ABSTRACT
The aim of this study was to evaluate for the cytotoxicity, genotoxicity and antioxidant/oxidant activity of GYZ on human peripheral blood lymphocytes (PBLs). Guaiazulene (GYZ) was added into culture tubes at various concentrations (0-400 µg/mL-1). Cytotoxicity against the human lymphocytes cultures was examined by lactate dehydrogenase (LDH) release assay. The proliferative response was estimated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Antioxidant/oxidant activity was evaluated by measuring the total oxidant status (TOS) and total antioxidant capacity (TAC) levels. Micronucleus (MN) and chromosomal aberration (CA) tests were used in genotoxicity studies. The results showed that GYZ caused cytotoxicity in the PBLs at high concentrations, but TOS level were not affected, while the level of TAC was significantly increased. GYZ also did not induce chromosomal aberrations when compared to that of the control group. Results this study clearly revealed that GYZ was not genotoxic and also increased the capacity of the antioxidant in the culture of human PBL cells. This report is first report on the impact of GYZ on human PBL cells.
ABSTRACT
Diffractaic acid (DA) is a naturally occurring depside derivative found in several lichen species. It has a wide range of important biological effects such as analgesic and antiviral properties, although its cytotoxic, cytogenetic and oxidative effects have not been investigated in human blood tissue yet. Therefore, increasing concentrations (1, 5, 10, 25, 50, 100 and 200 mgL-1) of DA was added into human whole blood cultures. 3-(4.5-dimethylthiazol-2-yl)-2.5-diphenyl tetrazolium bromide (MTT) assay was used to assess the cell viability and/or cytotoxicity and genotoxic damage potential of DA using chromosome aberration (CA) and micronucleus (MN) tests were performed. In addition, oxidative alterations were determined by the total antioxidant capacity (TAC) and total oxidant status (TOS) assays. The results revealed that DA reduced cell viability at higher concentrations than 50 mgL-1. The all tested concentrations of DA were non-genotoxic. In vitro treatments with DA led to increases of TAC levels in the cultured blood cells without changing the TOS levels as compared to the control group. Consequently, DA exhibited a significant non-mutagenic and antioxidant potential in vitro.
ABSTRACT
Tungsten (VI) oxide (WO3) nanoparticles (NPs) are used for many industrial purposes in everyday life. However, their effects on human health have not been sufficiently evaluated. Therefore, the present study was designed to investigate the toxicity potentials of various concentrations (0 to 1000 ppm) of WO3 NPs (<100 nm particle size) in cultured primary rat hepatocytes. The results of cell viability assay showed that the higher concentrations of dispersed WO3 NPs (300, 500 and 1000 ppm) caused significant (p<0.05) decreases of cell viability. Also, dose dependent negative alterations were observed in oxidative status and antioxidant capacity levels after the application of WO3 in cultured rat primary hepatocytes. The results of genotoxicity tests revealed that these NPs did not cause significant increases of micronucleated hepatocytes (MNHEPs) but increased 8-oxo-2-deoxyguanosine (8-OH-dG) levels as compared to the control culture.
ABSTRACT
The aim of this work was to investigate the genetic effects of resveratrol (RSV) at concentrations of 10, 15, 25, 40, 75 and 100 µM and its activities on the genotoxicity induced by the permethrin (PM) (200 µM). After the application of PM and RSV, separately and together, cultured human lymphocytes were assessed by chromosome aberrations (CA) and sister chromatid exchange (SCE) tests. According to results, the frequencies of CA and SCE rates in the peripheral lymphocytes were significantly increased by PM compared with the controls. However, RSV had no genotoxic effect. Furthermore, the findings revealed that PM-induced increases in the mean frequencies of both genotoxic indices were diminished by RSV in a clear dose dependent manner, indicating its protective role towards the cells from PM exerted injury. In conclusion, these effects of RSV should be considered while evaluating the possible use of RSV as a therapeutic agent.
ABSTRACT
This study was designed to investigate the effects of selenium and aflatoxin on human whole blood cultures (WBC) in relation to induction of sister-chromatid exchange (SCE). The results showed that the frequency of SCEs in peripheral lymphocytes was significantly increased by the direct-acting mutagen AFB1 (at doses 5 and 10 µM except for 1µM) compared to controls. When sodium selenite (Na2SeO3) was added alone at a molar ratio of 5x10-7 and 1x10-6, cells did not show significant increase in SCE frequency. Whereas, SCE rates induced by the various AFB1 concentrations could be significantly reduced by the presence of Na2SeO3 in a clear dose-related manner. These results indicated that selenite and AFB1 mutually antagonized their ability to cause DNA damage leading to the formation of SCEs. However, selenium didn't completely inhibit induction of SCEs by AFB1 compared to controls. This is first report describing, the protective ability of selenium againist AFB1 genotoxicity on human WBC.
ABSTRACT
The aim of this study was to investigate the effects of selenium and aflatoxin on human whole blood cultures (WBC) in relation to induction of sister-chromatid exchange (SCE). Results showed that the frequency of SCEs in peripheral lymphocytes was significantly increased by the direct-acting mutagen AFB1 (at doses 5 and 10 æM except for 1æM) compared with controls. When sodium selenite (Na2SeO3) was added at a molar ratio of 5x10-7 and 1x10-6, cells did not show significant increase in SCE frequency. Whereas, SCE rates induced by the various AFB1 concentrations could be significantly reduced by the presence of Na2SeO3 in a clear dose-related manner. These results indicated that selenite and AFB1 mutually antagonized their ability to cause DNA damage leading to the formation of SCEs. However, selenium didn't completely inhibit induction of SCEs by AFB1 compared with controls. AFB1 induced oxidative damage contributed to its genotoxicity in human WBC.