A prospective study of total urinary deoxynivalenol in adolescents in Shanghai, China.

There is growing interest in deoxynivalenol (DON) exposure during puberty because experimental evidence shows that DON-exposed to adolescents are more sensitive to DON and have limited detoxification ability. Nevertheless, there have been few surveys of DON exposure for adolescents in China. Furthermore, little is known about the effects of collection times on risk exposure. In the study, we estimated the risk of DON exposure for adolescents in Shanghai and explore the effects of collection time, areas, sex and BMI on intake estimates. A total of 315 adolescents aged 14-16 years, including 161 boys and 154 girls, were recruited. Urine samples were collected for three consecutive days and digested with ß-glucuronidase and then purified using a DON-immunoaffinity column (IAC). Total deoxynivalenol levels were measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in combination with a stable isotope dilution assay (SIDA). DON was detected in 945 morning urine samples taken from 315 individuals for three consecutive days. The mean estimated dietary intake of DON did not exceed the tolerable daily intake (TDI) of l µg/kg·bw/day, showing that exposure of adolescents in Shanghai is not of concern. However, 10-20% of probable daily intake (PDI) values exceed the TDI, indicating potential adverse effects. In addition, the DON concentration at the population level did not differ for urine samples collected at different times except for those of overweight adolescents. Therefore, assessment of exposure to DON by monitoring the morning urine of a healthy adolescent, except for overweight people, provides an appropriate estimate of exposure and related risk at the population level, but intake estimates for individuals are uncertain; these could be used to assess exposure of adolescents to DON rapidly and effectively for epidemiological investigations.

Ochratoxin A Induces Steatosis via PPARγ-CD36 Axis.

Ochratoxin A(OTA) is considered to be one of the most important contaminants of food and feed worldwide. The liver is one of key target organs for OTA to exert its toxic effects. Due to current lifestyle and diet, nonalcoholic fatty liver disease (NAFLD) has been the most common liver disease. To examine the potential effect of OTA on hepatic lipid metabolism and NAFLD, C57BL/6 male mice received 1 mg/kg OTA by gavage daily. Compared with controls, OTA increased lipid deposition and TG accumulation in mouse livers. In vitro OTA treatment also promoted lipid droplets accumulation in primary hepatocytes and HepG2 cells. Mechanistically, OTA prevented PPARγ degradation by reducing the interaction between PPARγ and its E3 ligase SIAH2, which led to activation of PPARγ signaling pathway. Furthermore, downregulation or inhibition of CD36, a known of PPARγ, alleviated OTA-induced lipid droplets deposition and TG accumulation. Therefore, OTA induces hepatic steatosis via PPARγ-CD36 axis, suggesting that OTA has an impact on liver lipid metabolism and may contribute to the development of metabolic diseases.