摘要:
研究增塑剂邻苯二甲酸二异壬酯(diisononyl phthalate, DINP)对雄性小鼠生殖毒性的氧化损伤机制,以昆明雄性小鼠为受试动物,随机分为7组,包括空白对照组(生理盐水),4个DINP暴露组(0.2、2、20和200 mg·kg-1)和褪黑素(melatonin, Mel)对照组50 mg·kg-1、Mel处理组(200 mg·kg-1 DINP+50 mg·kg-1 Mel),灌胃14 d。以睾丸组织匀浆测定活性氧(ROS)、还原型谷胱甘肽(GSH)和8-羟基脱氧鸟苷(8-OHdG)含量;以睾丸组织细胞测定DNA-蛋白交联(DPC)系数。随着DINP暴露剂量的增加,DINP暴露组睾丸组织ROS、8-OHdG含量和DPC系数逐渐上升,GSH含量逐渐降低,差异有统计学意义(P<0.05,P<0.01);Mel处理组ROS、8-OHdG含量和DPC系数相应降低,GSH含量逐渐上升。雄性小鼠睾丸组织形态观察结果表明,随着DINP暴露剂量的增加,小鼠睾丸组织的病理损伤程度呈上升趋势。实验结果表明,较高剂量(≥ 20 mg·kg-1)的DINP能造成小鼠睾丸组织的病理损伤和氧化损伤,50 mg·kg-1 Mel的抗氧化能力可以有效对小鼠睾丸组织起保护作用,使组织损伤减轻,即生殖毒性减弱。
Abstract:
To investigate the oxidative damage mechanism of plasticizer diisononyl phthalate on reproductive system in male mice, Kunming male mice were divided randomly into seven groups and administered daily for fourteen days. The groups included saline group, four DINP exposure groups (0.2, 2, 20 and 200 mg·kg-1), melatonin control group (50 mg·kg-1), and melatonin treatment group (200 mg·kg-1 DINP+50 mg·kg-1 Mel). The contents of reactive oxygen species (ROS), reduced glutathione (GSH) and 8-OhdG, and DNA-protein crosslinking (DPC) coefficients were determined by testicular homogenate. With the increasing dose of DINP exposure, the content of ROS and 8-OhdG, and DPC coefficients in testis tissue of DINP exposure group gradually increased and the content of GSH gradually decreased. The differences was statistically significant (P<0.05, P<0.01). Meanwhile, the content of 8-OHdG and DPC coefficients decreased correspondingly, and the content of GSH gradually increased in melatonin treatment group. The differences was statistically significant (P<0.05, P<0.01). Morphological observation of testis in male mice showed that the pathological damage of testis was more serious with the increase of the DINP exposure dose. Our results revealed that DINP at higher dose (≥ 20 mg·kg-1) could cause pathological damage and oxidative damage in mouse testis. The 50 mg·kg-1 Mel could effectively protect the testicular tissue of mice and alleviate the tissue damage. In short, the reproductive toxicity of DINP is weakened.
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