Glutathione-mediated effects of lithium in decreasing protein oxidation induced by mitochondrial complex I dysfunction

The aim of this study was to elucidate whether glutathione is involved in lithium’s ability to decrease carbonylation and nitration produced by complex I inhibition, which is consistently found in BD. Neuroblastoma cells were treated with rotenone, a complex I inhibitor. Our results suggest that glu...

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Veröffentlicht in:	Journal of Neural Transmission 2015-06, Vol.122 (6), p.741-746
Hauptverfasser:	Nascimento, Camila, Kim, Helena Kyunghee, Young, L. Trevor, Mendonça, Karina Martinez, Grinberg, Lea Tenenholz, Lafer, Beny, Andreazza, Ana Cristina
Format:	Artikel
Sprache:	eng
Schlagworte:	Cell Line, Tumor Cell Survival - drug effects Cell Survival - physiology Electron Transport Complex I - antagonists & inhibitors Glutathione - metabolism Humans Immunohistochemistry Lithium Compounds - pharmacology Medicine Medicine & Public Health Neuroblastoma - metabolism Neurology Neurosciences Protein Carbonylation - drug effects Psychiatry Rotenone - pharmacology Translational Neurosciences - Short communication Tyrosine - analogs & derivatives Tyrosine - metabolism Uncoupling Agents - pharmacology
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Zusammenfassung:	The aim of this study was to elucidate whether glutathione is involved in lithium’s ability to decrease carbonylation and nitration produced by complex I inhibition, which is consistently found in BD. Neuroblastoma cells were treated with rotenone, a complex I inhibitor. Our results suggest that glutathione is essential for lithium’s ability to ameliorate rotenone-induced protein carbonylation, but not nitration.
ISSN:	0300-9564 1435-1463
DOI:	10.1007/s00702-014-1318-8