氨基脲的毒性效应研究进展

环境及食品中的氨基脲主要来源于硝基呋喃类药物及偶氮二甲酰胺的分解；同时,次氯酸盐与氨基酸的作用也能产生氨基脲. 氨基脲曾在食品动物、玻璃包装食品等多种食品中被检出,近期在我国东营潮河入海口邻近海域也有检出. 早期的研究表明,氨基脲具有致诱变性和潜在的致癌性；而近期的研究表明,氨基脲不仅能够在组织形态学水平上导致多种组织器官的形态改变,而且还可对神经系统、内分泌系统的功能产生影响. 50~150mg/L氨基脲可导致大鼠胎儿肺和肝脏器官内核酸水平显著降低,增加幼年小鼠肺肿瘤发生率；此外,能够显著增加鼠骨髓嗜多染红细胞的微核率,表现出弱遗传毒性. 氨基脲是GABA合成酶GAD(谷氨酸脱羧酶)的抑制剂,并且对NMDAR(N-甲基-D-天氡氨酸受体)具有拮抗作用,从而产生神经毒性. 氨基脲可致大鼠多个靶组织器官形态结构的改变且具有一定的性别差异,其中,对胸腺及肾上腺的组织学改变仅在雌性中表现出来,而对甲状腺组织结构的改变仅在雄性中表现明显,对生殖器官的毒性表现为其能够改变雌性卵巢和雄性睾丸显微结构. 雌性大鼠口服40、75、140mg/kg氨基脲28d能够降低其血浆内E₂(雌二醇)水平,并且呈剂量-效应关系,表现出抗雌激素效应. 未来应继续补充氨基脲的毒性数据,以揭示其毒性作用机制；同时,应从其衍生物降解规律、环境风险评价等角度进行深入研究. 

Research Progress on the Toxicity of Semicarbazide

The main sources of semicarbazide (SEM) residual in the environment and food are the decomposition of nitrofuran drugs and azodicarbonamide blowing agents. Besides, SEM can also be produced by the interaction of hypochlorite and amino acids during bleaching process. SEM presents in animal-derived and glass jar packaged food, and recently SEM was detected in coastal waters adjacent to the Chaohe River estuary in reports. Earlier studies showed that SEM has mutagenic activity and latent carcinogenicity, while recent researches proved that SEM not only causes histological and morphological alternation in target organs, but also disturbs the nervous and endocrine systems. SEM with doses between 50and 150mg/kg can significantly decrease the nucleic acid level in the lung and liver of rat fetuses. Moreover, this chemical could also accelerate the development of lung tumors in newborn mice. SEM could also increase the frequencies of micronuclei in polychromatic erythrocytes for bone marrow cells of rat or mouse by showing their weak genotoxicity. SEM was an inhibitor in GABA synthesizing enzyme GAD and can interfere with NMDAR by acting as an antagonist. This demonstrated the existence of neurotoxicity of SEM. Moreover, experiments in vivo showed that SEM can cause histological and morphological alternation on potential target organs in a sex-related way:histological alternations of thymus and adrenals were only observed for female while thyroid altered more significantly for male. The microscopic structures of the ovary and testis were also affected by SEM treatments with potential toxicity on reproductive function. Serum estrogen levels for female rats were dose-dependently reduced after oral administration of SEM for 28days at 40,5, 140mg/kg, and this suggested that SEM has an anti-estrogenic activity. Future research on SEM should mainly concentrate on the toxic effects and mechanisms, degradation pattern of its derivatives and its environmental risk assessment.