title: Protective effects of apigenin against furan-induced toxicity in mice.
abstract: Furan, a food contaminant formed by heating, is possibly carcinogenic to humans. In this study, we discussed the effect of administration of apigenin on furan-induced toxicity by determining the ROS content, oxidative damage, cytokine levels, DNA damage, and the liver and kidney damage in a mouse model. Our data showed that apigenin administered at 5, 10, and 20 mg kg(-1) bw per day could decrease the toxicity induced by furan to different extents. On one hand, apigenin has the ability to increase the oxidative damage indexes of glutathione (GSH) and glutathione-S-transferase (GST) as well as superoxide dismutase (SOD) activities but decrease myeloperoxidase (MPO) activities and maleic dialdehyde (MDA) content in the liver and kidney of mice treated with furan. On the other hand, it could decrease cytokine levels of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, and interleukin (IL)-6 but increase interleukin (IL)-10 in the serum of furan-treated mice. At the same time, the three concentrations of apigenin elected in this paper all could decrease the ROS content, DNA damage index of 8-hydroxy-desoxyguanosine (8-OHdG), the liver and kidney damage indexes of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic dehydrogenase (LDH), and blood urea nitrogen (BUN) and creatinine content in furan-treated mice to different extents. The protective effects of apigenin against furan-induced toxicity damage were mainly due to its excellent ability to scavenge free radicals and inhibit lipid oxidation. This is important when considering the use of apigenin as a dietary supplement for beneficial chemoprevention of furan toxicity.
authors.affiliation: College of Quartermaster Technology, Jilin University, Changchun, China130062. yuanyuan1024@gmail.com.
authors.forename: Enting
authors.initials: E
authors.lastname: Wang
authors.forename: Fang
authors.initials: F
authors.lastname: Chen
authors.forename: Xiaosong
authors.initials: X
authors.lastname: Hu
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yuan
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D047310:Apigenin / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000097:blood; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D004249:DNA Damage / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005663:Furans / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D016753:Interleukin-10 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000447:Aldehydes; D000975:Antioxidants; D005663:Furans; D053583:Interleukin-1beta; D015850:Interleukin-6; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; C015977:malealdehyde; D047310:Apigenin; D003404:Creatinine; D009195:Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione; C039281:furan