust activation of the interferon signaling pathway, implying that PETE MPs are perceived by cells by similar mechanisms as those employed to recognize pathogens. The PETE MPs of heterogenous size and shapes induced cell injury, triggering cell death, inflammatory cascade, and DNA damage, hallmark in vitro events indicative of potential in vivo tissue injury. The study establishes toxicity of specific types of plastic materials in micron and nano size.

BACKGROUND: Previous studies reported that lead (Pb) exposure induced adverse health effects at high exposure concentrations, however, there have been limited data on sensitivity comparisons among different health outcomes at low blood Pb levels.
OBJECTIVE: To compare sensitivity between blood parameters and a genotoxic biomarker among workers exposed to low blood Pb levels (< 20 µg/dl), and to estimate a benchmark dose (BMD).
METHODS: Pb-exposed workers were recruited from a lead-acid storage battery plant. Their blood lead levels (BLLs) were measured. Blood parameters and micronuclei (MN) frequencies were determined. Multivariate linear or Poisson regression was used to analyze relationships between blood parameters or MN frequencies with BLLs. Two BMD software were used to calculate BMD and its 95 % lower confidence limit (BMDL) for BLLs.
RESULTS: The median BLL for 611 workers was 10.44 µg/dl with the 25th and 75th percentile being 7.37 and 14.62 µg/dl among all participants. There were significantly negative correlations between blood parameters and BLLs. However, MN frequencies correlated positively with BLLs (all P<0.05). Results from the two BMD software revealed that the dichotomous model was superior to the continuous model, and the BMDL for BLL derived from red blood cell (RBC) was 15.11 µg/dl, from hemoglobin (HGB) was 8.50 µg/dl, from mean corpuscular hemoglobin (MCH) was 7.87 µg/dl, from mean corpuscular hemoglobin concentration (MCHC) was 3.98 µg/dl, from mean corpuscular volume (MCV) was 11.44 µg/dl, and from hematocrit (HCT) was 6.65 µg/dl. The conservative BMDL obtained from the MN data was 7.52 µg/dl.
CONCLUSIONS: Our study shows that low dose Pb exposure caused decrease of blood parameters and increase of MN frequencies. The genotoxic biomarker was more sensitive than most blood parameters. BMDLs for BLL derived from MN frequencies and the red blood cell indicators should be considered as new occupational exposure limits. Our results suggest that MN assay can be considered as a part of occupational health examination items.

UNASSIGNED: Nowadays people are exposed to radiation due to various reasons, including natural, diagnostic, occupational or accidental exposure. High level of exposure to ionizing radiation can be fatal to human body. Synthetic drugs used to prevent radiation-induced damage are toxic in nature. Recently, Herbal drugs are being screened as an alternative due to their mechanism of action. Garcinia indica (G. indica) is one of the traditional medicinal plant which contains phytochemicals having several medicinal properties.
UNASSIGNED: In this study, G. indica extract was observed for its modulatory effect against 3 Gray (Gy) gamma radiation-induced damages in human peripheral blood lymphocytes. Various concentrations of G. indica extract ranging from 1 to 25 µg/mL was added to the blood post irradiation at 0 hr. Chromosomal aberration (CA) and Cytochalasin B blocked Micronuclei Cytome (CBMN) Assay were performed as per standard procedure.
UNASSIGNED: Radiomodulatory effect of Garcinia indica fruit rind extract (GIFRE) on CA and MN formation was observed in this study. Treatment of GIFRE did not affect the mitotic index. Positive inhibition percentages for dicentrics, total chromosomal aberrations and micronuclei were observed except for one instance.
UNASSIGNED: Owing to the various properties of Garcinia extracts, it makes it a potential candidate to be tested for its radiomodulatory effect. Based on the results observed in this preliminary study, it could act as a radiomodulatory agent. Radiomodulatory effect of GIFRE could possibly serve it as a potential herbal medicinal alternative to current drugs. However, results of this study need to be validated on larger sample size.

The extraction and burning of coal release genotoxic pollutants, and understanding the relationship between genetic damage and the spatial distribution of residences in coal-using regions is crucial. The study aimed to conduct a spatial analysis of genotoxic damage through the of micronuclei (MNs) number and their proximity to coal mining/burning in the largest coal exploration region in Brazil. In this study, the detection of genotoxic damage was performed using the MN assay in oral cells of residents exposed to coal mining activities. Spatial analysis was conducted using QGIS 3.28.10 based on information obtained from a questionnaire administered to the population. Multiple linear regression analysis was carried out to assess the influence of the distance from residential areas to polluting sources on the number of MNs found. Additionally, Spearman\'s correlation was performed to identify the strength and direction of the association between the frequency of MNs and each of the polluting sources. A total of 147 MNs were quantified among all participants in the coal mining region. Notably, residents living within 2 km and 10 km of pollution sources exhibited the highest prevalence of MNs. The analysis demonstrated a significant correlation between closer proximity to pollution sources and increased MN frequency, underscoring the spatial relationship between these sources and genotoxic damage. Environmental pollutants from anthropogenic sources present a major health risk, potentially leading to irreversible damage. The spatial analysis in this study highlights the importance of targeted public policies. These policies should aim for a sustainable balance between economic development and public health, promoting effective measures to mitigate environmental impacts and protect community health.

Per- and polyfluoroalkyl substances (PFAS) comprise many chemicals with strong carbon-carbon and carbon-fluorine bonds and have extensive industrial applications in manufacturing several consumer products. The solid covalent bonding makes them more persistent in the environment and stays away from all types of degradation, naming them \'forever chemicals.\' Zebrafish (Danio rerio) was used to evaluate the genotoxic and cytotoxic effects of legacy PFAS, Perfluorooctane sulfonate (PFOS), and its alternatives, such as Perfluoro-2-methyl-3-oxahexanoic acid ammonium (GenX) and 7H-Perfluoro-3,6-dioxa-4-methyl-octane-1-sulfonic acid (Nafion by-product 2 [NBP2]) upon single and combined exposure at an environmental concentration of 10 µg/L for 48-h. Erythrocyte micronucleus cytome assay (EMNCA) revealed an increased frequency of micronuclei (MN) in fish erythrocytes with a significant increase in NBP2-treated fish. The order of genotoxicity noticed was NBP2 > PFOS > Mixture > GenX in D. rerio. Fish exposed to PFOS and its alternatives in single and combined experiments did not cause any significant difference in nuclear abnormalities. However, PFOS and combined exposure positively inhibit cytokinesis, resulting in an 8.16 and 7.44-fold-change increase of binucleated cells. Besides, statistically, increased levels of reactive oxygen species (ROS) and malondialdehyde (MDA) content indicate oxidative stress in D. rerio. In addition, \'forever chemicals\' resulted in cytotoxicity, as evident through changes in nucleus width to the erythrocyte length in NBP2 and mixture exposure groups. The findings revealed that PFAS alternative NBP2 is more toxic than PFOS in inducing DNA damage and cytotoxicity. In addition, all three tested \'forever chemicals\' induced ROS and lipid peroxidation after individual and combined exposure. The present work is the first to concern the genotoxicity and cytotoxicity of \'forever chemicals\' in the aquatic vertebrate D. rerio.

Micronucleus (MN) cell counting emerged in 1973-1975 as a valid alternative for characterizing chromosomal damage caused by different agents. It was first described in mammals, but its application was rapidly extended to other vertebrates, mainly fish. However, it was not until 28 years later that this test was implemented in studies on reptiles. Nowadays, reptiles are found to be excellent non-target species from environmental contamination exposure and MN test has become a fundamental tool for analyzing genotoxic effects induced by various xenobiotics. In this article we provide an updated review of the application of the MN test in reptile species, from an ecotoxicological perspective. Therefore, we present (I) a bibliometric analysis of the available research on genotoxic-induced MN formation in reptile species; (II) the use of reptiles as sentinel organisms in ecotoxicological studies; and (III) the strength and weakness of the application of the MN test in this group. With this review, we aim to provide a comprehensive view on the use of the MN test in ecotoxicology and to encourage further studies involving reptile species.

Glyphosate is the most widely used systemic herbicide. There is ample scientific literature on the effects of this compound and its metabolite aminomethylphosphonic acid (AMPA), whereas their possible combined genotoxic action has not yet been studied. With the present study, we aimed to determine the level of genomic damage caused by glyphosate and AMPA in cultured human lymphocytes and to investigate the possible genotoxic action when both compounds were present at the same concentrations in the cultures. We used a micronuclei assay to test the genotoxicity of glyphosate and AMPA at six concentrations (0.0125, 0.025, 0.050, 0.100, 0.250, 0.500 μg/mL), which are more realistic than the highest concentrations used in previous published studies. Our data showed an increase in micronuclei frequency after treatment with both glyphosate and AMPA starting from 0.050 μg/mL up to 0.500 μg/mL. Similarly, a genomic damage was observed also in the cultures treated with the same concentrations of both compounds, except for exposure to 0.0065 and 0.0125 μg/mL. No synergistic action was observed. Finally, a significant increase in apoptotic cells was observed in cultures treated with the highest concentration of tested xenobiotics, while a significant increase in necrotic cells was observed also at the concentration of 0.250 μg/mL of both glyphosate and AMPA alone and in combination (0.125 + 0.125 μg/mL). Results of our study indicate that both glyphosate and its metabolite AMPA are able to cause genomic damage in human lymphocyte cultures, both alone and when present in equal concentrations.

UNASSIGNED: Coal mining is a vital sector in Colombia, contributing significantly to the nation\'s economy and the development of its regions. However, despite its importance, it has led to a gradual decline in the health of mine workers and nearby residents. While the adverse health effects of open-pit coal mining on exposed individuals have been well-documented in Colombia and globally, studies investigating genetic damage in underground coal miners are lacking.
UNASSIGNED: The aim of our study was to evaluate chromosomal and genotoxic damage, in peripheral blood samples from a group of underground coal miners and residents of areas exposed to coal, in the town of Samacá, Boyacá-Colombia, and in a group of unexposed individuals by using banding and molecular cytogenetic techniques, as well as cytokinesis block micronucleus assays.
UNASSIGNED: Our results suggest that occupational exposure to coal induces chromosomal and genotoxic damage in somatic cells of underground coal miners. Chromosomal and genotoxic damage is an important step in carcinogenesis and the development of many other diseases. Our findings provide valuable insights into the effects of coal dust exposure on chromosomal integrity and genetic stability.
UNASSIGNED: Our pilot study suggests that occupational exposure to coal induces chromosomal damage in underground coal miners, highlighting the importance of validating these findings with a larger sample size. Our results highlight the need to implement prevention and protection measures, as well as educational programs for underground coal miners. Characterizing and estimating exposure risks are extremely important for the safety of people exposed occupationally and environmentally to coal and its derivatives.