Enantioselective apoptosis and oxidative damage induced by individual isomers of profenofos in primary hippocampal neurons.

The purpose of this study was to investigate the apoptosis-related cytotoxic effects and molecular mechanisms of individual isomers of profenofos (PFF) on primary hippocampal neurons at 1.0 to 20 mg L-1. The cell viability and lactate dehydrogenase (LDH) efflux indicated that (-)-PFF exposure was associated with more toxic effects than (+)-PFF above the concentration of 5 mg L-1 (P < 0.5). Flow cytometric results showed that the percentages of apoptotic cells incubated with 20 mg L-1 (-)-PFF, (+)-PFF and rac-PFF for 24 h reached 23.4%, 9.2% and 14.2% (P < 0.01), respectively. Hippocampal neurons incubated with (-)-PFF, (+)-PFF and rac-PFF exhibited a dose-dependent accumulation of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) and a dose-dependent inhibition of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activity, implying that the defense system of the tests induces oxidative damage. A statistically significant difference was observed between the two enantiomers at 5 mg L-1 and above. Moreover, the results showed that (-)-PFF exposure caused a significant loss in mitochondrial transmembrane potential (MMP), an upregulation of Ca2+ and Bax protein expression, a downregulation of Bcl-2 protein expression, and the activation of caspase-3 and caspase-9 in a dose-dependent manner; (+)-PFF and rac-PFF exhibited these effects to a lesser degree. All results suggest that PFF induced apoptosis in rat hippocampal neurons via the mitochondria-mediated pathway, and oxidative stress is one of the factors of PFF-induced apoptosis. In addition, (-)-PFF appears to play an important role in oxidative stress and apoptosis, indicating that enantioselectivity should be considered when assessing ecotoxicological effects and health risks of chiral pesticides.

Residues and potential health risks of DDTs and HCHs in commercial seafoods from two coastal cities near Yangtze River Estuary.

Five species of commercial seafoods collected from the local markets in two coastal cities near Yangtze River Estuary (Ningbo and Zhoushan) in 2010 were analyzed to study the residues, potential sources, and health risks of dichlorodiphenyltrichloroethanes (DDTs) and hexachlorocyclohexanes (HCHs) in these areas. The total levels of DDTs and HCHs in the samples ranged from 1.13-20.2 ng g(-1) and 1.23-3.05 ng g(-1) wet weight, respectively, and were at a middle level compared with those from other marine systems. Results from one-way analysis of variance (ANOVA) indicated species-specific distributions of DDTs and HCHs in the seafoods of the studied area, which may be related to their different lipid contents and ecological characteristics. Compositional analysis suggested that historical usage dominates in this area, and fresh inputs of lindane and dicofol may also have part contributions. With respect to DDTs, it can be metabolized into both DDD and DDE simultaneously in seafoods tested. Assessment based on maximum residue levels, acceptable or tolerable daily intakes, and hazard ratios for non-carcinogens suggested no obvious adverse health effects, while the lifetime cancer risks may be increased from dietary exposure to DDTs and HCHs.

Cytotoxicity and DNA damage of five organophosphorus pesticides mediated by oxidative stress in PC12 cells and protection by vitamin E.

Previous studies have demonstrated that pesticides could induce cytotoxicity and genotoxicity in vivo and in vitro, and that oxidative stress may be an important factor involved. However, investigations comparing the capability of different organophosphorous (OP) compounds to induce cytotoxicity, genotoxicity and oxidative stress are limited. Hence, the aim of this paper was to access the cytotoxic and genotoxic effects of five OPs or metabolites, Acephate (ACE), Methamidophos (MET), Chloramidophos (CHL), Malathion (MAT) and Malaoxon (MAO), and to clarify the role of oxidative stress, using PC12 cells. The results demonstrated that MET, MAT and MAO caused significant inhibition of cell viability and increased DNA damage in PC12 cells at 40 mg L(-1). MAO was more toxic than the other OPs. ACE, MET, MAT and MAO increased the levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), and decreased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) at 20 mg L(-1) and 40 mg L(-1) to different degrees. Pre-treatment with vitamin E(600 µM)caused a significant attenuation in the cytotoxic and genotoxic effect; pre-treatment reversed subsequent OP-induced elevation of peroxidation products and the decline of anti-oxidant enzyme activities. These results indicate that oxidative damage is likely to be an initiating event that contributes to the OP-induced cytotoxicity.