Assessment of genotoxicity biomarkers in gasoline station attendants due to occupational exposure.

Gasoline station attendants are exposed to numerous chemicals that might have genotoxic and carcinogenic potential, such as benzene in fuel vapor and particulate matter and polycyclic aromatic hydrocarbons in vehicle exhaust emission. According to IARC, benzene and diesel particulates are Group 1 human carcinogens, and gasoline has been classified as Group 2A "possibly carcinogenic to humans." At gas stations, self-service is not implemented in Turkey; fuel-filling service is provided entirely by employees, and therefore they are exposed to those chemicals in the workplace during all working hours. Genetic monitoring of workers with occupational exposure to possible genotoxic agents allows early detection of cancer. We aimed to investigate the genotoxic damage due to exposures in gasoline station attendants in Turkey. Genotoxicity was evaluated by the Comet, chromosomal aberration, and cytokinesis-block micronucleus assays in peripheral blood lymphocytes. Gasoline station attendants (n = 53) had higher tail length, tail intensity, and tail moment values than controls (n = 61). In gasoline station attendants (n = 46), the frequencies of chromatid gaps, chromosome gaps, and total aberrations were higher compared with controls (n = 59). Increased frequencies of micronuclei and nucleoplasmic bridges were determined in gasoline station attendants (n = 47) compared with controls (n = 40). Factors such as age, duration of working, and smoking did not have any significant impact on genotoxic endpoints. Only exposure increased genotoxic damage in gasoline station attendants independently from demographic and clinical characteristics. Occupational exposure-related genotoxicity risk may increase in gasoline station attendants who are chronically exposed to gasoline and various chemicals in vehicle exhaust emissions.

Chromosomal Damage, Chromosome Instability, and Polymorphisms in GSTP1 and XRCC1 as Biomarkers of Effect and Susceptibility in Farmers Exposed to Pesticides.

In the department of Boyacá, Colombia, agriculture stands as one of the primary economic activities. However, the escalating utilization of pesticides within this sector has sparked concern regarding its potential correlation with elevated risks of genotoxicity, chromosomal alterations, and carcinogenesis. Furthermore, pesticides have been associated with a broad spectrum of genetic polymorphisms that impact pivotal genes involved in pesticide metabolism and DNA repair, among other processes. Nonetheless, our understanding of the genotoxic effects of pesticides on the chromosomes (as biomarkers of effect) in exposed farmers and the impact of genetic polymorphisms (as susceptibility biomarkers) on the increased risk of chromosomal damage is still limited. The aim of our study was to evaluate chromosomal alterations, chromosomal instability, and clonal heterogeneity, as well as the presence of polymorphic variants in the GSTP1 and XRCC1 genes, in peripheral blood samples of farmers occupationally exposed to pesticides in Aquitania, Colombia, and in an unexposed control group. Our results showed statistically significant differences in the frequency of numerical chromosomal alterations, chromosomal instability, and clonal heterogeneity levels between the exposed and unexposed groups. In addition, we also found a higher frequency of chromosomal instability and clonal heterogeneity in exposed individuals carrying the heterozygous GSTP1 AG and XRCC1 (exon 10) GA genotypes. The evaluation of chromosomal alterations and chromosomal instability resulting from pesticide exposure, combined with the identification of polymorphic variants in the GSTP1 and XRCC1 genes, and further research involving a larger group of individuals exposed to pesticides could enable the identification of effect and susceptibility biomarkers. Such markers could prove valuable for monitoring individuals occupationally exposed to pesticides.

Genotoxicity evaluation of food additive titanium dioxide using a battery of standard in vivo tests.

The increasing use of titanium dioxide (TiO2) nanoparticles (NPs) has raised concern about the safety of food additive TiO2. TiO2 has been considered no longer safe by EFSA due to concerns over genotoxicity, however, there are conflicting opinions upon the safety of TiO2 as a food additive, and the number of in vivo genotoxicity studies conducted on food additive TiO2 was limited. In order to investigate the potential genotoxicity of food additive TiO2, we evaluated the genotoxicity of a commercial food additive TiO2 (average size of 135.54 ± 41.01 nm, range from 60.83 to 230.16 nm, NPs account for 30% by number) using a battery of standard in vivo tests, including mammalian erythrocyte micronucleus test, mammalian bone marrow chromosomal aberration test and in vivo mammalian alkaline comet test. After 15 days of consecutive intragastric administration at doses of 250, 500, and 1000 mg/kgBW, food additive TiO2 neither increased the frequencies of bone marrow micronuclei or chromosomal aberration in mice, nor induced DNA strand breakage in rat liver cells. These results indicate that under the condition of this study, food additive TiO2 does not have genotoxic potential although it contains a fraction of NPs.

Safety assessment of high fructose corn syrup and fructose used as sweeteners in foods.

High Fructose Corn Syrup (HFCS) and Fructose (FR) are widely used sweeteners in many foods and beverages. This study aimed at investigating the cytotoxic effects of HFCS (5%-30%) and FR (62.5-2000 µg/mL) using MTT assay in Human Hepatocellular Carcinoma (HepG2) cells, and genotoxic effects of using Chromosome Aberrations (CAs), Sister Chromatid Exchanges (SCEs), Micronuclei (MN) and comet assays in human lymphocytes. HFCS significantly reduced the cell viability in HepG2 cells at between 7.5% and 30% for 24 and 48 h. 30% HFCS caused a very significant toxic effect. FR had a cytotoxic effect in HepG2 cells at all treatments. However, as fructose concentration decreased, the cell viability decreased. HFCS (10%-20%) and FR (250-2000 µg/mL) decreased the mitotic index at higher concentrations. IC50 value was found to be a 15% for 48 h. IC50 value of FR was detected as 62.5 µg/mL for 24 h and 48 h. HFCS significantly increased CAs frequency at 15% and 20%. FR significantly increased the frequency of CAs at 250, 1000, and 2000 µg/mL for 48 h. Both sweeteners increased the frequency of SCEs at all concentrations. HFCS (15% and 20%) and FR (250, 1000, and 2000 µg/mL) induced MN frequency at higher concentrations. HFCS caused DNA damage in comet assay at 10% -30%. FR increased tail intensity and moment at 125-2000 µg/mL and tail length at 62.5, 250 and 500 µg/mL. Therefore, HFCS and FR are clearly seen to be cytotoxic and genotoxic, especially at higher concentrations.

HFCS and FR exhibited cytotoxic effect at HepG2 and human lymphocytes at higher concentrations.Both sweeteners increased the frequencies of CAs and SCEs at higher concentrations.HFCS caused DNA damage at 10% -30% concentrations.HFCS (15% and 20%) and FR (250, 1000, and 2000 µg/mL) induced MN frequency.

Effect of Melissa officinalis L. leaf extract on manganese-induced cyto-genotoxicity on Allium cepa L.

Although the antioxidant properties of Melissa officinalis extract (Mox) are widely known, little work has focused on its protective capacity against heavy metal stress. The primary objective of this study was to determine the potential of Mox to mitigate manganese (II) chloride (MnCI2)-induced cyto-genotoxicity using the Allium and comet assays. Physiological, genotoxic, biochemical and anatomical parameters as well as the phenolic composition of Mox were examined in Allium cepa (L.). Application of 1000 µM MnCl2 reduced the rooting percentage, root elongation, weight gain, mitotic index and levels of chlorophyll a and chlorophyll b pigments compared to the control group. However, it increased micronuclei formation, chromosomal abnormality frequencies, tail DNA percentage, proline amount, lipid peroxidation level and meristematic damage severity. The activities of superoxide dismutase and catalase also increased. Chromosomal aberrations induced by MnCl2 were fragment, sticky chromosome, vagrant chromosome, unequal distribution of chromatin and bridge. Application of 250 mg/L Mox and 500 mg/L Mox along with MnCl2 significantly alleviated adverse effects dose dependently. The antioxidant activity bestowed by the phenolic compounds in Mox assisted the organism to combat MnCl2 toxicity. Consequently, Mox exerted remarkable protection against MnCl2 toxicity and it needs to be investigated further as a potential therapeutic option.

Eco-corona formation diminishes the cytogenotoxicity of graphene oxide on Allium cepa: Role of soil extracted-extracellular polymeric substances in combating oxidative stress.

Graphene oxide (GO) is widely acknowledged for its exceptional biological and industrial applications. However, its discharge into the environment negatively impacts the ecosystem. This study aimed to investigate the toxicity of GO in Allium cepa root tip cells and the role of extracellular polymeric substances (EPS) in modulating its toxic effects. To evaluate toxicity, various endpoints like cell viability using Evans blue dye, cytotoxicity (mitotic index), genotoxicity (chromosomal aberrations), and oxidative stress assessments (total ROS, superoxide, hydroxyl radical production, and lipid peroxidation) were considered. The results suggest that pristine GO caused a dose-dependent increase in various toxicity parameters, especially the genotoxic effects. Oxidative stress generation by GO is proposed to be the principal mode of action. The EPS-corona formed on GO could potentially counteract the toxic effects, substantially reducing the oxidative stress within the cells.

Genotoxicity assessment of titanium dioxide nanoparticles using a standard battery of in vivo assays.

As one representative of nanometal oxides, titanium dioxide nanoparticles (TiO2-NPs) have been widely used, particularly in the food industry. The genotoxicity of TiO2-NPs has attracted great attention over the years. This study was undertaken to investigate the chromosome and DNA damage effects of TiO2-NPs (0, 50, 150, and 500 mg/kg BW) using rodent models. After a comprehensive characterization, we conducted a standard battery of in vivo genotoxicity tests, including the chromosomal aberration test (CA), micronucleus (MN) test, and the comet test. The results of all these tests were negative. There were no structural or numerical chromosomal abnormalities in mice bone marrow cells, no increase in the frequency of micronucleated polychromatic erythrocytes in mice bone marrow cells, and no elevation in % tail DNA in rat hepatocytes. This indicated that TiO2-NPs did not cause chromosomal damage or have a direct impact on DNA. These findings suggested that TiO2-NPs did not exhibit genotoxicity and provided valuable data for risk assessment purposes.

Genetic and prenatal developmental evaluation of anthraquinone.

Anthraquinone is a recently identified contaminant present in teas globally, and its potential teratogenic and genotoxic impacts have yet to be fully comprehended. Hence, this study's objective was to determine anthraquinone's genotoxicity using various studies such as the Ames test, Mammalian erythrocyte micronucleus test, and in-vitro mammalian chromosome aberration study. Additionally, the study assessed its effects on maternal gestational toxicity and the fetus's teratogenicity through prenatal developmental toxicity research in rats. Results indicated that anthraquinone did not manifest mutagenic effects on Salmonella typhimurium histidine-deficient, did not cause chromosomal aberrations in Chinese hamster ovary cell subclone CHO-K1, and did not exhibit a genotoxic effect on mouse bone marrow erythrocytes. However, in the prenatal developmental toxicity study, administering anthraquinone orally to pregnant rats from day 5 to day 19 of gestation resulted in decreased body weight and food consumption of pregnant rats, along with a higher number of visceral malformations in the fetuses in the highest dose group (217.6 mg/kg BW). Additionally, two pregnant rats died in this group. The study has established the no observed adverse effect level (NOAEL) as 21.76 mg/kg BW, while the lowest observed adverse effect level (LOAEL) was 217.6 mg/kg BW.

Protective effect of quercetin and thymoquinone against genotoxicity and oxidative stress induced by ZnO nanoparticles in the Wistar rat model.

Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in a variety of consumer and other commercial products. Hence, man faces the risk of exposure to ZnO-NPs and the consequent adverse health effects. Mitigation/prevention of such effects using natural products has drawn the attention of scientists. Therefore, the aim of the present study has been to find the toxic effects associated with exposure to ZnO-NPs, and the protective role of the phytochemicals thymoquinone (TQ) and quercetin (QCT) in the rat model. ZnO-NPs were administered to male Wistar rats through oral route; TQ / QCT was concurrently administered through intra-peritoneal route. The response in the animal was analyzed adopting chromosomal aberration test, micronucleus test, and comet assay of bone marrow cells to assess the genotoxicity, and biochemical assays of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO), total extractable protein of liver, and reduced glutathione (GSH) of liver homogenate to monitor the changes in the antioxidant defense mechanism in response to the oxidative stress. Treatment of 300 mg/kg body weight (bw) of ZnO-NPs produced adverse effects on all aspects analyzed viz., structural chromosomal aberrations, micronuclei formation, DNA damage, SOD, catalase, lipid peroxidation, GSH, and extractable total protein of liver. Co-treatment of TQ / QCT offered protection against the toxicity induced by ZnO-NPs. The most optimum doses of TQ and QCT that offered the best protection were 18 mg/kg bw and 500 mg/kg bw, respectively. The study reveals that TQ / QCT supplementation is beneficial in the context of toxic effects of ZnO-NPs.

Cytotoxicity and genotoxicity evaluation of chloroform using Vicia faba roots.

Chloroform is a widely used industrial chemical that can also pollute the environment. The aims of this study were to examine the potential cytotoxicity and genotoxicity of chloroform on plant cells, using the Vicia faba bioassay. Chloroform was evaluated at concentrations of 0.1, 0.5, 1, 2, and 5 mg·L-1. The following parameters were analyzed: the mitotic index (MI), micronucleus (MN) frequency, chromosomal aberration (CA) frequency, and malondialdehyde (MDA) content. The results showed that exposure to increasing concentrations of chloroform caused a decrease in MI and an increase in the frequency of MN in Vicia faba root tip cells, relative to their controls. Moreover, various types of CA, including C-mitosis, fragments, bridges, laggard chromosomes, and multipolar mitosis, were observed in the treated cells. The frequency of MN was positively correlated with the frequency of CA in exposure to 0.1-1 mg·L-1 chloroform. Furthermore, chloroform exposure induced membrane lipid peroxidation damage in the Vicia faba radicle, and a linear correlation was observed between the MDA content and the frequency of MN or CA. These findings indicated that chloroform exposure can result in oxidative stress, cytotoxicity, and genotoxicity in plant cells.

Furan promotes cytotoxic effects through DNA damage and cell apoptosis in Leydig cells.

Furan is an organic chemical that can cause adverse effects on human health and is formed as a result of the thermal decomposition of many food components during cooking, storage, and processing techniques. Studies have shown that exposure to furan causes nephrotoxicity, hepatotoxicity, immunotoxicity, and reproductive toxicity. According to our current knowledge of the literature, the genotoxic mode of action of furan is highly controversial. The genotoxic effects of furan on the male reproductive system, however, have not been studied. In this study, the TM3 Leydig cell line was treated with 750, 1500, and 3000 µM concentrations of furan for 24 h. Following the completion of the exposure period, the cytotoxicity of furan in TM3 Leydig cells was assessed using a cell viability assay and a spectrophotometric measurement of lactate dehydrogenase (LDH) enzyme levels. The double fluorescence staining method was used to demonstrate furan-induced apoptosis, and DNA damage was shown using the micronucleus, comet, and chromosomal aberration assays. The result indicated that furan administration of Leydig cells resulted in an increase in structural chromosomal aberration, comet, and micronucleus formation, reduced cell viability, increased LDH activity, and a higher incidence of apoptotic cells. These findings revealed that furan induces DNA damage in TM3 Leydig cells, causing genotoxicity and DNA damage-induced cytotoxicity.

Lenalidomide treatment of Japanese patients with myelodysplastic syndromes with 5q deletion: a post-marketing surveillance study.

Lenalidomide was approved in Japan for the treatment of patients with myelodysplastic syndromes associated with a 5q deletion (del 5q-MDS) in August 2010. A post-marketing surveillance (PMS) study enrolled 173 patients with del 5q-MDS who started lenalidomide treatment between August 2010 and September 2011 (mean ± standard deviation [SD] age 72.4 ± 9.0 years) and observed for up to 6 cycles or 6 months. Adverse drug reactions (ADRs) and serious ADRs were reported in 78.0% and 50.9% of patients. The most commonly observed ADRs were thrombocytopenia or platelet count decreased (46.2%), neutropenia or neutrophil count decreased (42.2%), and rash (23.1%). Of 114 patients who were red blood cell transfusion-dependent at baseline, 39 (34.2%) achieved transfusion independence during lenalidomide treatment. Of 173 patients, 19 (11.0%) had confirmed acute myeloid leukemia (AML) progression during the study. Moreover, long-term follow-up (3 years) was available for 68 of the 173 patients, of whom 12 (17.6%) progressed to AML during the additional period. This PMS study investigated the safety and effectiveness of lenalidomide in patients with del 5q-MDS. No new safety concerns were noted in routine clinical use in Japan and no evidence was found for an increased risk of AML progression following lenalidomide treatment.

Chromosome damage in regions with different levels of air pollution.

Air pollution is an important environmental factor influencing human health. In this study, we compared chromosome damage in city policemen from three cities in the Czech Republic: industrial Ostrava characterized by high levels of benzo[a]pyrene, Prague with heavy traffic emitting nitrogen oxides, and relatively clean Ceske Budejovice located in an area with predominantly agricultural activity. Chromosomal aberrations in lymphocytes were evaluated by fluorescence in situ hybridization with painting probes for chromosomes 1, 2, 3, and 4 in spring and autumn. An increase in the frequency of unstable chromosome aberrations, that is, dicentric chromosomes and acentric fragments, was observed in spring samples from Ostrava (p = .014 and p = .044, respectively) and Prague (p = .002 and p = .006, respectively) in comparison with Ceske Budejovice. The difference was significant only for samples taken after the winter period, when the concentration of pollutants in the air increases due to poor dispersion conditions. An increased frequency of dicentric chromosomes was observed in spring compared to autumn in both Ostrava and Prague (p = .017 and p = .023, respectively), but not in Ceske Budejovice. More breakpoints were observed on chromosome 1 than on the other chromosomes examined (p < .001). The number of breakpoints in the heterochromatin region 1p11-q12 was lower than in other parts of chromosome 1 (p < .001), suggesting a protective function of heterochromatin against damage. Our study showed, that air pollution increased the frequency of unstable chromosome aberrations, especially dicentric chromosomes. However, we did not show an effect on stable chromosome rearrangements.

Assessment of Bio-physiological damages and cytological aberrations in cowpea varieties treated with gamma rays and sodium azide.

The assessment of mutagen induced biological damage forms an important study in determining the mutagenic potency and genotypic sensitivity, a vital aspect in mutation breeding programs. A prior assessment of lethal dose (LD50), mutagen induced biological damage (alterations in bio-physiological traits and frequency of cytological aberrations) is a prerequisite for determining an optimum mutagen dose in a successful mutation breeding experiment. Therefore, in a multi-year project of mutation breeding, two widely cultivated varieties of cowpea viz., Gomati VU-89 and Pusa-578, were treated with gamma (γ) rays and sodium azide (SA) doses. The results reflected a proportionate increase in bio-physiological damages with the increase in mutagenic doses and caused a substantial reduction in mean seed germination and seedling height. Different cytological aberrations such as cytomixis, univalents, chromosome stickiness, precocious separation, unequal separation, bridges, laggards, disturbed polarity, dyads, triads, and polyads were observed in both varieties. All the mutagen doses induced a broader spectrum of cytological aberrations with varying frequencies.

Genotoxic effect of iron oxide (Fe2 O3 ) nanoparticles on Triticum aestivum (wheat).

Industrial activities and unconscious consumption of natural resources cause environmental pollution with the rapid increase in the world population. As a result of the widespread use of iron oxide nanoparticles (Fe2 O3 NP) with nano-industrial activities, it is predicted that this NP will accumulate in the air, water, and soil. In the present study, the purpose was to find out the genotoxic effects on root meristem cells of the Triticum aestivum L. plant, which is an indicator organism exposed to 20-40 nm Fe2 O3 NPs at different concentrations (100, 200, and 400 ppm). The amount of Fe2 O3 NP accumulated in T. aestivum used in the study was determined with x-ray diffraction (XRD) spectroscopy, scanning electron microscopy (SEM), SEM element map, and EDS characteristic spectrum. All concentrations of Fe2 O3 NP caused significant decreases in the mitotic index. Fe2 O3 NPs significantly increased the frequency of mitotic abnormalities in T. aestivum root tip cells at all treatment times and all concentrations when compared to the control. Fe2 O3 NPs were formed by various mitotic abnormalities such as loss of genetic material, deconstructed prophase, adhesion, chromosome groupings in metaphase, deconstructed metaphase, C-Metaphase, chromosomal loss, chromosomal fracture, polyploidy, deconstructed anaphase, lagging chromosome, fragment, polar deviation, bridging, propagation, asynchronous division, star anaphase, multipolarity, and deconstructed telophase. All these results show that Fe2 O3 NPs are genotoxic and clastogenic and may also cause DNA damage. Briefly, these data show that Fe2 O3 NPs taken by organisms may pose a danger to the organism and the upper consumer. These findings also show that the production and use of Fe2 O3 NPs, which affect organisms, must be controlled, and ultimately, be safely disposed of to reduce their bioaccumulation. RESEARCH HIGHLIGHTS: In the present study, the purpose was to find out the genotoxic effects on root meristem cells of the Triticum aestivum L. (bread wheat) plant, which is an indicator organism exposed to 20-40 nm Fe2 O3 NPs at different concentrations (100, 200, and 400 ppm). The amount of Fe2 O3 NP accumulated in T. aestivum used in the study was determined with x-ray diffraction (XRD) spectroscopy, scanning electron microscopy (SEM), SEM element map, and EDS characteristic spectrum. The mitotic index was calculated to reveal the genotoxic effect. "Loss of genetic material, deconstructed prophase, adhesion, chromosome groupings in metaphase, deconstructed metaphase, C-Metaphase, chromosomal loss, chromosomal fracture, polyploidy, deconstructed anaphase, lagging chromosome, fragment, polar deviation, bridging, propagation, asynchronous division, star Chromosomal abnormalities such as anaphase, multipolarity, and deconstructed telophase" were visualized. Fe2 O3 NPs are genotoxic and clastogenic and may also cause DNA damage.

A study on Amygdalin's genotoxicological safety and modulatory activity in human peripheral lymphocytes in vitro.

Amygdalin (AMY), a plant secondary metabolite containing nitrile, is a major component of the seeds of Rosaceae family plants. It is known that this compound has many pharmacological activities such as cancer prevention, antipyretic, and cough suppressant. In this study, the genotoxic and modulatory effects of amygdalin were assessed by chromosomal aberration (CA), sister chromatid exchange (SCE), and cytokinesis-block micronucleus assay (CBMN) assays using human peripheral lymphocytes (HPLs) in the absence and presence of metabolic activator (S9 mix). Lymphocytes were exposed to various concentrations of amygdalin (0.86, 1.72, 3.43, 6.86, and 13.75 µg/mL) alone and in combination with mitomycin-C (MMC, 0.20 µg/mL) or cyclophosphamide (CP, 12 µg/mL). The mitotic index (MI), replication index (RI), cytokinesis-block proliferation index (CBPI), and cytostasis were also evaluated to determine cytotoxicity. Amygdalin alone did not exhibit genotoxic and cytotoxic effects at all the tested concentrations both in the absence and presence of the S9 mix. In contrast, amygdalin significantly reduced the frequencies of CA (especially at 48 h treatments), SCE, and MN (except 0.86 µg/mL in pre- and simultaneous treatment) induced by MMC in all the tested concentrations and treatment protocols. It has also considerably decreased CP-induced CA and SCE frequencies at all the concentrations (except 0.86 µg/mL) in simultaneous treatment. This study demonstrated that amygdalin alone was not genotoxic, on the contrary, it has revealed modulatory effects against chemotherapy agents that induced genomic damage in human lymphocytes, suggesting its chemopreventive potential.

DNA fragmentation and multifaceted toxicity induced by high-dose vanadium exposure determined by the bioindicator Allium test.

In this study, the toxicity of vanadium (VCI3) in Allium cepa L. was studied. Germination-related parameters, mitotic index (MI), catalase (CAT) activity, chromosomal abnormalities (CAs), malondialdehyde (MDA) level, micronucleus (MN) frequency and superoxide dismutase (SOD) activity were investigated. The effects of VCI3 exposure on the DNA of meristem cells were investigated with the help of comet assay, and the relationships between physiological, cytogenetic and biochemical parameters were revealed by correlation and PCA analyses. A. cepa bulbs were germinated with different concentrations of VCI3 for 72 h. As a result, the maximum germination (100%), root elongation (10.4 cm) and weight gain (6.85 g) were determined in the control. VCI3 treatment caused significant decreases in all tested germination-related parameters compared to the control. The highest percentage of MI (8.62%) was also observed in the control. No CAs were found in the control, except for a few sticky chromosomes and unequal distribution of chromatin (p > 0.05). VCI3 treatment caused significant decreases in MI and increases in the frequencies of CAs and MN, depending on the dose. Similarly, the comet assay showed that DNA damage scores increased with increasing VCI3 doses. The lowest root MDA (6.50 µM/g) level and SOD (36.7 U/mg) and CAT (0.82 OD240nmmin/g) activities were also measured in the control. VCI3 treatment caused significant increases in root MDA levels and antioxidant enzyme activities. Besides, VCI3 treatment induced anatomical damages such as flattened cell nucleus, epidermis cell damage, binuclear cell, thickening in the cortex cell wall, giant cell nucleus, damages in cortex cell and unclear vascular tissue. All examined parameters showed significant negative or positive correlations with each other. PCA analysis confirmed the relations of investigated parameters and VCI3 exposure.

Antigenotoxic effect of hyperoside against Mitomycin C and hydrogen peroxide-induced genotoxic damage on human lymphocytes.

Hyperoside is a flavonol glycoside isolated from various plant genera such as Hypericum and Crataegus. It has an important place in the human diet and is used medically to relieve pain and ameliorate cardiovascular functions. However, a comprehensive profile of the genotoxic and antigenotoxic effects of hyperoside is not known. The current study aimed to investigate the genotoxic and antigenotoxic effects of hyperoside against genetic damages induced by two genotoxins (MMC and H2O2) using chromosomal aberrations (CAs), sister chromatid exchanges (SCEs), and micronucleus (MN) assays in human peripheral blood lymphocytes in vitro. Blood lymphocytes were incubated with 7.8-62.5 µg/mL concentrations of hyperoside alone and simultaneously with 0.20 µg/mL Mitomycin C (MMC) or 100 µM Hydrogen peroxide (H2O2). Hyperoside did not exhibit genotoxic potential in the CA, SCE, and MN assays. Moreover, it did not cause a decrease in mitotic index (MI) which is an indicator of cytotoxicity. On the other hand, hyperoside significantly decreased CA, SCE, and MN (except for MMC treatment) frequencies induced by MMC and H2O2. Hyperoside, increased mitotic index against both mutagenic agents at 24-h treatment when compared to positive control. Our results demonstrate that hyperoside exhibited antigenotoxic effects rather than genotoxic in vitro human lymphocytes. Therefore, hyperoside may be a potential preventive agent in inhibiting chromosomal and oxidative damage induced by genotoxic chemicals.

The meta-analysis of cytogenetic biomarkers as an assessment of occupational risk for healthcare workers exposed to antineoplastic drugs.

OBJECTIVE: Antineoplastic drugs (ADs) are widely used in clinical practice and have been demonstrated to be effective in treating malignant tumors. However, they carry a risk of cytogenotoxicity for healthcare workers. Studies have reported that genotoxic biomarkers can be applied to assess the occupational health status of healthcare workers at an early stage, but results of different studies are variable. The objectives of the review were examine the association between long-term exposure to ADs and cytogenetic damage to healthcare workers. METHODS: We systematically reviewed studies between 2005 and 2021 using PubMed, Embase and Web of Science databases that used cytogenetic biomarkers to assess occupational exposure to ADs in healthcare workers. We used RevMan5.4 to analyze the tail length parameters of the DNA, frequency of the chromosomal aberrations, sister chromatid exchanges and micronuclei. A total of 16 studies were included in our study. The studies evaluate the quality of the literature through the Agency for Healthcare Research and Quality. RESULTS: The results revealed that under the random-effects model, the estimated standard deviation was 2.37 (95% confidence interval [CI] 0.92-3.81, P = 0.001) for the tail length parameters of the DNA, 1.48 (95% CI 0.71-2.25, P = 0.0002) for the frequency of chromosomal aberrations, 1.74 (95% CI 0.49-2.99, P = 0.006) for the frequency of sister chromatid exchanges and 1.64 (95% CI 0.83-2.45, P < 0.0001) for the frequency of micronuclei. CONCLUSIONS: The results indicate that there is a significant association between occupational exposure to ADs and cytogenetic damage, to which healthcare workers should be alerted.

Monitoring genotoxic, biochemical and morphotoxic potential of penoxsulam and the protective role of European blueberry (Vaccinium myrtillus L.) extract.

The present study aimed at exploring to explore the penoxsulam toxicity and protective effects of blueberry extract in roots of Allium cepa L. The effective concentration (EC50) of penoxsulam was determined at 20 µg/L by the root growth inhibition test as the concentration reducing the root length by 50%. The bulbs of A. cepa L. were treated with tap water, blueberry extracts (25 and 50 mg/L), penoxsulam (20 µg/L) and combination of blueberry extracts (25 and 50 mg/L) with penoxsulam (20 µg/L) for 96 h. The results revealed that penoxsulam exposure inhibited cell division, rooting percentage, growth rate, root length and weight gain in the roots of A. cepa L. In addition, it induced chromosomal anomalies such as sticky chromosome, fragment, unequal distribution of chromatin, bridge, vagrant chromosome and c-mitosis and DNA strand breaks. Further, penoxsulam treatment enhanced malondialdehyde content and SOD, CAT and GR antioxidant enzyme activities. Molecular docking results supported the up-regulation of antioxidant enzyme SOD, CAT and GR. Against all these toxicity, blueberry extracts reduced penoxsulam toxicity in a concentration-dependent manner. The highest amount of recovery for cytological, morphological and oxidative stress parameters was observed when using blueberry extract at a concentration of 50 mg/L. In addition, blueberry extracts application showed a positive correlation with weight gain, root length, mitotic index and rooting percentage whereas a negative correlation with micronucleus formation, DNA damage, chromosomal aberrations, antioxidant enzymes activities and lipid peroxidation indicating its protecting effects. As a result, it has been seen that the blueberry extract can tolerate all these toxic effects of penoxsulam depending on the concentration, and it has been understood that it is a good protective natural product against such chemical exposures.