Evaluation of genotoxicity of combined soil pollution by cadmium and imidacloprid

Cadmium (Cd) is one of the important pollutants of soil and the genotoxicity of Cd-contaminated soil was studied in combination with imidacloprid. The single cell gel electrophoresis or comet assay was used to quantify DNA strand breaks as a measure of DNA damage induced by Cd and imidacloprid contamination in soil. The soil was artificially contaminated by Cd 2 h at 25℃ and were used in the comet assay. DNA damage was measured as the values of percentage of nuclei with tails, tail length, tail DNA, tail moment (TM), and Olive tail moment (OTM). DNA damages of root tips of Vicia faba increased after Cd treatment and there were dose-related increases in DNA damage measured as these parameters. However, the addition of imidacloprid further increased the DNA damage. These data confirmed the genotoxic effect of Cd to plants, and that the combined pollution with imidacloprid can enhance the genotoxicity of Cd.     

In vivo evaluation of the toxic activity and genotoxicity of the Hymenaea courbaril L.’s resin in Drosophila melanogaster

Due to the negative consequences carried by the usage of synthetic insecticides, a global interest into finding substitutes for these chemical compounds through natural products has arisen. When yielded to external attacks, plants generally produce metabolites to defend themselves. The physicochemical characteristics of this kind of compounds have allowed their usage as potential bioinsecticides. The Hymenaea courbaril L. (algarrobo) has proven to be a plant rich in metabolites with outstanding biological activity, in such a way that some of its extracts have been tested as insecticides. The goal of this study was to know the phytochemical composition of Hymenaea courbaril L.’s resin and perform evaluations in vivo of its toxic and genotoxic effects in the biological model Drosophila melanogaster. For this, two resin extracts were prepared and both a phytochemical analysis were carried out on them, having found in the ethanolic total extract the presence of terpenes, flavonoids and coumarins, while in the partial ethanolic extract only presence of terpenes and flavonoids was found. Drosophila larvae were submitted to different concentrations of the extracts and both the survival and the sexual ratio were evaluated, finding that larvae are more sensitive to the partial ethanolic extract. Subsequently, the induction of somatic mutation and mitotic recombination (SMART) was evaluated in the flies’ eyes. The most significant affectations at a genotoxic level were found when larvae were tested with the partial extract, indicating that possibly the coumarins absence makes this insect more susceptible to damages at a genetic material level.     

Long-term exposure to a pulsed magnetic field (1.5 mT, 25 Hz) increases genomic DNA spontaneous degradation

The aim of this work is to investigate whether long-term pulsed magnetic field (MF) has genotoxic activity by induction of DNA damage on DNA molecules in vitro, in the absence of repair mechanisms. Yeast genomic DNA prepared by phenol extraction from S. cerevisiae cultures and the commercial DNA molecular weight marker Hyperladder I (HL-I) were exposed to 1.5?mT peak, pulsed 25?Hz MF, 8?h/day, 16 days. The total content of DNA (undamaged and damaged DNA) decreased during the exposure of genomic DNA to MF. On day 16 of exposure the DNA content was 41?±?8.1%. In addition, the undamaged DNA decreases until 6.2?±?3.1% for unexposed control samples and until 0.3?±?0.1% for pulsed MF-treated samples at day 16 of exposure. Therefore, the pulsed MF induced at day 16 an increase of 20.7-fold more degradation of DNA molecules >10?000?bp (undamaged DNA) than that observed for unexposed control samples. However, no effect was observed for HL-I DNA marker exposures. We conclude that long-term exposure to a pulsed MF (1.5?mT peak, 25?Hz, 8?h/day, 16 days) induces an increment in the DNA spontaneous degradation of yeast genomic DNA.     

Cytotoxicity and genotoxicity of xenoclauxin and desacetyl duclauxin fromPenicillium Duclauxii (delacroix)

The duclauxin derivatives xenoclauxin and desacetylduclauxin were examined for their effects on the growth of L-1210 murine leukemia cells, on the induction of DNA repair in the rat and mouse hepatocyte primary culture (HPC/DNA repair test), and on oxidative phosphorylation in mitochondria from rat livers in comparison to duclauxin. Both derivatives inhibited the growth of L-1210 culture cells as strongly as duclauxin. Duclauxin derivatives were negative in the HPC/DNA repair test. Xenoclauxin exhibited a potent uncoupling effect accompanying a marked depression of state 3 respiration of mitochondria in a similar fashion to that of duclauxin. Desacetylduclauxin significantly inhibited the state 3 respiration without causing uncoupling of oxidative phosphorylation in mitochondria. These results strongly suggest that xenoclauxin and desacetylduclauxin fromPenicillium duclauxii are not genotoxic but are cytotoxic mainly due to their potent inhibition of ATP synthesis in mitochondria.Abbreviations DNP 2,4-dinitrophenol - ETP electron transport particles - HPC hepatocyte primary culture cells - RC respiratory control - TdR thymine deoxyribonucleotide - UDS unscheduled DNA synthesis     

Absence of a synergistic effect between moderate-power radio-frequency electromagnetic radiation and adriamycin on cell-cycle progression and sister-chromatid exchange.

In our laboratories we are conducting investigations of potential interactions between radio-frequency electromagnetic radiation (RFR) and chemicals that are toxic by different mechanisms to mammalian cells. The RFR is being tested at frequencies in the microwave range and at different power levels. We report here on the 1) ability of simultaneous RFR exposures to alter the distribution of cells in first and second mitoses from that after treatment by adriamycin alone, and 2) on the ability of simultaneous RFR exposure to alter the extent of sister chromatid exchanges (SCEs) induced by adriamycin alone. This chemical was selected because of its reported mechanism of action and because it is of interest in the treatment of cancer. In our studies, Chinese hamster ovary (CHO) cells were exposed for 2 h simultaneously to adriamycin and pulsed RFR at a frequency of 2,450 MHz and a specific absorption rate of 33.8 W/Kg. The maximal temperature (in the tissue-culture medium) was 39.7 +/- 0.2 degrees C. The experiments were controlled for chemical and RFR exposures, as well as for temperature. Verified statistically, the data indicate that the RFR did not affect changes in cell progression caused by adriamycin, and the RFR did not change the number of SCEs that were induced by the adriamycin, which adriamycin is known to affect cells by damaging their membranes and DNA.     

Genotoxic activity of some mycotoxins using the SOS chromotest

The genotoxic activity of 11 mycotoxins was investigated inEscherichia coli K 12. The induction of the SOS functionsfi A whose level of expression is monitored by means of asfi A:: lac Z operon fusion was assayed by measuring the-galactosidase activity in the PQ 37 strain. Most of these fungal metabolites did not induce SOS response in this bacterial test. Only aflatoxicol, a reduced metabolite of aflatoxin B₁ was well detected as an SOS inducer if metabolic activation was performed. Patulin, penicillic acid and viomellein are only weak inducing agents. The other fungal compounds tested failed to demonstrate a positive SOS inducing activity. Relationship between SOS chromotest, mutagenicity toSalmonella typhimurium andin vivo carcinogenicity was discussed.     

The genotoxicity of lucidin,a natural component of Rubia tinctorum L., and lucidinethylether,a component of ethanolic Rubia extracts

The genotoxic activity of lucidin (1,3-dihydroxy-2-hydroxymethyl-9,10-anthraquinone), a natural component of Rubia tinctorum L., was tested in a battery of short-term tests. The compound was mutagenic in five Salmonella typhimurium strains without metabolic activation, but the mutagenicity was increased after addition of rat liver S9 mix. In V79 cells, lucidin was mutagenic at the hypoxanthine-guanine phosphoribosyl transferase gene locus and active at inducing DNA single-strand breaks and DNA protein cross-links as assayed by the alkaline elution method. Lucidin also induced DNA repair synthesis in primary rat hepatocytes and transformed C3HI M2-mouse fibroblasts in culture. We also investigated lucidinethylether, which is formed from lucidin by extraction of madder roots with boiling ethanol. This compound was also mutagenic in Salmonella, but only after addition of rat liver S9 mix. Lucidinethylether was weakly mutagenic to V79 cells which were cocultivated with rat hepatocytes. The compound did not induce DNA repair synthesis in hepatocytes from untreated rats, but positive results were obtained when hepatocytes from rats pretreated with phenobarbital were used. We conclude that lucidin and its derivatives are genotoxic.Abbreviations DMBA 7,12-dimethylbenz(a)anthracene - HA hydroxyanthraquinones - LUE lucidinethylether - PRH primary rat hepatocytes - UDS unscheduled DNA synthesis     

Effects of homogeneous and inhomogeneous static magnetic fields combined with gamma radiation on DNA and DNA repair

The aim of this study was to reveal whether static magnetic fields (SMFs) influence the repair of radiation‐damaged DNA on leukocytes or has any effect on DNA. After 4 Gy of ⁶⁰Co‐γ irradiation, some of the samples were exposed to inhomogeneous SMFs with a lateral magnetic flux density gradient of 47.7, 1.2, or 0.3 T/m by 10 mm lateral periodicity, while other samples were exposed to homogeneous SMF of 159.2 ± 13.4 mT magnetic flux density for a time period of 0.5 min, 1, 2, 4, 6, 18, 20, or 24 h. Another set of samples was exposed to the aforementioned SMFs before gamma irradiation. The following three groups were examined: (i) exposed to SMF only, (ii) exposed to SMF following irradiation by ⁶⁰Co‐γ, and (iii) exposed to SMF before ⁶⁰Co‐γ irradiation. The analysis of the DNA damage was made by single‐cell gel electrophoresis technique (comet assay). Statistically significant differences were found at 1 h (iSMF), 4 h (hSMF), and 18 h (hSMF) if samples were exposed to only SMF, compared to control. When the SMF exposure followed the ⁶⁰Co‐γ irradiation, statistically significant differences were found at 1 h (iSMF) and 4 h (hSMF). If exposure to SMF preceded ⁶⁰Co‐γ irradiation, no statistically significant difference was found compared to 4 Gy gamma‐irradiated group. Bioelectromagnetics 31:488–494, 2010. © 2010 Wiley‐Liss, Inc.     

Evaluation of genotoxic and immunotoxic activities of potential glucose biosensor components: ferrocenes

Three ferrocenes used in glucose biosensor construction were tested in the aspect of genotoxic and immunotoxic activities. All three ferrocenes were not mutagenic in the standard bacterial Ames test. Equally in the Sister Chromatid Exchanges test in human lymphocyte cultures, the genotoxic action of tested ferrocenes could be excluded. However, all three significantly decreased the rate of lymphocyte proliferation and especially diminished the numbers of B-lymphocytes and NK-cells after 72 hours of in vitro culture. Marked differences between the ferrocenes in their immunotoxic activities were noticed, and we were able to select those which would be relatively safe and those which should be avoided in further investigation of the glucose biosensor construction. Our results indicate the necessity to estimate immunotoxic effects as well as genotoxic effects, especially in biosensor components potentially used in vivo