Murray T G, Burton T C, Rajani C, Lewandowski M F, Burke J M, Eells J T
Department of Ophthalmology, Medical College of Wisconsin, Milwaukee 53226.
Arch Ophthalmol. 1991 Jul;109(7):1012-6. doi: 10.1001/archopht.1991.01080070124049.
Methanol ingestion can lead to visual impairment, central nervous system dysfunction, or death. The extent of ocular involvement has been difficult to determine because the toxicity is restricted to humans and nonhuman primates due to species differences in methanol metabolism. A rodent model of methanol toxicity recently developed by us was used to evaluate retinal dysfunction in methanol poisoning. Formic acidemia and visual toxic reactions developed in methanol-intoxicated rats. Electroretinographic analysis indicated a significant early deficit in b-wave amplitude followed by a temporally delayed, lesser reduction in a-wave amplitude. Histologic evaluation of the eyes 60 hours after methanol administration revealed generalized retinal edema and vacuolation in the photoreceptors and retinal pigment epithelium. Ultrastructural examination showed swelling and disruption of the mitochondria in photoreceptor inner segments, optic nerve, and the retinal pigment epithelium. These studies document direct retinal involvement in this nonprimate model of methanol toxicity.
摄入甲醇可导致视力损害、中枢神经系统功能障碍或死亡。由于甲醇代谢存在物种差异,毒性仅限于人类和非人类灵长类动物,因此眼部受累的程度一直难以确定。我们最近开发的一种甲醇毒性啮齿动物模型用于评估甲醇中毒时的视网膜功能障碍。甲醇中毒大鼠出现甲酸血症和视觉毒性反应。视网膜电图分析表明,b波振幅早期明显降低,随后a波振幅在时间上延迟、降低程度较小。给予甲醇60小时后对眼睛进行组织学评估,发现视网膜普遍水肿,光感受器和视网膜色素上皮出现空泡化。超微结构检查显示光感受器内节、视神经和视网膜色素上皮中的线粒体肿胀和破坏。这些研究证明在这种非灵长类甲醇毒性模型中视网膜直接受累。