Goncalves 2018 Life Sci
Gonçalves DF, de Carvalho NR, Leite MB, Courtes AA, Hartmann DD, Stefanello ST, da Silva IK, Franco JL, Soares FAA, Dalla Corte CL (2018) Caffeine and acetaminophen association: Effects on mitochondrial bioenergetics. Life Sci 193:234-41. |
Goncalves DF, de Carvalho NR, Leite MB, Courtes AA, Hartmann DD, Stefanello ST, da Silva IK, Franco JL, Soares FAA, Dalla Corte CL (2018) Life Sci
Abstract: Many studies have been demonstrating the role of mitochondrial function in acetaminophen (APAP) hepatotoxicity. Since APAP is commonly consumed with caffeine, this work evaluated the effects of the combination of APAP and caffeine on hepatic mitochondrial bioenergetic function in mice.
Mice were treated with caffeine (20mg/kg, intraperitoneal (i.p.)) or its vehicle and, after 30minutes, APAP (250mg/kg, i.p.) or its vehicle. Four hours later, livers were removed, and the parameters associated with mitochondrial function and oxidative stress were evaluated. Hepatic cellular oxygen consumption was evaluated by high-resolution respirometry (HRR).
APAP treatment decreased cellular oxygen consumption and mitochondrial complex activities in the livers of mice. Additionally, treatment with APAP increased swelling of isolated mitochondria from mice livers. On the other hand, caffeine administered with APAP was able to improve hepatic mitochondrial bioenergetic function. Treatment with APAP increased lipid peroxidation and reactive oxygen species (ROS) production and decreased glutathione levels in the livers of mice. Caffeine administered with APAP was able to prevent lipid peroxidation and the ROS production in mice livers, which may be associated with the improvement of mitochondrial function caused by caffeine treatment.
We suggest that the antioxidant effects of caffeine and/or its interactions with mitochondrial bioenergetics may be involved in its beneficial effects against APAP hepatotoxicity.
Copyright Β© 2017 Elsevier Inc. All rights reserved. β’ Keywords: Bioenergetics, High-resolution respirometry, Mitochondria, Oxidative stress β’ Bioblast editor: Kandolf G β’ O2k-Network Lab: BR Sao Gabriel Franco JL
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, mt-Medicine, Pharmacology;toxicology
Pathology: Other
Organism: Mouse Tissue;cell: Liver Preparation: Homogenate
Coupling state: LEAK, OXPHOS
Pathway: N, S, NS, ROX
HRR: Oxygraph-2k
2018-01