Effects of acute exposure to diisodecyl phthalate on kidney in mice and underlying mechanism
Balb/c小鼠随机分为空白对照组（生理盐水）、不同剂量DiDP组（0.15、1.5、15、150 mg/kg）、Vit E组（100 mg/kg）、联合处理组（150 mg/kg DiDP+100 mg/kg Vit E）共7组，每组8只。灌胃染毒14 d后，观察肾组织切片病理学变化，检测肾组织活性氧（ROS）、丙二醛（MDA）、还原型谷胱甘肽（GSH）、8-羟基脱氧鸟苷（8-OHdG）和血清尿素氮（UREA）、肌酐（CREA）水平。
与空白对照组比较，150 mg/kg DiDP组小鼠肾组织ROS、MDA、8-OHdG水平及血清UREA、CREA含量升高，GSH水平降低，差异均有统计学意义（
P< 0.05）；肾组织切片结果显示DiDP剂量越高，肾脏损伤越严重。加入Vit E干预后，与150 mg/kg DiDP组比较，联合处理组小鼠肾组织ROS、MDA、8-OHdG水平及血清UREA、CREA含量下降，GSH水平上升，差异均有统计学意义（ P< 0.05），同时肾组织切片结果也显示Vit E可在一定程度上降低150 mg/kg DiDP造成的肾损伤。 结论
Diisodecyl phthalate (DiDP) is a new type of plasticizer, and can enter the human body through a variety of ways. At present, there are few domestic studies on the nephrotoxicity of DiDP, and whether DiDP can cause renal injury in laboratory animals through oxidative stress is still unclear.
This experiment investigates the effects of different doses of DiDP on the kidney in male Balb/c mice, and explores the underlying mechanism.
Balb/c mice were randomly divided into control group (saline), DiDP groups (0.15, 1.5, 15, and 150 mg/kg), vitamin E (Vit E) group (100 mg/kg), and Vit E intervention group (150 mg/kg DiDP+100 mg/kg Vit E) (
n=8 in each group). After 14 d of the designed exposure by gavage, the pathological changes of renal tissue specimens were observed; reactive oxygen species (ROS), malondialdehyde (MDA), reduced glutathione (GSH), and 8-hydroxydeoxyguanosine (8-OHdG) in renal tissues, as well as urea nitrogen (UREA) and creatinine (CREA) in serum were measured. Results
The levels of ROS, MDA, and 8-OHdG in renal tissues and the levels of UREA and CREA in serum were significantly higher in the 150 mg/kg DiDP group than those in the control group, and the level of GSH was significantly lower (
P< 0.05). Moreover, the pathological results showed that higher doses of DiDP resulted in more serious renal injury. Compared with the 150mg/kg DiDP group, the levels of ROS, MDA, and 8-OHdG in renal tissues and the levels of UREA and CREA in serum were decreased, and the GSH level was increased in the Vit E intervention group ( P< 0.05). Meanwhile, the pathological results showed that Vit E somewhat relieved the renal injury caused by 150 mg/kg DiDP. Conclusion
DiDP can induce pathological damage of renal tissues in mice through oxidative stress.