The purpose of this study was to evaluate the effect of carotenoid astaxanthin (ASTA) on cultured primary rat hepatocytes treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, MTT), lactate dehydrogenase (LDH) activity, 8-oxo-2-deoxyguanosine (8-OH-dG), total antioxidant capacity (TAC), and total oxidative stress (TOS) levels, and liver micronucleus rates. ASTA (2.5, 5, and 10 µM) was added to cultures alone or simultaneously with TCDD (5 and 10 µM) for 48 h. The results of MTT and LDH assays showed that both doses of TCDD caused significant decrease in cell viability. Also, TCDD significantly increased TOS and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the dioxin caused significant increase in micronucleated hepatocytes) and 8-OH-dG level as compared to control culture. The presence of ASTA with TCDD minimized its effects on primary hepatocytes cultures and DNA damages.

Lichens are symbiotic organisms composed of fungi and algae and are very common in Turkey. Lichen secondary metabolites are mainly phenolic compounds produced by fungal partner of lichen symbiosis. Usnic acid (UA) is one of the most common lichen metabolites, and it was reported that to be effective for a wide range of pharmacological purposes including antiviral, antitumor, and antiprotozoal. However, there are limited data on the genotoxic and antioxidant effects of UA in cultured human peripheral blood cells. Therefore, the aim of this thesis study was to investigate the genetic and oxidative effects of UA in cultured human blood cells (n = 5). The UA was added into culture tubes at various concentrations (0-200 μg/ml). Chromosomal aberrations (CA) and micronuclei (MN) tests were performed for genotoxic damage influences estimation. In addition, biochemical parameters (total antioxidant capacity (TAC) and total oxidative status (TOS)) were examined to determine oxidative effects. In our in vitro test systems, it was observed that UA had no mutagenic effects on human lymphocytes. Furthermore, our results indicated that low concentrations (1 and 5 μg/ml) of UA caused increases of TAC levels in cultured human blood cells. And, the TOS levels were not changed (p > 0.05) when all the concentrations (except for 200 μg/ml) of UA were applied. In conclusion, UA can be a new resource of therapeutics as recognized in this study with their nonmutagenic and antioxidant features.