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N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes.
Chem Biol Interact. 2009 Sep 14; 181(1):95-106.CB

Abstract

D-Galactosamine (D-GalN) induces reactive oxygen species (ROS) generation and cell death in cultured hepatocytes. The aim of the study was to evaluate the cytoprotective properties of N-acetylcysteine (NAC), coenzyme Q(10) (Q(10)) and the superoxide dismutase (SOD) mimetic against the mitochondrial dysfunction and cell death in D-GalN-treated hepatocytes. Hepatocytes were isolated from liver resections. NAC (0.5 mM), Q(10) (30 microM) or MnTBAP (Mn(III)tetrakis(4-benzoic acid) porphyrin chloride (1mg/mL) were co-administered with D-GalN (40 mM) in hepatocytes. Cell death, oxidative stress, mitochondrial transmembrane potential (MTP), ATP, mitochondrial oxidized/reduced glutathione (GSH) and Q(10) ratios, electronic transport chain (ETC) activity, and nuclear- and mitochondria-encoded expression of complex I subunits were determined in hepatocytes. d-GalN induced a transient increase of mitochondrial hyperpolarization and oxidative stress, followed by an increase of oxidized/reduced GSH and Q(10) ratios, mitochondrial dysfunction and cell death in hepatocytes. The cytoprotective properties of NAC supplementation were related to a reduction of ROS generation and oxidized/reduced GSH and Q(10) ratios, and a recovery of mitochondrial complexes I+III and II+III activities and cellular ATP content. The co-administration of Q(10) or MnTBAP recovered oxidized/reduced GSH ratio, and reduced ROS generation, ETC dysfunction and cell death induced by D-GalN. The cytoprotective properties of studied antioxidants were related to an increase of the protein expression of nuclear- and mitochondrial-encoded subunits of complex I. In conclusion, the co-administration of NAC, Q(10) and MnTBAP enhanced the expression of complex I subunits, and reduced ROS production, oxidized/reduced GSH ratio, mitochondrial dysfunction and cell death induced by D-GalN in cultured hepatocytes.

Authors+Show Affiliations

Liver Research Unit, Reina Sofía University Hospital, Córdoba, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19523936

Citation

González, Raúl, et al. "N-acetylcysteine, Coenzyme Q10 and Superoxide Dismutase Mimetic Prevent Mitochondrial Cell Dysfunction and Cell Death Induced By D-galactosamine in Primary Culture of Human Hepatocytes." Chemico-biological Interactions, vol. 181, no. 1, 2009, pp. 95-106.
González R, Ferrín G, Hidalgo AB, et al. N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes. Chem Biol Interact. 2009;181(1):95-106.
González, R., Ferrín, G., Hidalgo, A. B., Ranchal, I., López-Cillero, P., Santos-Gónzalez, M., López-Lluch, G., Briceño, J., Gómez, M. A., Poyato, A., Villalba, J. M., Navas, P., de la Mata, M., & Muntané, J. (2009). N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes. Chemico-biological Interactions, 181(1), 95-106. https://doi.org/10.1016/j.cbi.2009.06.003
González R, et al. N-acetylcysteine, Coenzyme Q10 and Superoxide Dismutase Mimetic Prevent Mitochondrial Cell Dysfunction and Cell Death Induced By D-galactosamine in Primary Culture of Human Hepatocytes. Chem Biol Interact. 2009 Sep 14;181(1):95-106. PubMed PMID: 19523936.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-acetylcysteine, coenzyme Q10 and superoxide dismutase mimetic prevent mitochondrial cell dysfunction and cell death induced by d-galactosamine in primary culture of human hepatocytes. AU - González,Raúl, AU - Ferrín,Gustavo, AU - Hidalgo,Ana B, AU - Ranchal,Isidora, AU - López-Cillero,Pedro, AU - Santos-Gónzalez,Mónica, AU - López-Lluch,Guillermo, AU - Briceño,Javier, AU - Gómez,Miguel A, AU - Poyato,Antonio, AU - Villalba,José M, AU - Navas,Plácido, AU - de la Mata,Manuel, AU - Muntané,Jordi, Y1 - 2009/06/11/ PY - 2009/01/12/received PY - 2009/05/28/revised PY - 2009/06/03/accepted PY - 2009/6/16/entrez PY - 2009/6/16/pubmed PY - 2009/8/19/medline SP - 95 EP - 106 JF - Chemico-biological interactions JO - Chem. Biol. Interact. VL - 181 IS - 1 N2 - D-Galactosamine (D-GalN) induces reactive oxygen species (ROS) generation and cell death in cultured hepatocytes. The aim of the study was to evaluate the cytoprotective properties of N-acetylcysteine (NAC), coenzyme Q(10) (Q(10)) and the superoxide dismutase (SOD) mimetic against the mitochondrial dysfunction and cell death in D-GalN-treated hepatocytes. Hepatocytes were isolated from liver resections. NAC (0.5 mM), Q(10) (30 microM) or MnTBAP (Mn(III)tetrakis(4-benzoic acid) porphyrin chloride (1mg/mL) were co-administered with D-GalN (40 mM) in hepatocytes. Cell death, oxidative stress, mitochondrial transmembrane potential (MTP), ATP, mitochondrial oxidized/reduced glutathione (GSH) and Q(10) ratios, electronic transport chain (ETC) activity, and nuclear- and mitochondria-encoded expression of complex I subunits were determined in hepatocytes. d-GalN induced a transient increase of mitochondrial hyperpolarization and oxidative stress, followed by an increase of oxidized/reduced GSH and Q(10) ratios, mitochondrial dysfunction and cell death in hepatocytes. The cytoprotective properties of NAC supplementation were related to a reduction of ROS generation and oxidized/reduced GSH and Q(10) ratios, and a recovery of mitochondrial complexes I+III and II+III activities and cellular ATP content. The co-administration of Q(10) or MnTBAP recovered oxidized/reduced GSH ratio, and reduced ROS generation, ETC dysfunction and cell death induced by D-GalN. The cytoprotective properties of studied antioxidants were related to an increase of the protein expression of nuclear- and mitochondrial-encoded subunits of complex I. In conclusion, the co-administration of NAC, Q(10) and MnTBAP enhanced the expression of complex I subunits, and reduced ROS production, oxidized/reduced GSH ratio, mitochondrial dysfunction and cell death induced by D-GalN in cultured hepatocytes. SN - 1872-7786 UR - https://www.unboundmedicine.com/medline/citation/19523936/N_acetylcysteine_coenzyme_Q10_and_superoxide_dismutase_mimetic_prevent_mitochondrial_cell_dysfunction_and_cell_death_induced_by_d_galactosamine_in_primary_culture_of_human_hepatocytes_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(09)00219-1 DB - PRIME DP - Unbound Medicine ER -