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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 |
Publicado: |
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 |
Sumario: | 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. |
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