摘要:
探究邻苯二甲酸二异癸酯(diisodecyl phthalate,DIDP)对小鼠肺组织的氧化损伤。以BALB/c小鼠为受试动物,随机分为7组,包括1个阴性对照组(生理盐水)、4个DIDP染毒组(0.15,1.5,15,150 mg·kg-1)、1个维生素E (100 mg·kg-1)组和1个高剂量DIDP (150 mg·kg-1)加维生素E (100 mg·kg-1)组,灌胃染毒14 d。处死小鼠,制备肺组织匀浆样品,以化学荧光法检测活性氧(reactive oxygen species,ROS)含量,以分光光度试剂盒法检测还原型谷胱甘肽(glutathione,GSH)的含量、以硫代巴比妥酸(TBA)法检测丙二醛(malondialdehyde,MDA)的含量、以酶联免疫吸附(EILSA)试剂盒法检测8-羟基脱氧鸟苷(8-hydroxy-deoxyguanosine,8-OHdG)的含量,同时观察肺组织的病理变化与荧光染色结果。随着DIDP染毒剂量的升高,肺组织的ROS、MDA、8-OHdG含量逐渐上升,GSH含量逐渐降低,各指标呈一定的剂量-效应关系。染毒剂量为15 mg·kg-1时,ROS、GSH、8-OHdG含量差异有统计学意义(P<0.05,P<0.01);染毒剂量为150 mg·kg-1时,上述指标差异均有统计学意义(P<0.05,P<0.01)。小鼠肺组织H&E染色和荧光染色观察结果表明,随着DIDP染毒剂量的增加,小鼠肺细胞的病理损伤越严重。与150 mg·kg-1 DIDP剂量组比较,150 mg·kg-1 DIDP+维生素E组的ROS、MDA和8-OHdG含量均有下降,GSH含量上升(P<0.05,P<0.01);小鼠肺组织病理损伤减轻。以上结果说明,较高剂量(≥15 mg·kg-1)的DIDP能造成小鼠肺组织的氧化损伤,维生素E对其损伤有拮抗作用。
Abstract:
This study investigates the oxidative damage induced by diisodecyl phthalate (DIDP) on mouse lung tissue. BALB/c mice are randomly classified into seven groups and orally administered with drugs daily for fourteen days. Those groups include one solvent control group (normal saline), four diisodecyl phthalate groups, one vitamin E (100 mg·kg-1) group and one high dose DIDP (150 mg·kg-1) plus vitamin E (100 mg·kg-1) group. The exposure doses of diisodecyl phthalate groups are 0.15, 1.5, 15 and 150 mg·kg-1 respectively. The content of reactive oxygen species (ROS) is detected by chemiluminescence method in mice lung tissue homogenate samples. The content of reduced glutathione (GSH) is measured by spectrophotometric kit. The content of malondialdehyde (MDA) was determined by barbituric acid (TBA) method and the content of of 8-hydroxy-deoxyguanosine (8-OHdG) was detected by enzyme-linked immunosorbent assay (EILSA) kit. At the same time, the pathological changes and fluorescent staining results of lung tissue are observed. With the increase of DIDP dose, the contents of ROS, MDA and 8-OHdG in lung tissue increase gradually, and the content of GSH decreases gradually. Each indicator has a certain dose-effect relationship. In the 15 mg·kg-1 exposure group, the contents of ROS, GSH and 8-OHdG are higher compared with the control group (P<0.05, P<0.01). In the high-dose exposure groups, the differences of the above indicators are all statistically significant (P<0.05, P<0.01). H&E staining and fluorescence staining of mouse lung tissue shows that the pathological damage of mouse lung cells are more serious with the increase of DIDP dose. Compared with the 150 mg·kg-1 DIDP dose group, the levels of ROS, MDA and 8-OHdG in the 150 mg·kg-1 DIDP+vitamin E group are lower while that of the GSH content is increasing (P<0.05, P<0.01), and tissue damage is alleviated. The above results indicate that high dose (≥ 15 mg·kg-1) of DIDP can cause oxidative damage in mouse lung tissue, whereas, vitamin E has antagonistic effect on the damage.
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