The purine analogues abacavir and didanosine increase acetaminophen-induced hepatotoxicity by enhancing mitochondrial dysfunction
Author(s) -
Ana BlasGarcía,
Alberto Martí-Rodrigo,
Víctor M. Víctor,
Miriam Polo,
Fernando Alegre,
Haryes A. Funes,
Nadezda Apostolova,
Juan V. Esplugues
Publication year - 2016
Publication title -
journal of antimicrobial chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.124
H-Index - 194
eISSN - 1460-2091
pISSN - 0305-7453
DOI - 10.1093/jac/dkv424
Subject(s) - didanosine , abacavir , mitochondrial toxicity , pharmacology , context (archaeology) , mitochondrion , acetaminophen , medicine , toxicity , purine , chemistry , biology , immunology , human immunodeficiency virus (hiv) , biochemistry , antiretroviral therapy , enzyme , viral load , paleontology
NRTIs are essential components of HIV therapy with well-documented, long-term mitochondrial toxicity in hepatic cells, but whose acute effects on mitochondria are unclear. As acetaminophen-induced hepatotoxicity also involves mitochondrial interference, we hypothesized that it would be exacerbated in the context of ART.
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