Organic and inorganic selenium compounds were used to examinewhether low selenium concentrationis able to trigger apoptotic degeneration in a human neuron cell line in vitro and to explore changes inreactive oxygen and nitrogen species and antioxidant protein content during the apoptotic processes.The results indicated that: (1) SKNBE neuroblastoma cells treated with sodium selenite, sodium selenateand seleno-methionine (0.1, 0.5 and 0.5 mM, respectively) for 24 h exhibited a viability decrease, unlikekidney or prostatic cells; (2) the PARP (poly-ADP-ribose-polymerase) degradation and caspase activationdetected by Western blot and flow cytometry fluorimetric examination showed induction of apoptosis;(3) during selenium treatment, a ROS/RNS increase occurred despite the GSH increment, as revealed byfluorimetric analysis; (4) the RNS production could be blocked by a peroxynitrite scavenger; (5) afterexposure to selenium compounds, the concentration of nitric oxide synthase, manganese superoxidedismutase (SOD2), P-NF-kB (phospho nuclear factor kB), glutathione reductase and glutathioneperoxidase increased, whereas that of P-ERK (phospho extracellular signal-regulated kinase) decreased;(6) selenium presence induced copper/zinc superoxide dismutase (SOD1) translocation into mitochondria,in a way similar to what is observed in amyotrophic lateral sclerosis (ALS). This study supportsepidemiologic studies showing the possibility that excess environmental exposure to Se represents a riskfactor for a devastating human neurodegenerative disease.

Low levels of selenium compounds are selectively toxic for a human neuron cell line through ROS/RNS increase and apoptotic process activation / Maraldi, Tullia; Riccio, Massimo; L., Zambonin; Vinceti, Marco; DE POL, Anto; G., Hakimb. - In: NEUROTOXICOLOGY. - ISSN 0161-813X. - STAMPA. - 32:(2011), pp. 180-187. [10.1016/j.neuro.2010.10.008]

Low levels of selenium compounds are selectively toxic for a human neuron cell line through ROS/RNS increase and apoptotic process activation

MARALDI, Tullia;RICCIO, Massimo;VINCETI, Marco;DE POL, Anto;
2011

Abstract

Organic and inorganic selenium compounds were used to examinewhether low selenium concentrationis able to trigger apoptotic degeneration in a human neuron cell line in vitro and to explore changes inreactive oxygen and nitrogen species and antioxidant protein content during the apoptotic processes.The results indicated that: (1) SKNBE neuroblastoma cells treated with sodium selenite, sodium selenateand seleno-methionine (0.1, 0.5 and 0.5 mM, respectively) for 24 h exhibited a viability decrease, unlikekidney or prostatic cells; (2) the PARP (poly-ADP-ribose-polymerase) degradation and caspase activationdetected by Western blot and flow cytometry fluorimetric examination showed induction of apoptosis;(3) during selenium treatment, a ROS/RNS increase occurred despite the GSH increment, as revealed byfluorimetric analysis; (4) the RNS production could be blocked by a peroxynitrite scavenger; (5) afterexposure to selenium compounds, the concentration of nitric oxide synthase, manganese superoxidedismutase (SOD2), P-NF-kB (phospho nuclear factor kB), glutathione reductase and glutathioneperoxidase increased, whereas that of P-ERK (phospho extracellular signal-regulated kinase) decreased;(6) selenium presence induced copper/zinc superoxide dismutase (SOD1) translocation into mitochondria,in a way similar to what is observed in amyotrophic lateral sclerosis (ALS). This study supportsepidemiologic studies showing the possibility that excess environmental exposure to Se represents a riskfactor for a devastating human neurodegenerative disease.
32
180
187
Low levels of selenium compounds are selectively toxic for a human neuron cell line through ROS/RNS increase and apoptotic process activation / Maraldi, Tullia; Riccio, Massimo; L., Zambonin; Vinceti, Marco; DE POL, Anto; G., Hakimb. - In: NEUROTOXICOLOGY. - ISSN 0161-813X. - STAMPA. - 32:(2011), pp. 180-187. [10.1016/j.neuro.2010.10.008]
Maraldi, Tullia; Riccio, Massimo; L., Zambonin; Vinceti, Marco; DE POL, Anto; G., Hakimb
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11380/649076
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