| With the extensive use in addition agent of multipara,the arsanilic acid has resulted in remnant in products and environment pollution.So we carry out this research.Research Aim:We adopted this study of organic arsenic - the arsanilic acid in mice liver toxicity damage and identify its mechanism,so as to improve the arsanilic acid toxicity studies and a comprehensive objective evaluation of the arsanilic acid,for the provision of information on livestock and poultry production.Research Methods:We use this experiment in mice to 18-25g test object,the arsanilic acid infection,15 days after the anatomy of the liver from mouse experiments conducted as follows: conventional pathological observed pathological changes in liver tissue in mice;using Kits was detected liver function;Conventional method used to detect the activity of SOD,GSH-PX and CAT in liver tissue;TUNEL method used to detect the hepatocytes apoptosis and changes in the rate of apoptosis.Research Results:The dose the mice were shown varying degrees of hepatocytes degeneration and necrosis,hepatic cord disorders,nuclear enrichment,fragmentation,margination,such as pathological changes.With the higher dose,The DNA damage on the liver cell caused by the arsanilic acid is very obvious.In liver function tests,ALT and AST activity increased significantly. Compared with the control group,the dose group showed a very significant difference,with the increasing concentration of each group ALT,AST activity gradually increased,showing a dose-response relationship.Conventional methods that detected the impact about the arsanilic acid on the liver lipid peroxidation showed:1/4 LD50,1/8 LD50,1/16 LD50,1/32 LD50 group compared with the control group showed a significant difference(P <0.01),and 1/64 LD50 group with no significant difference(P> 0.05),But still lower SOD activity;CAT activity of 1/4 LD50,1/8 LD50,1/16 LD50 group was significantly lower than the control group(P <0.01),and 1/32 LD50, 1/64 LD50 with the control group showed significant differences(P < 0.05);GSH-PX activity of 1/64 LD50 group(649.5619±0.9431 U / mgProt) was significantly lower than the control group (729.5091±26.4308 U / mgProt)(P <0.05),and 1/4 LD50,1/8 LD50,1/16 LD50,1/32 LD50 group compared with the control group showed a significant difference(P <0.01);Each dose group MDA content in the liver of mice are significant changes,compared with the control group showed a significant difference(P <0.01),and with the increased concentration,MDA content increasingly shown significant dose-response relationship.TUNEL results:There were no hepatocytes apoptosis in 1/4 LD50 and 1/8 LD50 group,the main reason may be the role of high-dose caused acute hepatocytes necrosis,cell broken to pieces and dissolved,the nucleus broken and degradated,moreover there was nothing in the cells.In 1/16 LD50,1/32 LD50 and 1/64 LD50 group there were obvious hepatocytes apoptosis,and with the increased concentration,the more obvious apoptosis.The apoptosis rate of 1/16 LD50,1/32 LD50 and 1/64 LD50 Group compared with the control group showed a significant difference(P <0.01),The RT-PCR results showed that:The expression of Bax and Bcl-2 is very few in 1/4 LD50 and 1/8 LD50 group;In 1/16 LD50,1/32 LD50 and 1/64 LD50 group,With the increased amount of poison attack,Bax gene expression increased,Bcl-2 gene expression is reduced accordingly.Research Conclusion:1.the arsanilic acid can cause liver function in mice injury,and with the increased concentration,ALT,AST level of liver tissue gradually increased,the morphology showed that hepatocytes necrosis and swelling,hepatic cord disorders;2,the arsanilic acid can cause DNA damage of liver cells;3,the arsanilic acid can reduce the activity of peroxidase(SOD, GSH-PX,CAT) in liver of mice,increased lipid peroxides(MDA),showed that the arsanilic acid can cause lipid peroxides in liver;4.Through the lipid peroxidation induced hepatocytes apoptosis or even death might be one of the mechanisms of the arsanilic acid toxicity,the arsanilic acid at low doses can increase the expression of Bax protein and reduce the expression of Bcl-2 protein to promot apoptosis of mouse liver cell,and in high doses is a direct result of liver necrosis, resulting in liver damage. |