[The mechanisms of 232Th and of Ce (III) toxic action on Chlorella vulgaris Beijer. Estimation of 232Th radiation impact contribution into toxic effect induced].

232Th and Ce (III) toxic effects and its modifications with caffeine and D,L-buthionine-(S,R)-sulphoximine on Chlorella vulgaris Beijer were studied using an optical density measure after 24 hours growth. Concentrations of 232Th or of Ce--toxic effect relationship were shown to be nonlinear. In the first (nontoxic) concentration range (for Ce 0.036-1.642 micromol/L and for 232Th 0.001-1.551 micromol/L) algae biomass production registered by optical density do not significantly differ from the control one. In the second (toxic) concentration range dose-effect relationship for 232Th is characterized with quadratic dependence and in the case of Ce--with exponential dependence. 232Th radiation component contribution into effect observed is appeared as induction of DNA damages additional to spontaneous at the radionuclide concentration (equal to 0.345 micromol/L) that is three times lower than in case of the non-radioactive chemical analog Ce (1.071 micromol/L).

Circadian rhythms of resistance to UV-C and UV-B radiation in Euglena as related to "escape from light" and "resistance to light".

Radiation-induced stress, either from visible or UV light, is strongest at midday. We found that, in the absence of stress or time cues, Euglena gracilis Z was the most resistant to UV-C and UV-B at subjective midday, whether judged from immediate or reproductive survival. The circadian UV-resistance rhythms were free-running in stationary cultures under 1-h light/1-h dark cycles or continuous darkness, indicating that cell-cycle dependent DNA susceptibility to UV was not involved. We moreover examined what was the primary cause of the circadian UV resistance, estimated as the immediate cell survival. The half-maximal lethal dose (LD(50)) of UV-C at subjective midday (the most resistant phase) was 156 J/m(2), which is approximately 3-fold that at subjective midnight. The same was true for UV-B, except the LD(50) was approximately 13-fold that of UV-C. Temperature during UV irradiation had little effect, indicating that survival was not mediated via enzymatic reactions. Non-enzymatic antioxidants were added 5 min before UV irradiation. Dimethylsulfoxide (a hydroxyl radical scavenger) increased survival after UV-B, but had little effect after UV-C; conversely, sodium ascorbate increased survival after UV-C, but not after UV-B. These findings suggest that circadian rhythms of resistance to UVs involve a common mechanism for maximizing non-enzymatic antioxidative capacity at subjective midday, but the specific antioxidants differ.