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In vivo toxicity assessment of aflatoxin B1-contaminated corn after ozone degradation Part A Chemistry, analysis, control, exposure & risk assessment
- Luo, Xiaohu, Li, Ke, Xing, Jiali, Qi, Lijun, Yang, Ming, Wang, Ren, Wang, Li, Li, Yanan, Chen, Zhengxing
- Food additives & contaminants 2018 v.35 no.2 pp. 341-350
- aflatoxin B1, alanine transaminase, albumins, alkaline phosphatase, aspartate transaminase, blood serum, body weight, corn, feeds, globulins, histopathology, kidneys, liver, mice, ozonation, ozone, protein content, tissues, toxicity, China
- Corn is an important food and feedstuff in China and worldwide. The problems caused by aflatoxin B₁-contaminated corn (ACC) are of great concern. Our previous studies have demonstrated that ozone can effectively degrade AFB₁ in corn, prompting us to investigate the in vivo toxicity of treated ACC. In this study, 35 Kunming mice were used to assess the in vivo toxicity of ozone treated ACC. Results indicated that compared to mice fed with basal feedstuff (provided by the Shanghai SLAC Laboratory), those fed with ACC have significantly decreased mean weight as well as total protein (TP), albumin (ALB), and globulin (GLB) contents (p < 0.05). On the other hand, the liver and kidney/body weight ratio as well as the serum alanine transaminase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels significantly increased (p < 0.05). Obvious histopathological changes were found in the liver and kidney. When mice were fed with the ozone-treated ACC, no significant differences were observed in the mean weight, the liver and kidney/body weight ratio and in the major serum indexes ALT, TP, ALB, and GLB (p > 0.05). However, AST and ALP significantly increased (p < 0.05), and slight histopathological changes were found in liver tissues. This study indicated that ACC may lead to significant changes in various physiological characteristics and biochemical indexes in liver and kidney tissues, but ozone treatment of ACC could significantly reduce these changes.