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Brain glutathione redox system significance for the control of silica-coated magnetite nanoparticles with or without mercury co-exposures mediated oxidative stress in European eel (Anguilla anguilla L.)
Authors:Naser A Anjum  Koigoora Srikanth  Iram Mohmood  Iqbal Sayeed  Tito Trindade  Armando C Duarte  Eduarda Pereira  Iqbal Ahmad
Institution:1. Department of Chemistry, Centre for Environmental and Marine Studies (CESAM), University of Aveiro, 3810-193, Aveiro, Portugal
2. Department of Emergency Medicine, Brain Research Laboratory, Emory University, 1365B Clifton Road NE, Suite 5100, Atlanta, GA, 30322, USA
3. Department of Chemistry, CICECO and CESAM, Aveiro Institute of Nanotechnology, University of Aveiro, 3810-193, Aveiro, Portugal
4. Department of Biology, Centre for Environmental and Marine Studies (CESAM), University of Aveiro, 3810-193, Aveiro, Portugal
Abstract:This in vitro study investigates the impact of silica-coated magnetite particles (Fe3O4@SiO2/SiDTC, hereafter called IONP; 2.5 mg L?1) and its interference with co-exposure to persistent contaminant (mercury, Hg; 50 μg L?1) during 0, 2, 4, 8, 16, 24, 48, and 72 h on European eel (Anguilla anguilla) brain and evaluates the significance of the glutathione (GSH) redox system in this context. The extent of damage (membrane lipid peroxidation, measured as thiobarbituric acid reactive substances, TBARS; protein oxidation, measured as reactive carbonyls, RCs) decreased with increasing period of exposure to IONP or IONP + Hg which was accompanied with differential responses of glutathione redox system major components (glutathione reductase, GR; glutathione peroxidase, GPX; total GSH, TGSH). The occurrence of antagonism between IONP and Hg impacts was evident at late hour (72 h), where significantly decreased TBARS and RC levels and GR and glutathione sulfo-transferase (GST) activity imply the positive effect of IONP + Hg concomitant exposure against Hg-accrued negative impacts vs. early (2 h) hour of exposure]. A period of exposure-dependent IONP alone and IONP + Hg joint exposure-accrued impact was perceptible. Additionally, increased susceptibility of the GSH redox system to increased period of exposure to Hg was depicted, where insufficiency of elevated GR for the maintenance of TGSH required for membrane lipid and cellular protein protection was displayed. Overall, a fine-tuning among brain glutathione redox system components was revealed controlling IONP + Hg interactive impacts successfully.
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