This study combined an in vivo Transgenic Rodent Gene Mutation Assay (TGRA) and Mammalian Erythrocyte Micronucleus Test (MNT) using male MutaMouse to assess the four positive control substances recommended by the OECD test guideline no. 488: benzo[a]pyrene (B[a]P), N-ethyl-N-nitrosourea (ENU), 2,4-diaminotoluene (2,4-DAT), and ethyl carbamate (EC). The studies followed the procedures described in the OECD guidelines 488 and 474. Gene mutations were assessed in site-of-contact organs, glandular stomach and small intestine, as well as in the liver, and germ cells isolated from testes and cauda epididymis. Micronuclei were measured in peripheral blood reticulocytes by flow cytometry. B[a]P and ENU induced dose-dependent increases in gene mutations in somatic and germ cells, as well as significant increases in the micronucleus rate in peripheral blood reticulocytes. In contrast, 2,4-DAT and EC induced weak gene mutation responses in some somatic tissues, but no significant effects in germ cells. This highlights the tissue-specific responses and thus a need for differentiated assessments. All test substances induced an increase of micronuclei to different extents in peripheral blood reticulocytes. The combined TGRA-MNT protocol enabled comprehensive evaluation of gene mutation and micronucleus induction within the same study, supporting reduction in animal use for in vivo mutagenicity testing. B[a]P and ENU can be used as positive control substances for the combined TGRA-MNT approach.
India's rapid population growth positively correlates with solid waste generation. Indiscriminate disposal in unsanitary landfills is dominant, and releases hazardous contaminants, that pose genotoxic risks to humans and biota. This study evaluated DNA damage and genome instability induced by solid waste emissions of Indian origin. Following PRISMA guidelines, 36 peer-reviewed studies published until 2025 were selected. These studies reported 40 bioindicators and 56 genotoxic biomarkers, with cell lines and comet assay most frequently reported. Significant DNA strand breaks, micronucleus formation, chromosomal aberrations, nuclear abnormalities, and sperm defects in exposed models were consistently reported, often in dose- and time-dependent patterns. Random-effects meta-analysis using pooled standardized mean differences showed significant positive effect sizes for micronucleus and comet endpoints (p ≤ 0.0001), confirming increased genetic damage in exposed groups. Although substantial heterogeneity was observed (I² = 95.73% for micronucleus; 87.66% for comet), the direction of effect remained consistently positive. Risk-of-bias assessment indicated overall moderate to high methodological quality, with common reporting gaps in exposure characterization and blinding procedures. Oxidative stress and ROS generation are dominant drivers of genome instability. Signaling pathways causing DNA adduct, DNA repair impairment, epigenetic dysregulation, and mitochondrial-mediated apoptosis were other mechanisms. Despite strong evidence of somatic and germline genotoxicity, epidemiological data and quantitative exposure assessments remain inadequate. Integrated exposure monitoring, advanced molecular and epigenetic biomarkers, dose-response characterization and long-term population-level biomonitoring are needed to strengthen causal inference and human health risk assessment. Emissions from solid waste facilities in India represent a credible genotoxic hazard warranting improved waste management, and regulatory enforcement.
Microplastics (MPs) and nanoplastics (NPs) are environmental pollutants with paramount implications for aquatic ecosystems and, through that route, human health, particularly due to their oxidative stress-mediated genotoxic potential. This review is a synthesis of findings from recent studies, with emphasis on the scenario in India, on the bioavailability, toxicological risks, and cellular mechanisms of MPs and NPs (MNPs) in various organisms, separately addressing evidence from aquatic models, including marine mussels, common carp, zebrafish, rotifers, etc., and mammalian systems relying essentially on in vitro studies. Key evidence indicates that MPs adsorb persistent organic pollutants like Polycyclic Aromatic Hydrocarbons (PAHs), enhancing their bioavailability and inducing oxidative stress, immunological alterations, and developmental toxicity, which are closely associated with DNA damage and chromosome instability. As regards aquatic organisms, combined exposure to MPs and heavy metals to fish models exacerbates biochemical disruptions and immune suppression, along with oxidative stress-linked genotoxic responses such as DNA strand breaks and micronucleus formation. Zebrafish embryos exhibit microcirculation dysfunction and pathological angiogenesis upon NP exposure. Mammalian cell studies reveal size-dependent cytotoxicity, with smaller NPs causing greater oxidative damage and membrane disruption, which triggers mitochondrial dysfunction, excessive ROS production, cell-cycle arrest, and activation of DNA damage response pathways, evidenced by micronucleus formation, chromosomal abnormalities, and oxidative DNA lesions. Overall, toxicity is influenced by particle size, charge and co-contaminants, with oxidative stress emerging as the central mechanism that connects cellular toxicity to genetic damage. This review underscores the urgent need for integrated, multidisciplinary approaches to assess the environmental and toxicological risks of MNPs with special emphasis on standardized genotoxicity assessment, while informing regulatory and mitigation strategies for the future.
The Chernobyl nuclear accident of April 1986 remains the most severe nuclear disaster in human history, with long-lasting consequences for ecosystems exposed to chronic ionizing radiation. In the decades since the event, the Chernobyl Exclusion Zone has become an unintended but invaluable natural laboratory for investigating the genetic and ecological effects of persistent radiation exposure. This review synthesizes current knowledge on both immediate and long-term biological consequences observed in plants and animals inhabiting contaminated areas. Initial impacts included acute mortality, reproductive failure, and ecosystem collapse, most notably exemplified by the "Red Forest." Over subsequent years, studies revealed elevated mutation rates, chromosomal aberrations, genomic instability, and heritable genetic damage across diverse taxa. At the same time, evidence of adaptive responses has emerged, including increased antioxidant defenses, epigenetic modifications, and phenotypic changes such as melanism in amphibians. Flora and fauna within the exclusion zone illustrate the dual narrative of vulnerability to mutagenic stress and resilience through evolutionary adaptation. Comparisons with the Fukushima accident demonstrate convergent biological responses across ecosystems while highlighting the importance of context, such as terrestrial versus marine contamination and remediation strategies. Future research must integrate advanced genomic and epigenomic tools, accurate dosimetry, and long-term monitoring to clarify thresholds for harmful versus adaptive outcomes. Chernobyl thus continues to provide critical insights into radiation biology, ecological recovery, and evolutionary toxicology under conditions of chronic environmental stress.
The long-term effects of COVID-19 infection on genomic integrity, along with hematological, biochemical, and inflammatory, remain poorly understood. Viral infections, including SARS-CoV-2, are known to induce genomic instability, potentially contributing to the persistence of post-COVID-19 symptoms. This study aimed to assess genomic instability in individuals with acute and chronic post-COVID-19 conditions, alongside hematological profiles, metabolic parameters, and inflammatory markers, compared to a SARS-CoV-2-negative control group. Participants (n = 231) from southern Brazil were stratified into acute post-COVID (n = 78), chronic post-COVID (n = 79), and control groups (n = 74). DNA damage was assessed using alkaline and enzyme-modified comet assays. Oxidative lesions were detected across all groups, but no significant differences were observed among them. Correlations with biochemical markers suggest inflammation and oxidative stress as central mechanisms in post-COVID-19 pathophysiology. Hematological and biochemical analyses revealed persistent inflammation, lipid metabolism disruptions, and gender-specific alterations, such as higher levels of inflammatory markers (C-reactive protein and ferritin) and lipid abnormalities in men, whereas women exhibited distinct hematological patterns. Age-related influences on metabolic and inflammatory markers further illustrate the systemic complexity of post-COVID-19 effects. The chronic group exhibited ongoing but attenuated markers of inflammation and oxidative stress compared to the acute group. These findings suggest that genetic instability alone may not fully explain the observed clinical manifestations, emphasizing the role of persistent inflammation and metabolic dysregulation. This study provides a comprehensive view of the interplay between genomic instability, inflammation, oxidative damage, and systemic alterations in post-COVID-19 condition. It underscores the importance of a multifaceted approach to understanding disease mechanisms and the need for longitudinal studies to explore the dynamic nature of these alterations and their long-term health implications.
Asthma is a chronic, non-communicable respiratory disorder affecting approximately 262 million people worldwide, with India projected to become one of the leading countries in prevalence. Asthma is well-established as a condition of chronic inflammation of the airways and related to systemic oxidative stress, but relatively not much is known about the genomic instability associated with asthma. On the other hand, obesity is found in 650 million people worldwide and 113 million people in India. Studies reported links between asthma and obesity, which include adipose tissue dysfunction and inefficient blood monocyte efferocytosis. Obesity enhances reactive oxygen species (ROS) production and inflammation, leading to DNA lesions. Thus, the aim of this study was to assess the DNA damage and frequencies of micronuclei (MNi), nucleoplasmic bridges (NPB), and nuclear buds (NBUD) in the lymphocytes of asthma patients and obese individuals. This study evaluates the DNA damage and nuclear anomalies in (n = 435) subjects (asthma patients n = 100, asthmatic obese patients n = 131, obese n = 100 and controls n = 104). An alkaline comet assay was used to assess DNA damage and nuclear anomalies were assessed by cytokinesis block micronucleus cytome (CBMN-Cyt) assay. All subjects were recruited between the age of 20 and 60 years. The total DNA damage, MNi, and frequency of total nuclear anomalies were found to be significantly higher in asthma male and female patients, asthmatic obese male and female patients, and obese males and females in comparison to control males and females (p < 0.05). The total comet score showed a positive correlation with the frequency of total nuclear anomalies in asthma male and female patients and obese males, respectively. Overall the findings demonstrate that inflammation and oxidative stress in asthma and obesity lead to DNA damage and genomic instability.
The increasing dissemination of microplastics (MPs) in the environment and their potential adverse effects on human and animal health have raised significant concerns in the scientific community. In this context, we aimed to investigate the toxicity induced by polyethylene (PE) MPs in the blood of Swiss mice (Mus musculus), focusing on biomarkers of oxidative and nitrosative stress and genotoxicity. Thirty mice were distributed across three experimental groups: two groups intravenously inoculated with polyethylene MPs at target systemic blood concentrations of 7.1 µg/mL and 355 µg/mL, respectively, and a non-exposed control group. After five days of intravenous (single) exposure to MPs, analyses revealed particles in the blood, liver, and kidneys, indicating selective retention in these tissues. While the Comet assay demonstrated increased DNA damage in peripheral blood, corroborating the genotoxicity of MPs, biochemical analyses revealed a complex response that depended on the organ and the biomarker evaluated. In the liver, we observed a significant reduction in the oxidative stress index, a metric that integrates pro-oxidant parameters (ROS and MDA) in relation to the endogenous antioxidant activities of SOD and CAT. At the same time, in the kidneys, there was an increase in the ratio between SOD and CAT activity. In both organs, increased nitrite production suggests the induction of marked nitrosative stress. On the other hand, in the liver, MDA levels surprisingly decreased, suggesting that MPs may interfere with lipid peroxidation pathways or promote the diversion of ROS toward NO-mediated peroxynitrite formation, reducing classical lipid oxidative damage. Principal Component Analysis (PCA) and cluster analysis provided an exploratory and integrative overview of the dataset, revealing distinct biochemical patterns between the control and MP-exposed groups, with higher MP concentrations associated with more pronounced oxidative and genotoxic responses. Thus, we conclude that exposure to MPs can cause significant cellular damage, reinforcing the need for further research to understand the risks associated with MP contamination and to develop effective mitigation strategies.
Environmental contamination by heavy metals poses a significant threat to aquatic biodiversity, however, the genotoxic effects in reptiles remain poorly understood, particularly in tropical ecosystems. This study provides the first genotoxic assessment of Caiman latirostris in northeastern Brazil, integrating cytogenetic biomarkers and trace metal analysis. Twenty-eight individuals were sampled from three areas representing distinct levels of anthropogenic pressure: a preserved reference site (Farming Area - FA), a moderately impacted reservoir (Tapacura Reservoir - TR), and a highly urbanized area (Urban Area - UA). Micronucleus frequency (MNF) was significantly higher in specimens from UA compared to FA (Kruskal-Wallis, p < 0.001), indicating potential genotoxic effects associated with untreated urban effluents and metal exposure. Although no significant differences in nuclear anomalies frequency (NAF) were found among sites, a moderate positive correlation was observed between MNF and NAF (Spearman's rho = 0.56; p = 0.026). MNF showed significant positive associations with blood concentrations of aluminum (p = 0.027), chromium (p = 0.049), iron (p = 0.035), manganese (p = 0.043), and zinc (p = 0.0083). Principal Component Analysis (PCA) confirmed these patterns, with MNF aligned along the same vector direction as Al and Cr, and opposed to Fe, Mn, Zn, and Pb, revealing distinct contamination profiles. No significant correlations were found between NAF and individual metals. These findings support the use of MNF and NAF as sensitive and complementary biomarkers for genotoxicity in reptiles. The integration of biomarker responses and multivariate analysis highlights C. latirostris as an effective sentinel species for environmental monitoring. This study provides novel baseline data on cytogenetic biomarkers in crocodilians from tropical freshwater ecosystems, underscoring the need for continued ecotoxicological monitoring in human-impacted areas.
Bacterial microbiome of the respiratory tract can influence the development of respiratory diseases, including lung cancer (LC). However, establishing a causal link between certain members of the respiratory microbiota and LC is challenging. This study aimed to analyze the sputum microbiome and its association with chromosome damage in leukocytes of LC patients and healthy controls. Sputum samples from 150 LC patients and 104 healthy donors were analyzed by 16S rRNA gene sequencing. Chromosomal aberrations (CA) were assessed cytogenetically in lymphocytes. Bioinformatics analyses examined correlations between sputum microbiome profiles and chromosome damage. The sputum microbiomes of LC patients and healthy controls did not have significant indicators for the species richness index and the Faith's phylogenetic diversity, whereas the comparison index in LC patients was significantly lower than that of healthy controls. Bacterial community structures (beta diversity) were also similar in patients and controls. We showed higher abundance of Bacillus, Prevotella, Granulicatella and Bergeyella in LC patients' sputum. LC patients exhibited increased aberrant metaphases, as well as all major CA types, compared to healthy subjects. Positive associations between aberrant metaphases and bacteria from Fusobacteria phylum, genera Bacteroidetes, Leptotrichia, Lactobacillus, Macellibacteroides, Mycoplasma, Lachnoanaerobaculum, Bulleidea, and Dialister were found in LC patients. In healthy donors, CA only correlated with Anaerorhabdus and Peptococcus. Streptobacillus and Zhouia positively correlated with the proportion of aberrant metaphases in both LC patients and in healthy individuals. Specific bacterial genera in sputum associate with chromosomal damage in host cells, suggesting possible genotoxic potential of these bacteria.
This paper is part of a series of publications developed by the Latin America-Comet assay (LA-COMET) group, which emerged in 2021, during the Asociacion Latinoamericana de Mutagenesis, Carcinogenesis y Teratogenesis Ambiental Congress, to organize the LA-COMET initiative. A total of 104 alkaline comet assay publications in animal (aquatic and terrestrial) and plant models, authored by members of this group, were analyzed to determine how DNA damage under experimental and environmental exposure conditions is assessed. The manuscript reflects the broad use and versatility of the comet assay in diverse taxonomic groups (invertebrates and vertebrates), in vivo research models, and cell types (e.g., erythrocytes, branchia cells, retinal epithelial cells, peripheral blood, liver, kidney, lung, bone marrow, testicle and nasal cells). Application of the comet assay in diverse biological systems requires careful methodological standardization to ensure reproducibility and allow for comparability of results. In order to unify the evaluations of the papers, a quality score system was developed, the 'quality score comet assay' (QSca), providing values reflecting the methodological rigor of the execution of the assay. The group identified key elements when performing the comet assay and uses them as the focus for the QSca score. The LA-COMET initiative will provide opportunities to strengthen collaborative networks among Latin American countries, promoting more integrative and regionally connected research where the comet assay can be used as a reliable and reproducible tool for the assessment of DNA damage in diverse biological models.
Arsenic and bisphenol A (BPA) are widespread environmental pollutants. We have studied the nephrotoxicity of arsenite (ARS), 10 mg/L in drinking water, plus BPA, 50 µg/kg oral dose, in juvenile Sprague-Dawley rats. Animals were randomized into seven groups and exposed to the chemicals either continuously or intermittently, for 8 weeks. The parameters evaluated were urine biomarkers, histopathological and transmission electron microscopic (TEM) examinations, DNA damage (halo assay), and protein expressions. Continuous exposure to AS and BPA significantly increased urinary creatinine, albumin, and total protein, and decreased blood urea nitrogen (BUN). Histopathological and TEM data showed brush border detachment, iron accumulation, podocyte injury, increased slit diaphragm space, and collagen deposition in both exposure groups. Significantly greater DNA damage was seen in the combined-exposure group than in the other experimental groups. Combination exposure in the continuous and intermittent groups showed renal fibrosis and ferroptosis and gene expression analysis revealed a significant increase in Bax and decrease in SIRT 1. Combination exposure was more harmful than the individual exposures in causing kidney injury in these animals.
The diesel exhaust constituent 1-nitropyrene (1-NP) is classified as a probable human carcinogen and other constituents 1,8-dinitropyrene (1,8-DNP) and 3-nitrobenzanthrone (3-NBA) are classified as possible human carcinogens by the International Agency for Research on Cancer. These nitroarenes are activated by nitroreduction via nitroso- and hydroxylamino- intermediates on route to the corresponding amine product(s). Two types of DNA adduct can occur in this sequence. First, the hydroxylamino- intermediate can undergo sulphonation or acetylation giving rise to a strong leaving group so that stable covalent adducts can form. Second, back oxidation of these air sensitive intermediates can give rise to reactive oxygen species and nitrogen species (ROS, RNS) so that oxidatively damaged bases can form. Human aldo-keto reductases AKR1C1, AKR1C2 and AKR1C3 play prominent roles in the nitroreduction of these nitroarenes in human lung cell lines. We now report that when AKR1C1-AKR1C3 are transfected into V79-4 cells we observe a significant increase in HPRT gene mutation. The mutation is dependent on AKR1C enzyme activity since isoform specific inhibitors reduced the number of mutant colonies formed. ROS scavengers reduced the number of mutant colonies formed with 1-NP, 1-8-DNP and 3-NBA in the presence of transfected AKR1C1. Ethyl gallate and the superoxide dismutase mimetic (MnTBAP) reduced the number of mutant colonies formed. Nitric oxide scavengers, 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazoyl-1-oxy-3-oxide and uric acid, also reduced the number of mutant colonies formed. Our results suggest that both 8-oxo-dG and 8-nitro-dG lesions may contribute to the mutation observed. Since AKR1C1-AKR1C3 are potently induced by NRF2, its activation might increase the mutagenicity of nitroarenes in the context of diesel exhaust exposure.
The DNA damage response (DDR) is crucial for maintaining genomic stability and preventing cancer development. Base excision repair (BER) and nucleotide excision repair (NER) play key roles in correcting oxidative and bulky DNA lesions, respectively. Alterations in these mechanisms have been implicated in breast and colorectal cancers (CRC), affecting both tumorigenesis and therapeutic responses. We have evaluated BER and NER activities in 85 cancer patients (58 breast cancer, 27 CRC) and 31 healthy controls. We used a comet assay-based approach to assess DNA repair capacity in peripheral blood lymphocytes. At diagnosis, patients exhibited lower BER and NER activities compared to controls, which suggests that impaired DNA repair mechanisms may contribute to cancer development. Following treatment, an overall increase in repair activity was observed, indicating cellular adaptation to therapy-induced DNA damage. This increase was greater in patients who later experienced relapse or metastasis, which suggests a possible link between enhanced repair capacity and treatment resistance. Our results also showed an interplay between BER and NER mechanisms, with their simultaneous activation potentially contributing to treatment resistance by enhancing tumour cell survival. These findings highlight the dual role of BER and NER in cancer progression and therapy outcomes, reinforcing their potential as biomarkers for predicting treatment response. Understanding the regulatory dynamics of these pathways may provide a foundation for improved personalized cancer treatment strategies.
The cytokinesis-block micronucleus (CBMN) assay is widely used for biomonitoring populations exposed to ionizing radiation as a simpler alternative to the chromosomal aberration (CA) assay. However, evidence regarding the concordance of these two assays under chronic low-dose occupational exposure remains limited and inconsistent. This study aimed to systematically evaluate the agreement and diagnostic performance of the micronucleus (MN) assay relative to the CA assay in a cohort of medical radiation workers chronically exposed to low doses. In this cross-sectional study, we analyzed 1226 concurrent MN and CA test results from 321 medical radiation workers. Both assays were performed on the same blood sample from each participant in accordance with national standards (GBZ/T 248-2014; GBZ/T 328-2023). Agreement between the two assays was assessed using Cohen's kappa statistic, and diagnostic performance (sensitivity, specificity, AUC) was assessed across MN thresholds ranging from 1 ‰ to 6 ‰. Although the MN and CA assays were statistically associated (χ² = 8.73, p = 0.003), their agreement was only slight (κ = 0.08). The MN assay showed poor diagnostic accuracy (AUC = 0.579). At the conventional 6 ‰ threshold, the MN assay demonstrated high specificity (91.2 %) and a high negative predictive value (NPV > 95 %), but very low sensitivity (19.7 %) and a low positive predictive value (PPV) of approximately 11 %. The MN assay shows limited concordance and diagnostic accuracy compared with the CA assay under chronic low-dose exposure conditions and therefore cannot be recommended as a standalone substitute. However, its consistently high NPV supports its use as an efficient rule-out tool within a tiered surveillance strategy, where negative MN results reliably exclude CA-detectable chromosomal damage and positive results trigger confirmatory CA testing.
Arsenic is a prevalent environmental contaminant recognized for its detrimental effects on several biological systems, particularly the male reproductive system. Although genotoxic effects linked to arsenite (As) exposure have been shown in various cell and tissue types, research concerning the male reproductive system is limited. In this study, the cytotoxic, apoptotic, and genotoxic effects of As exposure were evaluated using in vitro assays in TM3 Leydig cells, cells that play a critical role in testicular function. Leydig cells were exposed to increasing As concentrations (1, 2, 4, and 6 µM) for 24 h. Cell viability, oxidative stress (ROS production, SOD, CAT, GPx, and GSH levels), apoptosis (propidium iodide/Hoechst double fluorescent staining), and genotoxicity (micronucleus, comet, and chromosomal aberration tests) were analyzed. The administration of As markedly diminished cell viability in a concentration-dependent manner and inhibited antioxidant enzyme activity, resulting in a redox imbalance. An increase in the rate of apoptotic cells was noted in parallel to the As concentration. Genotoxicity analyses revealed an elevation in DNA damage, chromosomal aberrations, and micronucleus formation. In conclusion, As induces multifaceted toxic effects in TM3 Leydig cells by disrupting the oxidative balance, triggering apoptosis, and damaging genome integrity. This is the first in vitro study demonstrating genotoxicity of As in TM3 cells and offers an important contribution to the literature on male reproductive toxicity.
The widespread use of benzalkonium chloride (BAC) as a disinfectant necessitates a thorough evaluation of its toxicity. This study investigated the cytotoxic and genotoxic effects of BAC, alongside its recovery potential, using the Allium cepa test system. Roots were exposed to 5, 15, and 30 mg/L BAC for 24 and 48 h. EC₅₀ values were initially determined by linear interpolation as 38.3 mg/L (24 h) and 28.0 mg/L (48 h); a supplementary four-parameter nonlinear regression (Hill sigmoid model) yielded 31.79 mg/L (95 % CI: 18.56-45.03; R² = 0.9993) and 27.66 mg/L (95 % CI: 19.87-35.44; R² = 0.9995), respectively, confirming the robustness of dose selection. Cytogenetic analysis revealed significant, dose-dependent decreases in mitotic index and alterations in mitotic phase distribution. BAC induced clastogenic and aneugenic effects, manifesting as significant increases in C-mitosis, anaphase bridges, chromosome breakages, and stickiness. Micronucleus formation was statistically significant only at 30 mg/L after 24 h (p = 0.521 at 48 h). Roots transferred to distilled water for recovery demonstrated persistent mitotic suppression and genomic instability, indicating that BAC inflicts irreversible damage exceeding cellular repair capacity. These findings establish that BAC possesses significant genotoxic and cytotoxic hazard potential for non-target eukaryotic organisms.
This cross-sectional study evaluated dietary and lifestyle factors potentially contributing to DNA damage, cytokinetic defects, proliferative potential, and cell death among gym users in Brazil and Spain. We assessed demographic data, exercise habits, and nutrient estimated intake in 127 Brazilians and 101 Spaniards (≥18 years). DNA damage (micronuclei and/or nuclear buds), cytokinetic defects (binucleated cells), proliferative potential (normal cell frequency), and cell death (condensed chromatin, karyorrhexis, pyknotic, and karyolytic cells) were evaluated using the buccal micronucleus cytome assay (BMCyt). Multivariate analysis using partial least-squares discriminant analysis (PLS-DA) revealed significant discrimination between populations (AUC=0.976, sensitivity=90 %, specificity=95 %). Brazilians showed higher estimated carbohydrate consumption (220.9 vs 182.8 g/day, p = 0.001) and increased cell death markers, particularly karyorrhexis cells (p < 0.001; r = 0.94). Spaniards exhibited higher estimated intake of protein (121.1 vs 89.5 g/day), vitamins E and C, and manganese (all p < 0.001), with lower cellular damage frequencies. Results suggest a higher estimated intake of dietary antioxidants may provide protective effects against cytotoxic damage in different cultural contexts.
Type 1 diabetes (T1DM), an autoimmune disease, is the result of damage to pancreatic beta cells, and causes prolonged hyperglycaemia. In males, diabetic hyperglycaemia can perturb sperm morphology and motility, reduce semen volume, and lower fertility. We have investigated the protective effects of dimethyl itaconate (DMI) on diabetes-induced germ cell damage in male SD rats. Diabetes was induced with streptozotocin and animals with blood glucose levels ≥ 250 mg/dL were included in the study. DMI was administered orally for four weeks. Testicular damage was evaluated by examining morphology, oxidative stress, inflammation, and hormonal levels. Diabetes increased oxidative stress (elevated MDA, reduced GSH levels), decreased sperm count and motility, and increased abnormal sperm morphology and fragmented sperm DNA. It also altered the expressions of key proteins in rat testes, including increased 8-OHdG, Caspase-3, p-NF-κB p65 and IL-6, and decreased 3β-HSD, Nrf2, HO-1 and SOD-1. DMI treatment significantly ameliorated these effects, demonstrating its protective role against diabetes-induced germ cell damage in rats.
This study assessed the water quality of the Capibaribe River, a major water resource in the state of Pernambuco, Northeastern Brazil. In vivo toxicogenetic analyses were conducted using the Comet assay in Drosophila melanogaster, together with physicochemical assessments at four sampling points along the river. Genotoxicity analyses revealed a progressive increase in DNA damage that corresponded to the degree of urbanization along the river. The lowest Damage Index (DI) was recorded at point P1, in the municipality of Paudalho (DI = 35.67), an environmental protection area. The highest DI levels were observed along the two most urbanized stretches of Recife (DI = 68.67), at points P3 and P4. At these sites, concentrations of Total Dissolved Solids (TDS), chloride, sulfate, phosphate, and nitrate exceeded the limits set by the Brazilian National Council for the Environment (CONAMA). Additionally, elevated levels of sulfur (S), aluminum (Al), potassium (K), sodium (Na), phosphorus (P), and magnesium (Mg), elements known to cause genetic damage, were also detected. These findings underscore the importance of assessing genotoxic effects in model organisms, particularly in the more urbanized stretch of the Capibaribe River. They also highlight the urgent need for pollution control measures, continuous monitoring, and the implementation of strict environmental policies to safeguard both human and environmental health.
Computed tomography (CT) is a widely used diagnostic imaging modality that contributes significantly to human healthcare. Despite the advantage, its extensive use increased concerns due to receiving radiation doses to pediatric patient's over adults during CT imaging. We evaluated the biological effects (Gamma-H2AX (γ-H2AX) foci and micronucleus (MN) formation) of low-dose X-radiation on the peripheral blood lymphocytes of pediatric (n = 45) and adult (n = 38) participants before and after CT imaging. Participant-specific organ doses were calculated using VirtualDose™CT software, weighted to the corresponding organ's blood volume, summed to derive the blood dose, and then related to induced DNA damage. A significant (p < 0.001) increase in γ-H2AX foci and MN frequencies was observed in both pediatric and adult groups after CT imaging. While the mean effective dose (ED) in pediatric and adult (16.21 ± 11.33 mSv and 31.30 ± 16.25 mSv) participants were significantly different (p < 0.001), the mean blood doses did not differ (9.83 ± 6.34 mGy and 12.82 ± 5.96 mGy) (p > 0.05), respectively. A weak correlation was observed between the induced DNA damage to that of ED and blood dose. The results suggest that damage to blood lymphocytes after CT imaging was observed by an increased γ-H2AX foci result of DNA double-strand breaks. The increase in MN frequency suggests activation of DNA repair, thereby contributing to minimal damage, although they are unstable. Therefore, it is necessary to follow up on the pediatric participants to look for stable aberrations to better relate DNA damage to exposure and long-term health effects, if any.