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Lipoic acid increases glutamate uptake, glutamine synthetase activity and glutathione content in C6 astrocyte cell line
Author(s) -
KleinkaufRocha Juliana,
Bobermin Larissa Daniele,
Machado Priscila de Mattos,
Gonçalves CarlosAlberto,
Gottfried Carmem,
QuincozesSantos André
Publication year - 2013
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2012.12.006
Subject(s) - glutamine synthetase , glutathione , glutamate receptor , astrocyte , neuroprotection , oxidative stress , glutamine , glutamatergic , biochemistry , nitric oxide , reactive oxygen species , excitotoxicity , glutathione synthetase , neuroglia , chemistry , biology , pharmacology , enzyme , amino acid , endocrinology , central nervous system , receptor
Alpha lipoic acid (LA) is a sulfhydryl compound, used as dietary supplement and to treat a variety of conditions associated to oxidative stress. Glial cells are key modulators of neuroprotection. We show here that LA modulates specific glial parameters in C6 astrocyte cell line, such as glutamate uptake, glutamine synthetase (GS) activity and glutathione content, commonly associated with the protective role of glial cells. LA (10 and 50 μM) after 24 h of treatment significantly decreased the formation of reactive oxygen species (ROS) and nitric oxide (NO) levels, and increased glutamate uptake (up to 20%), GS activity (25%) and GSH content (up to 40%). LA increase glutamate uptake probably by decreasing oxidizing conditions and/or by mechanism dependent of protein kinase C (PKC). In contrast, high concentrations of LA (1000 μM) decreased these glial functions. Moreover, this concentration increased ROS production and NO levels. In summary, these findings show that low doses of LA were able to modulate glial functions and it appears to have remarkable therapeutic potential in neurological diseases involving oxidative stress by improving glutamatergic metabolism.