Toxicity Of Pesticide Trichlorphon On Bufo Raddei Tadpoles

Amphibian populations have globally declined over the past decades, including a number of species extinction. Now, some reports have proved the pesticide (herbicide, insecticide et al) was one resulting in amphibian population declination. In order to evaluate the toxicity and discuss the toxic mechanism of the organophosphorus pesticide (OP) trichlorphon to Bufo raddei Strauch, tadpole early development, activities of Acetylcholinesterase (AChE), Superoxide dismutase(SOD) and Catalase(CAT), erythrocyte micronucleus ratio and DNA-single strand break in tadpoles.The experiment included tow parts: one was on tadpole early development experiment in which the tadpoles of B. raddei were exposed to trichlorfon at concentration o f 0.5 mg/L, 1.0mg/L, 5.0mg/L for 40d respectively. Another experiment was on the activities of antioxidant enzymes and genotoxicity of trichlorfon in B. raddei tadpoles exposed to trichlorfon at concentration of 0.05 mg/L, 0.05 mg/L, 1.0 mg/L, 2.5 mg/L for 7d, 14d, 21d or 28d respectively. The results showed that:When the tadpoles of B. raddei were exposed to trichlorfon at concentration o f 0.5 mg/L,1.0mg/L,5.0mg/L for 30d respectively, the development of tadpoles had no significant difference with those of the relative control groups(P>0.05). After 30d, the 0.5 mg/L and 1.0mg/L groups grew up quicker than the relative control groups but the 5.0 mg/L groups inhibited the development of tadpoles. Tadpoles with tail flexure and swirling in each treating group were found.The results indicated that the lower concentration (0.05 mg/L) had no significant effect on the activities of SOD and CAT in the short term (7d). But, after 21d, the activity of SOD at the concentration of 0.05mg/L marked lower than control group and the activity of CAT at the concentration of 0.05mg/L significantly (P>0.05) higher than control group that indicated the lower concentration (0.05mg/L) could inhibit the activity of SOD and induced the activity of CAT in the long term exposure (>21d). But the activities of SOD and CAT were both inhibited at each higher concentration (>0.05mg/L) exposure. The activity of AChE was inhibited both at the lower and higher level of trichlofon.The results also showed that frequency of micronuclei and nuclear anomalies of each concentration group for the tadpoles exposed to trichlorfon were higher than those of the control group (P <0. 01) except the tadpoles exposed to trichlorfon for 7d at the concentration of 0.05 mg/L which had no significant difference respect to those from control group. The level of DNA damage in each concentration group for the tadpoles exposed to trichlorfon was significantly higher than that of control group (P < 0. 05, P< 0. 01) and increased gradually with the dose increasing of trichlorfon in the same exposure period. There existed dose-effect but no time-effect relationship among the tested concentrations.In one word, the organophosphorus pesticide (OP) trichlorphon did harms to B. raddei tadpoles by inhibiting the activity of AChE, and by affecting antioxidant defense system and genetic materials.For more credibility of the result, the biomarkers are signed out in our experiment. Through detecting the activity of AChE, SOD and CAT, the number of erythrocytes nucleus anomalies and tadpole live cell DNA damage, the toxicity of trichlorphon is evaluated, which indicates that trichlorphon has toxicity on aquatic animals.