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Alkaloid gây độc tế bào, được tìm thấy trong một số chi của cyanobacteria, là một bổ sung gần đây lĩnh vực nghiên cứu độc tố. Đánh giá độc tính của chất chiết xuất từ vi khuẩn cyanobacterium raciborskii Cylindrospermopsis bắt đầu khi nó được xác định là nguyên nhân có thể xảy ra của bệnh bí ẩn Palm Island, thảo luận trong Chương 5 (Hawkins, Runnegar et al. 1985). Đánh giá của các độc tố tinh khiết bắt đầu chỉ trong 1992, khi nó lần đầu tiên được phân lập và xác định cấu trúc (Ohtani, Moore và các. | 6 Cylindrospermopsin Toxicity This cytotoxic alkaloid found in several genera of cyanobacteria is a recent addition to the field of toxin research. Evaluation of the toxicity of extracts of the cyanobacterium Cylindrospermopsis raciborskii began when it was identified as the probable cause of the Palm Island mystery disease discussed in Chapter 5 Hawkins Run-negar et al. 1985 . Evaluation of the purified toxin started in only 1992 when it was first isolated and the structure identified Ohtani Moore etal. 1992 . Research activity into the toxicity of this alkaloid is rapidly intensifying as a result of its detection in drinking water sources in the U.S. Europe Israel Brazil Southeast Asia Japan and Australia. 6.1 TOXICITY OF CYLINDROSPERMOPSIN WHOLE-ANIMAL STUDIES The oral and intraperitoneal toxicity to mice of C. raciborskii extracts and of purified cylindrospermopsin have been investigated. The first report on the toxicity of the organism cultured from the Solomon Dam Palm Island was published by Hawkins Runnegar et al. 1985 . This examined the effect of intraperitoneal injection of a saline extract of freeze-dried cells on young male mice. The lethal dose killing 50 of the animals LD50 over 24 h was 64 mg of freeze-dried cells per kilogram of body weight per mouse. Mice surviving beyond 24 h after receiving the LD50 died up to 5 days later indicating a prolonged action of the poison. At a dose of 168 mg kg survival time was 6 to 9 h increasing the dose beyond this by 2 to 10 times increased survival time to 10 to 12 h an unexpected observation as the expected effect of increasing the dose of a toxin is to shorten survival. Postmortem examination of mice that received doses at or below the LD50 showed pale livers with white foci and focal hemorrhages in the lungs. Histopathological examination of these livers showed centrilobular necrosis. Higher doses resulted in swollen livers mottled red with a lobular pattern of congestion and hemorrhage. The histology showed
