Search

Humans have been using plants in the treatment of various diseases for millennia. Currently, even with allopathic medicines available, numerous populations globally still use plants for therapeutic purposes. Although plants constitute a safer alternative compared to synthetic agents, it is well established that medicinal plants might also exert adverse effects. Thus, the present investigation aimed to assess the phytotoxic, cytotoxic, and genotoxic potential of two plants from the Brazilian Cerrado used in popular medicine, Davilla nitida (Vahl) Kubitzki, and Davilla elliptica (A. St.-Hil.). To this end, germination, growth, and cell cycle analyses were conducted using the plant model Lactuca sativa. Seeds and roots were treated with 0.0625 to 1 g/L for 48 hr under controlled conditions. The germination test demonstrated significant phytotoxic effects for both species at the highest concentrations tested, while none of the extracts produced significant effects in the lettuce growth test. In the microscopic analyses, the aneugenic and cytotoxic action of D. elliptica was evident. In the case of D. nitida greater clastogenic action and induction of micronuclei, (MN) were noted suggesting that the damage initiated by exposure to these extracts was not repaired or led to apoptosis. These findings indicated that the observed plant damage was transmitted to the next generation of cells by way of MN. These differences in the action of the two species may not be attributed to qualitative variations in the composition of the extracts as both are similar, but to quantitative differences associated with synergistic and antagonistic interactions between the compounds present in these extracts. [ABSTRACT FROM AUTHOR]

Natural products are usually considered harmless; however, these substances need to be consumed with caution. Biological assays with plant models are a suitable alternative for prospective studies to assess natural product-initiated toxicity. The aim of this study was to examine the toxic potential of leaf and flower extracts derived from Tropaeolum majus L. a widely used plant in traditional medicine. Seeds of Lactuca sativa L. were exposed to T. majus extracts and based upon the seedling growth curve values, the 50% Inhibition Concentration (IC50) was calculated and applied for cell cycle analysis exposure. Both extracts contained organic acids, proteins, amino acids, and terpene steroids. Sesquiterpene lactones and depside were detected in leaf extracts. The higher concentration tested exhibited a marked phytotoxic effect. The extracts induced clastogenic, aneugenic cytotoxic, and potential mutagenic effects. The possible relationships between the classes of compounds found in the extracts and effects on cells and DNA were determined. [ABSTRACT FROM AUTHOR]

Many of the higher plants can be genetic models for the detection of environmental mutagens. One of the species often used in monitoring environmental pollution with pesticides is onion (Alium cepa). The Allium assay (Aa) is used with a high frequency in many studies to evaluate the cytotoxic and genotoxicity effects of various chemical substances in agricultural plants. This is based on the fact that compared to using animals for testing the Aa is more cost-effective and provides a large amount of data using a simple cultivation protocol without ethical concerns. In this context, the purpose of this study was to evaluate the clastogenic potential of two pesticides (Rancona fungicide and Mospilan insecticide) in plants through the Allium assay, using onion meristematic roots as biological material. The meristematic roots were exposed for 24 h to three different concentrations of pesticides as follows: 0.5, 1, and 2 µg/mL (Rancona) and 0.05, 0.1, 0.2 µg/mL (Mospilan). The obtained results showed that the tested pesticides induced the decrease, in variable percentages, of the mitotic index (MI %) in the onion meristematic cells, in all tested variants. Thus, compared to the control variant, the values of MI in the variants exposed to the pesticide treatment were between 38-54% (Rancona), respectively 30-48% in the variants treated with Mospilan. At the same time, there was a direct correlation between the pesticides concentration and the clastogenic effect observed in onion cells, through the appearance of several types of chromosomal and nuclear aberrations: sticky, fragments, bridges and chromosomal loss; nuclear dissolution and ring chromosomes. These results suggest caution when using the tested pesticides and mandatory compliance with the concentrations recommended by the producers, to avoid negative impact on plants and environment. [ABSTRACT FROM AUTHOR]

Background/Aim: Exposure to chromium (VI) [Cr(VI)] has been postulated to be associated with the induction of cancer. In vivo studies utilizing biomarkers of genotoxic damage could aid in elucidating the mechanisms underlying the genotoxic effects of Cr(VI) and their relationship with carcinogenesis. In this study, the origin (clastogenic and/or aneugenic damage) and kinetics of micronuclei (MN) induced by Cr(VI) were investigated. Materials and Methods: Hsd:ICR female mice were divided into groups of five individuals each. MN kinetics were measured in groups treated with 20 or 25 mg/kg CrO3 intraperitoneally using acridine orange-coated slides in peripheral blood obtained from the caudal vein 0, 12, 24, 36, 48, 60, and 72 h after treatment. Whereas identification of MN with centromeric DNA (MNK+) was measured at the dose of 20 mg/kg of CrO3, using fluorescence in situ hybridization (FISH) with a centromere-specific probe in peripheral blood obtained at 0, 12, and 48 h after treatment. Control groups were administered vehicle only. Results: Total MN were quantified and the clastogenic/aneugenic effects of Cr(VI) were evaluated based on the proportion of MNK+ versus micronuclei without centromeric DNA (MNK-). There was a significant increase in MN frequencies beginning at 12 h in the Cr(VI)-treated groups demonstrating its genotoxicity. When calculating the MNK+ as a percentage of the total MN, the increase was significant beginning 12 h after treatment. Conclusion: The fact that the MNK+ and MNK-were observed at both evaluation times corroborates Cr(VI) as a genotoxic agent and demonstrates that both clastogenic and aneugenic damages are involved in the formation of MN. [ABSTRACT FROM AUTHOR]

Abstract The urbanization contributes to environment contamination, mainly by the increased vehicle traffic. This intense traffic releases in the air chemical compounds with mutagenic properties that can affect the entire ecosystem. The birds for the flight accumulate air, absorbing gases or particles. The absorption of this polluted air may be causative agent responsible for micronucleus (MN) induction in bird erythrocytes. The quantitative analysis of MN in birds can assists in the monitoring environmental quality of various places. The study aimed to quantify the MN frequency in birds and compare their variation: I) among forest fragments distant from and near to urbanization, II) among species and populations of birds and III) to find if there is a relation between vehicle traffic and MN induction. The capture of the birds took place in four forest fragments in central Brazil (two distant and two near the city) using mist nets. Blood smears were prepared with blood collected from the tarso-metatarsal vein. A total of 354 individuals were analyzed and MN were found in 52% of the individuals analyzed. All sampled birds were identified and resulted to belong to 50 different species, only 4 of which were captured in all the 4 forest fragments. The average MN frequency, regardless of bird species and sampling area, was 1.04/10,000 erythrocytes. From an overall analysis carried out on all birds, the MN frequencies were found to vary among forest fragments distant from and near to urbanization (x2 =15.513; p < 0.001) and demonstrated positive correlation between vehicle traffic intensity and the MN frequency (r = 0.988; df=2; p = 0.011). The species of birds presented variation in the amount of MN (x2 = 84.64; df=49; p = 0.001). Therefore, a restricted analysis carried out on the 4 species of birds present in all the forest fragments showed that the populations of Antilophia galeata (x2 =6.029; p = 0.014), Basileuterus culicivorus (x2 =9.53; p = 0.002), Eucometis penicillata (x2 =8.067; p = 0.005) and Myiothlypis flaveola (x2 =4.771; p = 0.029) showed difference in the MN frequency, when compared between forest fragments distant from and near to cities. The analysis demonstrated that birds living in forest areas near to the city presented higher MN frequency, probably because pollutants generated by urbanization affect birds and that the larger the vehicle traffic the greater the induced MN in the birds. Graphical abstract fx1 Highlights • Birds living near the city presented more micronuclei than those distant from it. • The higher the vehicle traffic the greater the development of micronuclei in birds. • Four bird populations presented more micronuclei in areas near the city. • The analysis of micronuclei in birds can indicate mainly air pollution. • Birds can be used as bioindicators for air quality biomonitoring. [ABSTRACT FROM AUTHOR]

Solanum lycocarpum St.-Hil popularly known as ‘fruta-de-lobo’ or ‘lobeira’ is native to the Brazilian Cerrado, and used in folk medicine due to its phytotherapic properties. The action of S. lycocarpum on the cell cycle and chromosomes in order to demonstrate whether there are aneugenic and/or clastogenic effects is unknown. Thus, this study aimed at investigating the cytotoxic and genotoxic potential of methanol and hexane extracts of S. lycocarpum on growth and cell cycle of Lactuca sativa and Allium cepa. Roots from both species were exposed for 72 hours to methanol and hexane extracts with 50, 100, and 200 µg mL-1 of S. lycocarpum. Slides were prepared by the squash technique and then analyzed to determine the mitotic index and the total of chromosomal and nuclear abnormalities. The frequencies of chromosomal and nuclear abnormalities were high and significant with a dose-dependent effect, indicating that S. lycocarpum has a cytotoxic and genotoxic action depending on the dose used on meristem cells of A. cepa and L. sativa.

Copyright of Acta Scientiarum: Biological Sciences is the property of Universidade Estadual de Maringa and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background/aim: Exposure to chromium (VI) [Cr(VI)] has been postulated to be associated with the induction of cancer. In vivo studies utilizing biomarkers of genotoxic damage could aid in elucidating the mechanisms underlying the genotoxic effects of Cr(VI) and their relationship with carcinogenesis. In this study, the origin (clastogenic and/or aneugenic damage) and kinetics of micronuclei (MN) induced by Cr(VI) were investigated., Materials and Methods: Hsd:ICR female mice were divided into groups of five individuals each. MN kinetics were measured in groups treated with 20 or 25 mg/kg CrO 3 intraperitoneally using acridine orange-coated slides in peripheral blood obtained from the caudal vein 0, 12, 24, 36, 48, 60, and 72 h after treatment. Whereas identification of MN with centromeric DNA (MNK+) was measured at the dose of 20 mg/kg of CrO 3 , using fluorescence in situ hybridization (FISH) with a centromere-specific probe in peripheral blood obtained at 0, 12, and 48 h after treatment. Control groups were administered vehicle only., Results: Total MN were quantified and the clastogenic/aneugenic effects of Cr(VI) were evaluated based on the proportion of MNK+ versus micronuclei without centromeric DNA (MNK-). There was a significant increase in MN frequencies beginning at 12 h in the Cr(VI)-treated groups demonstrating its genotoxicity. When calculating the MNK+ as a percentage of the total MN, the increase was significant beginning 12 h after treatment., Conclusion: The fact that the MNK+ and MNK- were observed at both evaluation times corroborates Cr(VI) as a genotoxic agent and demonstrates that both clastogenic and aneugenic damages are involved in the formation of MN., (Copyright © 2023, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Abstract: The purpose of this study was to further investigate the cytotoxic and genotoxic effects of dicamba and Banvel® employing the cytokinesis-block micronucleus cytome (CBMN-cyt) assay estimated by the analysis of the nuclear division index (NDI), the frequency of micronucleus (MN), nucleoplasmic bridges (NPBs), and nuclear buds (NBUDs). Besides, for mechanism of MN induction CREST anti-kinetochore antibody analysis was performed. The activities of both compounds were tested within the range of 50–500μg/ml on Chinese hamster ovary (CHO-K1) cells. Overall, dicamba and Banvel® produced a NDI dose-dependent decrease but the response was statistically significant only in cultures treated with Banvel® at a 100–500μg/ml concentration range. A dose-dependent induction of MN was observed after dicamba- and Banvel®-treatments within the 50–400μg/ml and 50–500μg/ml concentration-ranges, respectively. Induction of NPBs and NBUDs was significantly enhanced by both test compounds. The NPBs/MN ratio values found for dicamba and Banvel® were 0.04–0.11 and 0.05–0.18, respectively. Results clearly demonstrated that dicamba and Banvel® exerted both cyto- and genotoxic damage on CHO-K1 cells. Furthermore, the CBMN-cyt assay employed confirmed our previous investigations concerning the cellular and DNA damaging capabilities of dicamba and highlights that both clastogenic and aneugenic mechanisms are implicated in the MN induction. [Copyright &y& Elsevier]

Abstract: The concentrations of the benzoxazinoids (BAs), 2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one (DIMBOA) and 2,4-dihydroxy-1,4-benzoxazin-3-one (DIBOA) were determined in four selected Triticum aestivum cultivars. The impact of the cultivation period on the overall concentrations in the cultivars was determined by HPLC. Furthermore, the distribution of the two BAs was analysed in aerial and subterranean parts of the seedlings after different time periods. The highest levels were detected after 3days. Subsequently, the levels of DIMBOA declined in all cultivars (reduction between 84% and 93%), while DIBOA was not detectable after 7days. The distribution between aerial parts and roots varied substantially in the different cultivars. In addition, DIMBOA amounts, expressed in per cent, as well as in mg per seedling, were determined in one selected cultivar during the entire time course for better understanding of eventual dilution effects during plant growth. Our findings indicate that the consumption (up to several 100g) of fresh sprouts (as suggested by suppliers) may already lead to exposure levels of up to 470mg DIMBO and 190mg of DIBOA per 100g each. The potential adverse health effects of these doses are discussed. [Copyright &y& Elsevier]

Abstract: Trifluralin is a herbicide capable of interfering in mitotic cell division due to either microtubule depolymerization or alteration in the concentration of calcium ions within the cell. The aim of this study was to investigate the effects of trifluralin in Allium cepa meristematic cells, evaluating the induction mechanisms of the chromosomal and nuclear aberrations. In this study, A. cepa root tips were submitted for 24h treatment to several concentrations of this herbicide and 48h recovery post-treatment. The results showed that some concentrations of trifluralin can lead to a mitotic index inhibition, besides inducing chromosomal and nuclear alterations throughout the mitotic cycle. Some of the alterations found seem to be resulting from the herbicide action in different phases and in more than one consecutive cell cycle. [Copyright &y& Elsevier]

Abstract: Semicarbazide, mainly produced for research purposes, has been known for various reasons within foods. It occurs as one of the break-down products of nitrofurans, a group of widely used veterinary drugs, and as a break-down product of azodicarbonamide used as a flour treatment agent to improve baking properties. Furthermore, it occurs in carrageenan, a food additive (thickener). Semicarbazide was tested for genotoxicity. In this study, we present results from the flow cytometer-based micronucleus assay in peripheral blood of mice. Male CBA and Balb/C mice were intraperitoneally (i.p.) injected with semicarbazide (hydrochloride). The doses were: 0, 40, 80, 120mg/kg body weight. Blood samples were collected and the frequency of micronucleated polychromatic erythrocytes, fMPCE, and the cell proliferation, %PCE, was determined. In order to further increase the sensitivity of the test for agents with an aneugenic property, also the fMPCE restricted to micronuclei containing a high mean DNA content, was measured. Neither of the different analyses disclosed any adverse effect in either of the two mouse strains. [Copyright &y& Elsevier]

• Nickel metal is a naturally occurring element currently classified as possibly carcinogenic to humans. • Gene and Micronucleus mutation studies of nickel metal were conducted in V79 Hamster cells by following OECD guidelines. • These studies demonstrate that nickel metal does not cause gene mutations nor micronucleus mutations. • These studies do not unequivocally support respiratory carcinogenicity of nickel metal. Nickel metal is a naturally occurring element used in many industrial and consumer applications. Human epidemiological data and animal cancer bioassays indicate that nickel metal is not likely to be a human carcinogen. Yet, nickel metal is classified as a suspected human carcinogen (CLP) and possibly carcinogenic to humans (IARC). There are no reliable studies on the potential for nickel metal to induce gene and micronucleus (MN) mutations. To fill these datagaps and increase our understanding of the mechanisms underlying the lack of nickel metal carcinogenicity, gene and micronucleus mutation studies were conducted with nickel metal powder (N36F) in V79 Chinese Hamster cells following OECD 476 and 487 guidelines, respectively, under GLP. Gene mutation at the hprt locus was tested, with and without metabolic activation, after 4-h treatment with 0.05–2.5 mM nickel metal powder. Cytokinesis-block MN frequency following exposure to 0.25–1.5 mM nickel metal was tested after 4-h treatment, with and without metabolic activation, followed by a 24-h treatment without metabolic activation. In the gene mutation assay, there were modest increases in hprt mutants observed at some test concentrations, not exceeding 2.2-fold, which were either within the historical control values and/or showed no concentration-response trend. The positive controls showed increases of at least 7-fold. Likewise, no increases in the MN frequency exceeding 1.5-fold were observed with nickel metal, with no concentration-response trends. Taking these results together, it can be concluded that nickel metal is non-mutagenic and does not cause gene nor chromosomal mutations. [ABSTRACT FROM AUTHOR]