tailieunhanh - Cyanobacterial Toxins of Drinking Water Supplies: Cylindrospermopsins and Microcystins - Chapter 7

Các gia đình microcystin của peptide đã nhận được sự chú ý nghiên cứu nhiều hơn có bất kỳ độc tố cyanobacteria khác. Đây là một hệ quả của cái chết vật nuôi gây ra bởi tiêu thụ của độc Microcystis aeruginosa (trước đó được biết đến như Anacystis cyanea và Microcystis toxica) và nguy cơ tiềm tàng đối với sức khỏe con người từ microcystin-ô nhiễm nước uống. Bao gồm gần đây của microcystin-LR là một chất hóa học độc hại trong Tổ chức Y tế Thế giới (WHO) uống hướng dẫn nước có điều tra tiếp tục tăng. | 7 Microcystin Toxicity The microcystin family of peptides has received more research attention than have any other cyanobacterial toxins. This is a consequence of the many livestock deaths caused by consumption of toxic Microcystis aeruginosa earlier known as Anacystis cyanea and Microcystis toxica and the potential risk to human health from microcystin-contaminated drinking water. The recent inclusion of microcystin-LR as a toxic chemical in the World Health Organization WHO drinking water guidelines has further accelerated investigation of the adverse effects of these peptides on mammals. ACUTE TOXICITY OF MICROCYSTIN TO RODENTS Careful research into this toxicity commenced in the . with a histopathological study of poisoning by M. aeruginosa extracts containing microcystin which was published in 1946 in the American Journal of Pathology. In these experiments a toxic extract of M. aeruginosa was administered by intraperitoneal injection into rats detailed examination was then carried out on these animals from 15 min to 1 month after injection. The findings of this study were that changes in the liver could be discerned within 15 min with increased blood content which by 3 h had increased liver weight by 25 . The hepatic parenchyma was engorged with blood with partial liquefaction of the cells. In animals surviving to 2 to 3 days the liver was shrunken yellow and mottled by 5 days it was recovering and after 1 month it was apparently normal. Histology of the liver showed centrilobular necrosis by 4 h with breakup of the liver architecture and sinusoids filled with red cells. Cell cytoplasm was seen in the central vein area of lobules and the sinusoidal endothelium was destroyed in some areas. By 3 to 5 days the liver architecture was reformed and mitotic figures were commonly seen indicating regeneration of the hepatocyte population. Kidney injury was also seen with necrosis of epithelial cells in the convoluted tubules. Heart and lungs showed small .