Sakamoto M, Wakabayashi K, Kakita A, Adachi T, Nakano A
Department of Epidemiology, National Institute for Minamata Disease, 4058-18 Hama, Minamata, Kumamoto 867, Japan.
Brain Res. 1998 Feb 16;784(1-2):351-4. doi: 10.1016/s0006-8993(97)01400-5.
The neurotoxicity of methylmercury (MeHg) treatment during the postnatal developing phase in rats was studied. Rats on postnatal day 1 were orally administered 5 mg/kg/day methylmercury chloride (MMC) for more than 30 consecutive days. Body weight loss began 26 days after MMC was administered, and severe paralysis of the hind-limbs and unsteadiness appeared subsequently. Histopathologically, the widespread neuronal degeneration was observed in the cerebral neocortex, neostriatum, red nucleus, brainstem, cerebellum and spinal dorsal root ganglia on day 32. The widespread distribution of the lesions was quite similar to that in fetal cases of MeHg intoxication in Minamata, Japan. These findings suggest that MMC treatment during the postnatal development phase in rats produce a good model of fetal-type Minamata disease.
研究了大鼠出生后发育阶段甲基汞（MeHg）处理的神经毒性。出生第1天的大鼠连续30多天口服给予5 mg/kg/天的氯化甲基汞（MMC）。给予MMC后26天开始体重减轻，随后出现严重的后肢麻痹和步态不稳。组织病理学检查显示，在第32天，大脑新皮质、新纹状体、红核、脑干、小脑和脊髓背根神经节出现广泛的神经元变性。病变的广泛分布与日本水俣病胎儿甲基汞中毒病例非常相似。这些发现表明，大鼠出生后发育阶段给予MMC可建立胎儿型水俣病的良好模型。
