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The heavy metal thallium is an emerging pollutant among the most potentially toxic species to which human populations are exposed. Its harmful effects on living organisms are well-known at high doses, typical of acute intoxication. Its harmful effects at low doses are by far less known. In a previous paper, we reported a TlCl-induced metabolic shift to lactate and ethanol production in living hippocampal HN9.10e neurons that appeared after a single short exposure (48 h) at low doses (1-100 μg/L). This metabolic shift to lactate and ethanol suggests a marked impairment of cell bioenergetics. In this work, we provide detailed evidence for TlCl-induced changes of neuronal morphology and mitochondrial activity. Confocal microscopy and fluorescent probes were used to qualitatively and quantitatively analyze, at the subcellular level, living HN9.10e neurons during and after TlCl exposure. An early onset mitochondrial dysfunction appeared, associated with signs of cellular deregulation such as neurite shortening, loss of substrate adhesion, and increase of cytoplasmic calcium. The dose-dependent alteration of mitochondrial ROS (mtROS) level and of transmembrane mitochondrial potential (ΔΨm) has been observed also for very low TlCl doses (1 μg/L). The treatment with the ATP synthase inhibitor oligomycin revealed a severe impairment of the mitochondrial function, more significant than that measured by the simple quantification of the tetramethylrhodamine methyl ester (TMRM) fluorescence. These results highlight that mitochondria are a key subcellular target of TlCl neurotoxicity. The transmembrane mitochondrial potential was significantly correlated with the ethanol concentration in cell culture medium ( P < 0.001, r = -0.817), suggesting that ethanol could be potentially used as a biomarker of mitochondrial impairment.

AbstractThe possible effects on cognitive processes of external electric fields, such as those generated by power line pillars and household appliances are of increasing public concern. They are difficult to study experimentally, and the relatively scarce and contradictory evidence make it difficult to clearly assess these effects. In this study, we investigate how, why and to what extent external perturbations of the intrinsic neuronal activity, such as those that can be caused by generation, transmission and use of electrical energy can affect neuronal activity during cognitive processes. For this purpose, we used a morphologically and biophysically realistic three‐dimensional model of CA1 pyramidal neurons. The simulation findings suggest that an electric field oscillating at power lines frequency, and environmentally measured strength, can significantly alter both the average firing rate and temporal spike distribution properties of a hippocampal CA1 pyramidal neuron. This effect strongly depends on the specific and instantaneous relative spatial location of the neuron with respect to the field, and on the synaptic input properties. The model makes experimentally testable predictions on the possible functional consequences for normal hippocampal functions such as object recognition and spatial navigation. The results suggest that, although EF effects on cognitive processes may be difficult to occur in everyday life, their functional consequences deserve some consideration, especially when they constitute a systematic presence in living environments.