Abstract: 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.