The Study On The Toxicity And Toxicological Mechanism Of Microcystin-LR

Microcystin-LR is a secondary metabolize production of poisonous cyanobacteria. It is a kind of toxin in cells which only can be released into water with the death and decomposing of these cells. In the recent, with the increasing of human population and the consequent intensification of agricultural and industrial activities, a great deal of sewage riched in nitrogen and phosphorus streams into freshwater bodies. The enhancement of eutrophication leads to the frequent formation of surface planktonic cyanobacteria. The occurrence of blue-green algae blooms contributes to deterioration of water which cause the death of fish. And the biotoxins released by decayed cyanobacteria do great harm to the health of human beings and other creatures.People contact these toxins mainly by drinking water or eating foods contaminated by them. MCLR is liver specific toxins, which can lead to the damage of liver. The development of enteron cancer, such as primary liver cancer, has been linked to long-term chronic exposure to MCLR. MCLR, being a tumour promoter, may induce the overproduction of free radicals. Oxidative stress can lead to severe adverse effects on cells by causing lipid peroxidation. But we still need more research on injury caused by oxidative stress, such as membranous toxicity, protein and DNA damage. On the other hand, according to most researches MCLR is a tumour promotor, but not a carcinogen with genotoxicity. However, there are still some scholars who believe that MCLR results in the damage of genetic material. To strengthen the perception of people on the toxicity and toxicological mechanism of Microcystin, We treat human hepatoma cells with MCLR in vitro. In the article, we mainly explore the combinative toxicity of MCLR, Aflatoxin B1 and Fumonisin B1, the combinative action of MCLR and Carbon Tetrachloride on DNA Damage. Moreover, we also investigate cytotoxicity, oxidative stress, membrane toxicity and DNA damage. We can conclude that:1, MCLR may enhance oxidative stress in Hep G2 cells. The excessive production of reactive oxygen species(ROS) and the lipid peroxidation products, malondialdehyde(MDA), was significantly increased in microcystin-treated cells. And after exposure to MCLR, membrane fluidity of these cells decreases. MCLR can lead to the injury of biomembrane. But in the experimental dosage scope, MCLR fails to influence membrane permeability and Na+,K+-ATPase activity. This possibly is because different cells have different sensitivity to MCLR. In addition, according to the results of MCLR-induced DNA damage in vitro, MCLR can result in DNA strand break, but can not cause DNA Cross-links of the Calf Thymus DNA and Hep G2 Cells DNA.2, According to the research on combinative toxicity of MCLR and other hazardous substance, combinative toxicity of MCLR, Aflatoxin B1 and Fumonisin B1 falls into the category of additive effect. So after treatment by the three biotoxins, cytotoxicity of human hepatoma cells is enhanced. Moreover, we explore the effect of DNA Damage of MCLR and Carbon Tetrachloride, which is the by-product of chlorination disinfection with factorial analysis. According to the result, we can see that each of the two...