Gong H, Amemiya T
Department of Ophthalmology, Nagasaki University School of Medicine, Nagasaki, Japan.
Exp Eye Res. 2001 Apr;72(4):363-9. doi: 10.1006/exer.2000.0958.
In this study the optic nerve changes in zinc (Zn)-deficient rats are examined. Zinc is one of the essential trace elements and is known to be related to optic nerve diseases such as ethambutol neuropathy. However, the effect of Zn on the optic nerve has not been studied experimentally in animals. We used 3 week old weanling male Wistar Kyoto rats weighing 40-50 g. Rats were fed a Zn-deficient diet containing 0.007 mg of Zn per 100 g, all other nutrients and distilled and deionized water. The same water supplemented with 3 mg Zn per 100 g was given to the control group. After 4 or 7 weeks on a Zn-deficient diet, the optic nerve was examined with an electron microscope. A recovery group was fed a Zn-containing diet for 5 weeks after 7 weeks on the Zn-deficient diet. The serum Zn levels of the deficient group were significantly decreased at both 4 and 7 weeks. Most of the Zn-deficient rats showed hair loss around the eyes and on the extremities. Ultrastructural findings were as follows. The number of myelinated axons of Zn-deficient rats at 4 and 7 weeks were significantly decreased and the myelin sheaths were significantly thinner in the Zn-deficient groups and in the recovery group. Unmyelinated axons were more numerous than in the control rats. Destruction of myelin and proliferation of glial cells were found in the optic nerves of Zn-deficient rats. This study suggests that the optic nerve needs Zn for the maintenance of its cell structure and even if Zn is supplied to the Zn-deficient rats, destruction of the myelin structure may continue. Zn-deficiency induce a decrease of myelinated nerve fibers, and it is thought that optic neuropathy in patients treated with some drugs such as ethambutol may be a secondary change due to Zn-deficiency following drug administration.
在本研究中，对缺锌大鼠的视神经变化进行了检查。锌是必需的微量元素之一，已知与视神经疾病如乙胺丁醇神经病有关。然而，锌对视神经的影响尚未在动物实验中进行研究。我们使用了3周龄、体重40 - 50克的断乳雄性Wistar Kyoto大鼠。给大鼠喂食含锌量为每100克0.007毫克的缺锌饮食，其他所有营养素以及蒸馏水和去离子水。对照组给予每100克补充3毫克锌的相同饮水。在缺锌饮食4周或7周后，用电子显微镜检查视神经。在缺锌饮食7周后，恢复组喂食含锌饮食5周。缺锌组在4周和7周时血清锌水平均显著降低。大多数缺锌大鼠在眼睛周围和四肢出现脱毛。超微结构结果如下。缺锌大鼠在4周和7周时的有髓轴突数量显著减少，缺锌组和恢复组的髓鞘明显变薄。无髓轴突比对照大鼠更多。在缺锌大鼠的视神经中发现了髓鞘破坏和胶质细胞增殖。本研究表明，视神经维持其细胞结构需要锌，并且即使给缺锌大鼠补充锌，髓鞘结构的破坏可能仍会继续。缺锌导致有髓神经纤维减少，并且认为用乙胺丁醇等一些药物治疗的患者中的视神经病变可能是给药后缺锌引起的继发性变化。
