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.

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.

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.

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 µM except for 1µM) 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.