Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes.
- Author:
Geun Hye HWANG
1
;
Yu Jin JEON
;
Ho Jae HAN
;
Soo Hyun PARK
;
Kyoung Min BAEK
;
Woochul CHANG
;
Joong Sun KIM
;
Lark Kyun KIM
;
You Mie LEE
;
Sangkyu LEE
;
Jong Sup BAE
;
Jun Goo JEE
;
Min Young LEE
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: apoptosis; butylated hydroxyanisole; primary mouse hepatocytes; reactive oxygen species
- MeSH: Animals; Apoptosis/*drug effects; Butylated Hydroxyanisole/chemistry/*pharmacology; Cell Survival/drug effects; Cells, Cultured; Hepatocytes/*drug effects; Hydrogen Peroxide/*toxicity; Male; Mice; Mice, Inbred ICR; Molecular Structure
- From:Journal of Veterinary Science 2015;16(1):17-23
- CountryRepublic of Korea
- Language:English
- Abstract: 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 (H2O2)-induced apoptosis in primary cultured mouse hepatocytes. Cell viability was significantly decreased by H2O2 in a dose-dependent manner. Additionally, H2O2 treatment increased Bax, decreased Bcl-2, and promoted PARP-1 cleavage in a dose-dependent manner. Pretreatment with BHA before exposure to H2O2 significantly attenuated the H2O2-induced decrease of cell viability. H2O2 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). H2O2-induced decrease of cell viability was also attenuated by pretreatment with BHA and NAC. Furthermore, H2O2-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 H2O2-induced apoptosis by inhibiting ROS generation.
