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Study of CeO2 nanoparticle interactions with biological cells and lipid bilayers

A.L. Popov, I.I. Selezneva, N.S. Kurnakov, V.K. Ivanov and P.A. Grigoriev§,∗
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, Russia
Kurnakov Institute of General and Inorganic Chemistry Russian Academy of Sciences, Moscow, Russia
§ Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, Russia

DOI: 10.4024/01PO14A.jbpc.14.01
Publication date (web): 10 November 2014
Copyright © 2014 Collegium Basilea and AMSI

ABSTRACT. We studied the action of different doses of CeO2 nanoparticles on HEp-2 cells, NCTC L929 fibroblasts and model lipid bilayer membranes. The MTT-test of the mitochondrial dehydrogenase activity of the NCTC L929 fibroblasts and HEp-2 epithelial cells showed that there is no difference in the viability of the cells in media with 10–5–10–11 M of CeO2, stabilized by sodium citrate, and the viability of the cells in medium without CeO2. It was shown that neither the lipid membrane conductance nor the surface charge of the lipid bilayer interface were changed in the 10–5–10–11 M range of nanoparticle concentrations. The results indicate low cell toxicity of the CeO2 nanoparticles.

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Autoantibody markers of neural degeneration are associated with post-mortem histopathological alterations of a neurologically-injured pilot

Mohamed B. Abou-Donia,†,∗ F.R.W. van de Goot and M.F.A. Mulder§
Duke University Medical Center, Durham, North Carolina 27710, USA
Symbiant BV, Wilhelminalaan 12, 1815 JD Alkmaar, The Netherlands
§ Aviation Medical Consult, Karbouwstraat 14, 1402 VC Bussum, The Netherlands

DOI: 10.4024/05AB14A.jbpc.14.03
Publication date (web): 27 July 2014
Copyright © 2014 Collegium Basilea and AMSI

ABSTRACT. There are numerous concerns regarding the neurotoxicity of contaminated air inside pressurized aircraft. Neurological symptoms have been seen in many aircrew personnel who have reportedly been exposed to the potentially toxic breathable air in airliners. Symptoms, allegedly contracted by aircrew and passengers, are thought to be caused by a single large exposure or repetitive cumulative low-level exposures to toxic chemicals in the airliner internal air. Genetic variation plays a rôle. We report here the case of a 43-year old airline pilot who presented with neurological deficits and other symptoms. The pilot died without regaining good health. In vivo blood had been collected ante mortem. Analysis of the serum confirmed grossly elevated levels of serum autoantibody biomarkers for neuronal cell degeneration compared with a control group. At autopsy, various tissues underwent histopathological assessment. Brain and spinal tissues exhibited axonal degeneration and demyelination. Peripheral nerves showed T-lymphocyte infiltration and demyelination. T-lymphocytes had infiltrated the heart muscle tissue. The post-mortem tests and pathological examination of the nervous system confirm the autoantibody biomarker results. Differential diagnosis showed that the work environment, clinical condition, histopathology and serum biomarkers for nervous system injury are consistent with organophosphate-induced neurotoxicity. The results also showed that exposure to organophosphates rendered the nervous system and heart tissue sensitive and predisposed to further injury.

Special copy editor's note(s) for this paper:
References to be renumbered and corrected.
Precise scale to be added to all micrographs.

Properties of ion channels formed by peroxiredoxin-6 in the lipid bilayers: cluster channel inactivation

P.A. Grigoriev, M.G. Sharapov and V.I. Novoselov

Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region, Russia

DOI: 10.4024/09GR14A.jbpc.14.03
Publication date (web): 9 December 2014
Copyright © 2014 Collegium Basilea and AMSI

ABSTRACT. We show that the antioxidant protein peroxirdoxin-6 forms cation-selective ion cluster-type channels in phosphatidylcholine bilayer membranes. The cluster channel consists of several (from three to ten) conducting subunits—monochannels—each with a conductance of about 350 pS in 200 mM KCl. Mean dwell time in the open state of the cluster is voltage-dependent. It exponentially diminishes with increasing membrane voltage. A possible molecular mechanism of the channel’s inactivation is discussed.

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