| A toxicity test was used to determine the 48h median lethal concentration (48h LC50 Value) of Methylamino abamectinaa on pomacea canaliculata. Using P. canaliculata as an experimental animal, the Methylamino abamectin was prepared into different concentrations (LC25, LC50, LC75), the effects of Methylamino abamectin on superoxide dismutase (SOD), catalase (CAT), and Phenoloxidse (PO), acetylcholinesterase (AChE), glutathione s-tranferase (GSTs) activity and malondialdehyde (MDA) content in hepatopancreas were studied in different exposure time (6,12,24,48 h). This research used the paraffin section method to compare five organs of control group and chemical treatments p. canaliculata on microexamination. The main results are as follows:1.800 mg/L concentrations of Methylamino abamectin led to high antifeedan rate of which was at 93.5% for 48 hours on P. canaliculata by using leaf immersion method. AFC50 is 4.13 mg/L.133 μ/g concentrations of Methylamino abamectin to feeding P. canaliculata for 48h led to highly lethal rate of 87.5% with agar cake bait containing, and LD50 is 67.57 μ/g. So we could conclude that Methylamino abamectin had stronger antifeedan effect and stomach poisonous. But different concentration of Methylamino abamectin had little toxicity effects to Pomacea Canaliculata’primes by contact method.2. Using "final screen method in the lab of snail killing drugs" by WHO, the effects of Methylamino abamectin with different concentration on the eggs, youngs snail、primes snail and adult snail were studied. The results showed that the Methylamino abamectin had no significant toxicity effect on the eggs of P. canaliculata, but had significant toxicity effect on the youngs snail、primes snail and adult snail. The median lethal concentration (LC50) in 48 h of Methylamino abamectin were 0.1067 mg/L,0.1873 mg/L,0.232 mg/L, respectively.3. At low (LC25) and moderate (LC50) doses of Methylamino abamectin, the activity of GSTs and AChE of hepatopancreas in primes and adult snail significantly higher than control group; to the peak in 12 h and decreased after 48 h (P<0.01); but the activity of AChE in LC25 group on adult snail increased compared with control whereas GSTs in joungs snail increased to the peak in 6 h than decreased significantly compared to control at high (LC75) dose of Methylamino abamectin. All concentration group, GSTs and AChE activity in hepatopancreas of youngs snail were induced remarkably first, then inhibited obviously as time prolonging.4. The influence of phenoloxidse (PO) was fluctuant for different growth phase of Pomacea Canaliculata. PO could be induced by low (LC25) dose of Methylamino abamectin; while PO in hepatopancreas of youngs snail and adult snail was induced remarkably first, then inhibited obviously at moderate (LC50) dose of Methylamino abamectin. PO in hepatopancreas of primes snail treated by moderate (LC50) and high (LC75) dose of Methylamino abamectin, rised sharply before 6 h, and declined between 6-12 h, then sharply dropped in the leavel of control group after 48 h.5. With different chemical treatments, CAT activity in general showed the high-low trend, and with the increase of exposure concentration and time, the CAT activity was obviously inhited. The CAT activities in hepatopancreas of youngs snail、primes snail and adult snail treated by high (LC75) dose of Methylamino abamectin for 6 h, attained to the maximum, which was 3.13、2.29、2.21 times that of the control group, respectively. As the extension of time, CAT activities dropped to the lowest after 48 h, significantly lower than the control group.6. At moderate (LC50) doses of Methylamino abamectin, SOD in the hepatopancreas followed an up-down-up-down pattern, whereas SOD in the hepatopancreas followed an up-down pattern at other treatment. SOD could be sharply induced in a short time of exposure (12 h). The activity of SOD in all group did not return to normal after 48 h, but SOD in primes snail still significantly elevated at low doses of Methylamino abamectin.7. Under the stress of Methylamino abamectin, P. canaliculata liver malondialdehyde (MDA) content had changed significantly higher than the control group. All concentration of Methylamino abamectin on primes snail, the MDA content increased with time, and with the dose of Methylamino abamectinm, being directly proportional to the concentration, in the maximum, concentration of 48 h reaching the maximum value. The concentration of MDA content was induced during the whole exposure process. In low (LC25) dose of Methylamino abamectin on adult snail, MDA content in 6 h, and 12 h, respectively had no significant change, while at other treatment, it was significantly or extremely significantly induced.8. Diffuse necrosis in liver tissue was observed. Liver was clearly damage with the increasing of exposure concentration and time with a good dose-response pattern. In the liver injury, diffuse congestion in connective tissue. High concentration of Methylamino abamectin can induce acute necrosis of liver congestion, cell degeneration, malformation, necrosis and cytolysis. The change of stomach and intestine cilia with Methylamino abamectin were observed on microexamination. Cells were lost and swelling in high concentration of Methylamino abamectin. Diffuse necrosis and edema in mucosa of stomach and intestine were observed. High concentration of Methylamino abamectin can cause similar pathological change to ovary and testicle of Potomac canaliculata:atrophied oocyte; spermatogoriium pyknosis; widened the distance between the folliculus.The results above suggest that oxidative damage may be one of the reasons for methylamino abamectin toxicity of hepatopancreas in P. canaliculata. |
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