6533b853fe1ef96bd12ad399
RESEARCH PRODUCT
Mitochondrial (dys)function - a factor underlying the variability of efavirenz-induced hepatotoxicity?
Fernando AlegreJuan V. EspluguesHaryes A. FunesNadezda ApostolovaMiriam PoloVictor M. VictorAna Blas-garciasubject
PharmacologyThapsigarginEfavirenzReverse-transcriptase inhibitorEndoplasmic reticulumRotenoneBiologyMitochondrionPharmacologychemistry.chemical_compoundchemistryUnfolded protein responseHepatic stellate cellmedicinemedicine.drugdescription
Background and Purpose The non-nucleoside analogue reverse transcriptase inhibitor efavirenz is associated with hepatic toxicity and metabolic disturbances. Although the mechanisms involved are not clear, recent evidence has pinpointed a specific mitochondrial action of efavirenz accompanied by the induction of an endoplasmic reticulum (ER) stress/unfolded protein response in human hepatic cells. The aim of this study was to further investigate the involvement of this organelle by evaluating efavirenz's effects in cells lacking functional mitochondria (rho°) and comparing them with those of the typical mitotoxic agent rotenone, a standard complex I inhibitor, and the ER stress inducer thapsigargin.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2015-01-08 | British Journal of Pharmacology |