Abstract
Saxitoxin (STX), a paralytic shellfish toxin (PST) produced from toxic bloom-forming dinoflagellates, was selected to comparatively investigate the induction of cytotoxicity and apoptosis and a possible mechanism based on changes in the antioxidant defence system of two cellular strains: the mouse neuroblastoma cell line Neuro-2a and the rainbow trout fish cell line RTG-2. Increasing concentrations of STX (0–256 nM) presented little cytotoxic or apoptotic effects on the two cell lines. Measurements of cellular viability, lethal ratio and LDH leakage showed slight changes in Neuro-2a and RTG-2 cells (p > 0.05), and similar results were observed for cellular morphology and apoptotic rates. The contents of the main reactive oxygen species (ROS) components, superoxide anion (O2−) and hydrogen peroxide (H2O2), were markedly increased in Neuro-2a cell with STX exposure at middle (15 nM) and high (150 nM) concentrations (p < 0.05), and the simultaneous increase of the ratio of reduced/oxidized glutathione (GSH/GSSG) (p < 0.05) inferred the occurrence of oxidative stress. However, little difference was observed in all treated groups of RTG-2 cells. The activities of three antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR), were significantly enhanced in Neuro-2a cells in the middle and high concentration groups (p < 0.05), while glutathione peroxidase (GPX) obviously decreased (p < 0.05) in all treated groups. Little change was found in RTG-2 cells with the same exposures. These results provided evidence that STX exposure altered the redox status of Neuro-2a cells and resulted in oxidative stress, but the same exposure exerted little effect on RTG-2 cells. Therefore, Neuro-2a cells are more sensitive than reproductive cells to STX exposure, and the antioxidant systems appears to be partly responsible for this differentiation response.
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