Methylseleninic Acid Prevents Patulin-Induced Hepatotoxicity and Nephrotoxicity via the Inhibition of Oxidative Stress and Inactivation of p53 and MAPKs

被引:43
|
作者
Lu, Xiaotong [1 ]
Zhang, Enxiang [1 ]
Yin, Shutao [1 ]
Fan, Lihong [2 ]
Hu, Hongbo [1 ]
机构
[1] China Agr Univ, Beijing Adv Innovat Ctr Food Nutr & Human Hlth, Coll Food Sci & Nutr Engn, Beijing Key Lab Food Nonthermal Proc, 17 Qnghua East Rd, Beijing 100083, Peoples R China
[2] China Agr Univ, Coll Vet Med, 2 Yuanmingyuan West Rd, Beijing 100193, Peoples R China
基金
中国国家自然科学基金;
关键词
patulin; methylseleninic acid; hepatotoxicity; nephrotoxicity; ROS; p53; MAPKs; HUMAN PROSTATE-CANCER; MYCOTOXINS CITRININ; INDUCED APOPTOSIS; IN-VITRO; SELENIUM; CELLS; MICE; CHEMOPREVENTION; SELENOPROTEINS; GENOTOXICITY;
D O I
10.1021/acs.jafc.7b01338
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Patulin is one of the common food-borne mycotoxins. Previous studies have demonstrated that patulin can cause diverse toxic effects in animals including hepatotoxicity and nephrotoxicity. In the present study, we have addressed the protective effect of two forms of selenium compounds methylseleninic acid (MSeA) and sodium selenite on patulin-induced nephrotoxicity and hepatotoxicity using both in vitro and in vivo models. Results showed that MSeA at concentrations of 3-5 mu M, not sodium selenite at the same concentrations, is capable of protecting against patulin-induced cytotoxicity in the cell culture model. Moreover, the hepatoprotective and nephroprotective effects of MSeA (2 mg/kg body weight, oral administration) on patulin-induced toxicity (10 mg/kg body weight, intraperitoneal injection) were also achieved in the animal model. A further mechanistic study revealed that the protective effect of MSeA on patulin-mediated toxicity is attributed to its ability to inhibit patulin-mediated ROS generation and inactivate p53 and mitogen-activated protein kinase (MAPK) signaling pathways. Our findings support a possible usefulness of MSeA as a novel detoxicant to mitigate the toxicities of patulin.
引用
收藏
页码:5299 / 5305
页数:7
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