ArticleJournal of veterinary science2015
Protective effect of butylated hydroxylanisole against hydrogen peroxide-induced apoptosis in primary cultured mouse hepatocytes.
Article in Journal of veterinary science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
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- Antioxidants Amelioration Is Insufficient to Prevent Acrylamide and Alpha-Solanine Synergistic Toxicity in BEAS-2B Cells.International journal of molecular sciences · 2023Article
- Ex Vivo Hepatic Perfusion Through the Portal Vein in Mouse.Journal of visualized experiments : JoVE · 2022Article
- MicroRNA-125b alleviates hydrogen-peroxide-induced abnormal mitochondrial dynamics in HT22 cells by inhibiting p53.Metabolic brain disease · 2021Article
- Lion's Mane Mushroom,Antioxidants (Basel, Switzerland) · 2019Article
- Overexpression of C‑sis inhibits H2O2‑induced Buffalo rat liver cell apoptosis in vitro and alleviates liver injury in a rat model of fulminant hepatic failure.International journal of molecular medicine · 2018Article
- Mixture Design and Doehlert Matrix for the Optimization of the Extraction of Phenolic Compounds fromFrontiers in chemistry · 2017Article
- The cytotoxicity and protective effects ofAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2016Article
- Promotion of behavior and neuronal function by reactive oxygen species in C. elegans.Nature communications · 2016Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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