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Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes
Butylated hydroxyanisole (BHA) is a synthetic phenolic compound consisting of a mixture of two isomeric organic compounds: 2-tert-butyl-4-hydroxyanisole and 3-tert-butyl-4-hydroxyanisole. We examined the effect of BHA against hydrogen peroxide (H(2)O(2))-induced apoptosis in primary cultured mouse h...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Society of Veterinary Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367145/ https://www.ncbi.nlm.nih.gov/pubmed/25798044 http://dx.doi.org/10.4142/jvs.2015.16.1.17 |
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author | Hwang, Geun Hye Jeon, Yu Jin Han, Ho Jae Park, Soo Hyun Baek, Kyoung Min Chang, Woochul Kim, Joong Sun Kim, Lark Kyun Lee, You-Mie Lee, Sangkyu Bae, Jong-Sup Jee, Jun-Goo Lee, Min Young |
author_facet | Hwang, Geun Hye Jeon, Yu Jin Han, Ho Jae Park, Soo Hyun Baek, Kyoung Min Chang, Woochul Kim, Joong Sun Kim, Lark Kyun Lee, You-Mie Lee, Sangkyu Bae, Jong-Sup Jee, Jun-Goo Lee, Min Young |
author_sort | Hwang, Geun Hye |
collection | PubMed |
description | Butylated hydroxyanisole (BHA) is a synthetic phenolic compound consisting of a mixture of two isomeric organic compounds: 2-tert-butyl-4-hydroxyanisole and 3-tert-butyl-4-hydroxyanisole. We examined the effect of BHA against hydrogen peroxide (H(2)O(2))-induced apoptosis in primary cultured mouse hepatocytes. Cell viability was significantly decreased by H(2)O(2) in a dose-dependent manner. Additionally, H(2)O(2) treatment increased Bax, decreased Bcl-2, and promoted PARP-1 cleavage in a dose-dependent manner. Pretreatment with BHA before exposure to H(2)O(2) significantly attenuated the H(2)O(2)-induced decrease of cell viability. H(2)O(2) exposure resulted in an increase of intracellular reactive oxygen species (ROS) generation that was significantly inhibited by pretreatment with BHA or N-acetyl-cysteine (NAC, an ROS scavenger). H(2)O(2)-induced decrease of cell viability was also attenuated by pretreatment with BHA and NAC. Furthermore, H(2)O(2)-induced increase of Bax, decrease of Bcl-2, and PARP-1 cleavage was also inhibited by BHA. Taken together, results of this investigation demonstrated that BHA protects primary cultured mouse hepatocytes against H(2)O(2)-induced apoptosis by inhibiting ROS generation. |
format | Online Article Text |
id | pubmed-4367145 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | The Korean Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-43671452015-03-20 Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes Hwang, Geun Hye Jeon, Yu Jin Han, Ho Jae Park, Soo Hyun Baek, Kyoung Min Chang, Woochul Kim, Joong Sun Kim, Lark Kyun Lee, You-Mie Lee, Sangkyu Bae, Jong-Sup Jee, Jun-Goo Lee, Min Young J Vet Sci Original Article Butylated hydroxyanisole (BHA) is a synthetic phenolic compound consisting of a mixture of two isomeric organic compounds: 2-tert-butyl-4-hydroxyanisole and 3-tert-butyl-4-hydroxyanisole. We examined the effect of BHA against hydrogen peroxide (H(2)O(2))-induced apoptosis in primary cultured mouse hepatocytes. Cell viability was significantly decreased by H(2)O(2) in a dose-dependent manner. Additionally, H(2)O(2) treatment increased Bax, decreased Bcl-2, and promoted PARP-1 cleavage in a dose-dependent manner. Pretreatment with BHA before exposure to H(2)O(2) significantly attenuated the H(2)O(2)-induced decrease of cell viability. H(2)O(2) exposure resulted in an increase of intracellular reactive oxygen species (ROS) generation that was significantly inhibited by pretreatment with BHA or N-acetyl-cysteine (NAC, an ROS scavenger). H(2)O(2)-induced decrease of cell viability was also attenuated by pretreatment with BHA and NAC. Furthermore, H(2)O(2)-induced increase of Bax, decrease of Bcl-2, and PARP-1 cleavage was also inhibited by BHA. Taken together, results of this investigation demonstrated that BHA protects primary cultured mouse hepatocytes against H(2)O(2)-induced apoptosis by inhibiting ROS generation. The Korean Society of Veterinary Science 2015-03 2015-03-18 /pmc/articles/PMC4367145/ /pubmed/25798044 http://dx.doi.org/10.4142/jvs.2015.16.1.17 Text en © 2015 The Korean Society of Veterinary Science. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Hwang, Geun Hye Jeon, Yu Jin Han, Ho Jae Park, Soo Hyun Baek, Kyoung Min Chang, Woochul Kim, Joong Sun Kim, Lark Kyun Lee, You-Mie Lee, Sangkyu Bae, Jong-Sup Jee, Jun-Goo Lee, Min Young Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title | Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title_full | Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title_fullStr | Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title_full_unstemmed | Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title_short | Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
title_sort | protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367145/ https://www.ncbi.nlm.nih.gov/pubmed/25798044 http://dx.doi.org/10.4142/jvs.2015.16.1.17 |
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