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Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes

Abstract

The intracellular oxidative stress has been involved in bile acid-induced cell death in hepatocytes. Nitric oxide (NO) exerts cytoprotective properties in glycochenodeoxycholic acid (GCDCA)-treated hepatocytes. The study evaluated the involvement of Ca{sup 2+} on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes. The regulation of Ca{sup 2+} pools (EGTA or BAPTA-AM) and NO (L-NAME or NO donor) production was assessed during NAC cytoprotection in GCDCA-treated HepG2 cells. The stimulation of Ca{sup 2+} entrance was induced by A23187 in HepG2. Cell death, Ca{sup 2+} mobilization, NOS-1, -2 and -3 expression, AP-1 activation, and NO production were evaluated. GCDCA reduced intracellular Ca{sup 2+} concentration and NOS-3 expression, and enhanced cell death in HepG2. NO donor prevented, and L-NAME enhanced, GCDCA-induced cell death. The reduction of Ca{sup 2+} entry by EGTA, but not its release from intracellular stores by BAPTA-AM, enhanced cell death in GCDCA-treated cells. The stimulation of Ca{sup 2+} entrance by A23187 reduced cell death and enhanced NOS-3 expression in GCDCA-treated HepG2 cells. The cytoprotective properties of NAC were related to the recovery of intracellular Ca{sup 2+} concentration, NOS-3 expression and NO production induced by GCDCA-treated HepG2 cells. The increase of NO  More>>
Publication Date:
Jan 15, 2010
Product Type:
Journal Article
Resource Relation:
Journal Name: Toxicology and Applied Pharmacology; Journal Volume: 242; Journal Issue: 2; Other Information: DOI: 10.1016/j.taap.2009.10.003; PII: S0041-008X(09)00425-6; Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BILE ACIDS; CALCIUM IONS; EGTA; GLUTATHIONE; LIVER CELLS; NITRIC OXIDE; OXIDATION; STIMULATION; STRESSES; ALCOHOLS; ANIMAL CELLS; CARBOXYLIC ACIDS; CHALCOGENIDES; CHARGED PARTICLES; CHELATING AGENTS; CHEMICAL REACTIONS; DRUGS; GLYCOLS; HYDROXY COMPOUNDS; IONS; NITROGEN COMPOUNDS; NITROGEN OXIDES; ORGANIC ACIDS; ORGANIC COMPOUNDS; OXIDES; OXYGEN COMPOUNDS; PEPTIDES; POLYPEPTIDES; PROTEINS; RADIOPROTECTIVE SUBSTANCES; RESPONSE MODIFYING FACTORS; SOMATIC CELLS; STEROIDS; STEROLS
OSTI ID:
21344837
Country of Origin:
United States
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0041-008X; TXAPA9; TRN: US10R1678075739
Availability:
Available from http://dx.doi.org/10.1016/j.taap.2009.10.003
Submitting Site:
INIS
Size:
page(s) 165-172
Announcement Date:
Oct 28, 2010

Citation Formats

Gonzalez-Rubio, Sandra, Linares, Clara I, Bello, Rosario I, Gonzalez, Raul, Ferrin, Gustavo, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Hidalgo, Ana B, Munoz-Gomariz, Elisa, Rodriguez, Blanca A, Barrera, Pilar, Ranchal, Isidora, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Duran-Prado, Mario, CIBER Fisiopatologia de la Obesidad y Nutricion CB06/03, Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo (Spain)], Aguilar-Melero, Patricia, De la Mata, Manuel, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Muntane, Jordi, and Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)]. Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes. United States: N. p., 2010. Web. doi:10.1016/j.taap.2009.10.003.
Gonzalez-Rubio, Sandra, Linares, Clara I, Bello, Rosario I, Gonzalez, Raul, Ferrin, Gustavo, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Hidalgo, Ana B, Munoz-Gomariz, Elisa, Rodriguez, Blanca A, Barrera, Pilar, Ranchal, Isidora, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Duran-Prado, Mario, CIBER Fisiopatologia de la Obesidad y Nutricion CB06/03, Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo (Spain)], Aguilar-Melero, Patricia, De la Mata, Manuel, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Muntane, Jordi, & Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)]. Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes. United States. doi:10.1016/j.taap.2009.10.003.
Gonzalez-Rubio, Sandra, Linares, Clara I, Bello, Rosario I, Gonzalez, Raul, Ferrin, Gustavo, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Hidalgo, Ana B, Munoz-Gomariz, Elisa, Rodriguez, Blanca A, Barrera, Pilar, Ranchal, Isidora, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Duran-Prado, Mario, CIBER Fisiopatologia de la Obesidad y Nutricion CB06/03, Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo (Spain)], Aguilar-Melero, Patricia, De la Mata, Manuel, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Muntane, Jordi, and Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)]. 2010. "Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes." United States. doi:10.1016/j.taap.2009.10.003. https://www.osti.gov/servlets/purl/10.1016/j.taap.2009.10.003.
@misc{etde_21344837,
title = {Calcium-dependent nitric oxide production is involved in the cytoprotective properties of n-acetylcysteine in glycochenodeoxycholic acid-induced cell death in hepatocytes}
author = {Gonzalez-Rubio, Sandra, Linares, Clara I, Bello, Rosario I, Gonzalez, Raul, Ferrin, Gustavo, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Hidalgo, Ana B, Munoz-Gomariz, Elisa, Rodriguez, Blanca A, Barrera, Pilar, Ranchal, Isidora, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Duran-Prado, Mario, CIBER Fisiopatologia de la Obesidad y Nutricion CB06/03, Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo (Spain)], Aguilar-Melero, Patricia, De la Mata, Manuel, Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)], Muntane, Jordi, and Centro de Investigacion Biomedica en Red de Enfermedades Hepaticas y Digestivas (CIBEREH o Ciberehd) (Spain)]}
abstractNote = {The intracellular oxidative stress has been involved in bile acid-induced cell death in hepatocytes. Nitric oxide (NO) exerts cytoprotective properties in glycochenodeoxycholic acid (GCDCA)-treated hepatocytes. The study evaluated the involvement of Ca{sup 2+} on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes. The regulation of Ca{sup 2+} pools (EGTA or BAPTA-AM) and NO (L-NAME or NO donor) production was assessed during NAC cytoprotection in GCDCA-treated HepG2 cells. The stimulation of Ca{sup 2+} entrance was induced by A23187 in HepG2. Cell death, Ca{sup 2+} mobilization, NOS-1, -2 and -3 expression, AP-1 activation, and NO production were evaluated. GCDCA reduced intracellular Ca{sup 2+} concentration and NOS-3 expression, and enhanced cell death in HepG2. NO donor prevented, and L-NAME enhanced, GCDCA-induced cell death. The reduction of Ca{sup 2+} entry by EGTA, but not its release from intracellular stores by BAPTA-AM, enhanced cell death in GCDCA-treated cells. The stimulation of Ca{sup 2+} entrance by A23187 reduced cell death and enhanced NOS-3 expression in GCDCA-treated HepG2 cells. The cytoprotective properties of NAC were related to the recovery of intracellular Ca{sup 2+} concentration, NOS-3 expression and NO production induced by GCDCA-treated HepG2 cells. The increase of NO production by Ca{sup 2+}-dependent NOS-3 expression during NAC administration reduces cell death in GCDCA-treated hepatocytes.}
doi = {10.1016/j.taap.2009.10.003}
journal = {Toxicology and Applied Pharmacology}
issue = {2}
volume = {242}
place = {United States}
year = {2010}
month = {Jan}
}