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Involvement of nitric oxide in the mitochondrial action of efavirenz: a differential effect on neurons and glial cells

By Nadezda Apostolova, Haryes A. Funes, Ana Blas García, Fernando Alegre, Míriam Polo and Juan V. Esplugues Mota

Abstract

The anti-human immunodeficiency virus (HIV) drug efavirenz (EFV) alters mitochondrial function in cultured neurons and glial cells. Nitric oxide (NO) is a mediator of mitochondrial dysfunction associated with HIV central nervous system symptoms. We show that EFV promotes inducible nitric oxide synthase (iNOS) expression in cultured glial cells and generated NO undermines their mitochondrial function, as inhibition of NOS partially reverses this effect. EFV inhibits mitochondrial Complex I in both neurons and glia; however, when the latter cells are treated for longer periods, other mitochondrial complexes are also affected in accordance with the increased NO production. These findings shed light on the mechanisms responsible for the frequent EFV-associated neurotoxicity

Topics: efavirenz, electron transport chain, HIV, mitochondria, nitric oxide, NNRTI, central nervous system
Publisher: Oxford University Press
Year: 2014
DOI identifier: 10.1093/infdis/jiu825
OAI identifier: oai:repositori.uji.es:10234/126965
Provided by: Repositori UJI
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