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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...

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Detalles Bibliográficos
Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Veterinary Science 2015
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
Descripción
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.