Common marmosets were used as model animals for methylmercury (MeHg) poisoning. Six marmosets were given MeHg of 5 ppm Hg in drinking water. The animals were divided into 3 groups of 2 each. The first group was examined for acute symptomatic MeHg poisoning. They were given MeHg for 70 and 90 days, respectively, to manifest severe symptoms. The second group was sacrificed after 38 days of MeHg exposure, when they had acute-subclinical MeHg poisoning. The third group of animals was exposed for 21 days, and then observed for 2.5 years without MeHg exposure. One of them showed typical symptoms of MeHg poisoning after MeHg exposure had ended, but the other one showed only slight symptoms without ataxia. This experiment demonstrated that MeHg causes pathological changes in neural tissues including the peripheral nerves in common marmosets. Furthermore, common marmosets were found to show MeHg-induced pathological changes similar to those in humans in the cerebrum and cerebellum.
Eto K. (1997). Pathology of Minamata disease. Toxicol Pathol25: 614—623.
2.
Eto K., Takeuchi T. (1978). A pathological study of prolonged cases of Minamata disease, with particular reference to 83 autopsy cases. Acta Pathol Jpn28: 565—584.
3.
Eto K., Yasutake Y., Kuwana T., Korogi Y., Akima M., Shimozeki T., Tokunaga H., Kaneko Y. (2001). Methylmercury poisoning in common marmosets—A study of selective vulnerability within the cerebral cortex. Toxicol Pathol29:565—573.
4.
Grant CA (1973). Pathology of experimental methyl mercury intoxication: Some problems of exposure and response. In: Mercury, Mercurials and Mercaptane, Miller MW, Clarkson TW (eds). Charles C Thomas Publishers , Springfield, IL, pp 284—312.
5.
Hunter D., Russell DS (1954). Focal cerebral and cerebellar atrophy in a human subject due to organic mercury compounds. J Neurol Neurosurg Psychiatry17: 235—241.
6.
Kawasaki Y., Ikeda Y., Yamamoto T., Ikeda K. (1986). Long-term toxicity study of methylmercury chloride in monkeys. J Food Hyg Soc Jpn27: 528— 552.
7.
Korogi Y., Takahashi M., Okajima T., Eto K. (1998). MR findings of Minamata disease—Organic mercury poisoning. JMRI (J Magn Reson Imag)8: 308— 316.
8.
Le Quesne PM , Damluji SF, Rustam H. (1974). Electrophysiologica l studies of peripheral nerves in patients with organic mercury poisoning. J Neurol Neurosurg Psychiatry37: 333—339.
9.
Matsumura A. , Eto K., Furuyoshi N., Okamura Y. (1993). Disturbances of accommodation in Minamata disease. Neuro-ophthalmology13: 331—339.
10.
Miyakawa T. , Deshimaru M., Sumiyoshi S., Teraoka A., Udo N., Hattori E., Tatetsu S. (1970). Experimental organic mercury poisoning. Pathological changes in peripheral nerves. Acta Neuropathol15: 45—55.
11.
Miyakawa T. , Sumiyoshi S., Deshimaru M. (1974). Late changes in sciatic nerve after a small dose of methyl methylmercuric sulfide. Acta Neuropathol30: 30—41.
12.
Ohkawa T., Uenoyama H., Tanida K., Ohmae T. (1977). Ultra trace mercury analysis by dry thermal decomposition in alumina porcelain tube. J Hyg Chem23: 13—22.
13.
Pentschew A. (1958). Quecksibervergiftung. Handbuch der Speziellen Pathologishen Anatomie und Histologie X III/2, B, Springer-Verlag , Berlin, pp 2007—2024.
14.
Raynolds ES (1963). The use of lead citrate at high pH as an electron-opaque stain in electron microscopy. J Cell Biol17: 208—212.
15.
Sakai K., Okabe M., Eto K., Takeuchi T. (1975). Histochemical demonstration of mercury in human tissue cells of Minamata disease by use of autoradiographic procedure. Acta Histochem Cytochem8: 257— 264.
16.
Shaw CM, Mottet NK, Body RL, Luschei ES (1975). Variability of neuropathologic lesions in experimental methylmercurial encephalopathy in primates. Am J Pathol80: 451—469.
17.
Shiraki H. (1979). Neuropathological aspects of organic mercury intoxication, including Minamata disease. In: Handbook of Clinical Neurology , Vol 36, Vinken PJ, Bruyn GW (eds). Elsevier, North-Holland, Amsterdam , pp 83—145.
18.
Shiraki H., Takeuchi T. (1971). Pathology of the nervous system. In: Minamata Disease, 2nd ed, Minckler J (ed). McGraw-Hill, New York, pp 1651—1665.
19.
Suda I., Eto, K., Tokunaga H., Furusawa R., Suetomi K., Takahshi H. (1989). Different histochemical findings in the brain produced by mercuric chloride and methyl mercury chloride in rats. Neurotoxicology10: 113—126.
20.
Takeuchi T. (1968). Pathology of Minamata disease. In: Minamata Disease, Kutsuna M (ed). Kumamoto University Study Group, Kumamoto , Japan, pp 141—252.
21.
Takeuchi T. (1977). Neuropathology of Minamata disease in Kumamoto, especially at the chronic stage. In: Neurotoxicology, Roizin L, Shiraki H, Grcevic N (eds). Raven Press, New York, pp 235—246.
22.
Takeuchi T., Eto K. (1975). Minamata disease. In: Studies on the Health Effects of Alkylmercury in Japan. Environment Agency, Tokyo, 28—62.
23.
Takeuchi T., Eto K. (1977). Pathology and pathogenesis of Minamata disease . In: Minamata Disease: Methylmercury Poisoning in Minamata and Niigata, Japan, Tsubaki T, Irukayama K (eds). Kodansha, Tokyo, pp 103— 141.
24.
Takeuchi T., Eto K. (1986). Pathology of mild prolonged cases of Minamata disease. In: Recent Advances in Minamata Disease Studies: Methylmercury Poisoning inMinamata and Niigata, Japan, Tsubaki T, Takahashi H (eds). Kodansha, Tokyo, pp 117—134.
25.
Takeuchi T., Eto K. (1999). Peripheral nerves in Minamata disease. In: The Pathology of Minamata Disease—A Tragic Story of Water Pollution. Nakayama H, Sumiyoshi A (editorial collaborations), Kyushu University Press, Inc, Fukuoka, Japan, pp 149—174.
26.
Tokuomi H., Uchino M., Imamura S., Yamanaga H., Nakanishi R., Ideta T. (1982). Minamata disease (organic mercury poisoning): Neuroradiologic and electrophysiologic studies. Neurology32: 1369—1375.
27.
Tryphonas L. , Nielsen NO (1973). Pathology of chronic alkyl mercurial poisoning in swine. Am J Vet Res34: 379—392.
28.
Yasutake A. , Hirayama K. (1990). Selective quantification of inorganic mercury in tissue of methylmercury-treated rats . Bull Environ Contam Toxicol45: 662—666.
