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]

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: 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]