Limited Link between Oxidative Stress and Ochratoxin A—Induced Renal Injury in an Acute Toxicity Rat Model
Liye Zhu,
Tao Yu,
Xiaozhe Qi,
Jing Gao,
Kunlun Huang,
Xiaoyun He,
Haoshu Luo,
Wentao Xu
Affiliations
Liye Zhu
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Tao Yu
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Xiaozhe Qi
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Jing Gao
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Kunlun Huang
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Xiaoyun He
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Haoshu Luo
State key Laboratory of Agrobiotechnology, Department of Animal Physiology, College of Biological Sciences, China Agricultural University, Beijing 100193, China
Wentao Xu
Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, No. 17 Tsinghua Donglu, Beijing 100083, China
Ochratoxin A (OTA) displays nephrotoxicity and hepatotoxicity. However, in the acute toxicity rat model, there is no evidence on the relationship between OTA and nephrotoxicity and hepatotoxicity. Based on this, the integrated analysis of physiological status, damage biomarkers, oxidative stress, and DNA damage were performed. After OTA treatment, the body weight decreased and AST, ALP, TP, and BUN levels in serum increased. Hydropic degeneration, swelling, vacuolization, and partial drop occurred in proximal tubule epithelial cells. PCNA and Kim-1 were dose-dependently increased in the kidney, but Cox-2 expression and proliferation were not found in the liver. In OTA-treated kidneys, the mRNA expressions of Kim-1, Cox-2, Lcn2, and Clu were dose-dependently increased. The mRNA expressions of Vim and Cox-2 were decreased in OTA-treated livers. Some oxidative stress indicators were altered in the kidneys (ROS and SOD) and livers (SOD and GSH). DNA damage and oxidative DNA damage were not found. In conclusion, there is a limited link between oxidative stress and OTA-induced renal injury in an acute toxicity rat model.
