Optic nerve changes in zinc-deficient rats

In this study the optic nerve changes in zinc (Zn)-deficient rats are exami ned. 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 bt cn studied experimentally in animals. We used 3 week Old weanling male Wistar Kyoto rats weighing 40-50 g. Rats w ere 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 wi th 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 microsco pe. 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 Mere significantly decreased at both 4 and 7 weeks. Most of the Zn-deficient rat s showed hair loss around the eyes and on the extremities. Ultrastructural findings were as follows. The number of myelinated axons of Zn-deficient ra ts at 4 and 7 weeks were significantly decreased and the myelin sheaths wer e significantly thinner in the Zn-deficient groups and in the recovery grou p. Unmyelinated axons were more numerous than in the control rats. Destruct ion of myelin and proliferation of glial cells were Found in the opt:ic ner ves 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 th e Zn-deficient rats, destruction of the myelin structure may continue. Zn-d eficiency induce a decrease of myelinated nerve fibers, and it is thought t hat, optic neuropathy in patients treated with some drugs such as ethambuto l may he a secondary change due to Zn-deficiency following drug administrat ion. (C) 2001 Academic Press.