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Optic nerve changes in zinc-deficient rats.

H Gong1, T Amemiya

  • 1Department of Ophthalmology, Nagasaki University School of Medicine, Nagasaki, Japan. hgong@net.nagiasaki-u.ac.jp

Experimental Eye Research
|March 29, 2001
PubMed
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Zinc deficiency in rats causes optic nerve damage, including thinner myelin sheaths and fewer myelinated axons. This suggests zinc is crucial for optic nerve health and may explain drug-induced optic neuropathies.

Area of Science:

  • Neuroscience
  • Trace Element Research
  • Ophthalmology

Background:

  • Zinc (Zn) is an essential trace element linked to optic nerve diseases like ethambutol neuropathy.
  • The specific effects of zinc deficiency on the optic nerve have not been experimentally established in animal models.

Purpose of the Study:

  • To investigate the ultrastructural changes in the optic nerve of rats subjected to experimental zinc deficiency.
  • To explore the potential role of zinc in maintaining optic nerve structure and function.

Main Methods:

  • Wistar Kyoto rats were fed a zinc-deficient diet (0.007 mg Zn/100g) or a control diet (3 mg Zn/100g) for 4 or 7 weeks.
  • Optic nerves were examined using electron microscopy.
  • A recovery group was established to assess reversibility of changes.

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Main Results:

  • Zinc-deficient rats exhibited significantly decreased serum Zn levels and characteristic hair loss.
  • Ultrastructural analysis revealed a significant decrease in myelinated axons and thinner myelin sheaths in deficient rats.
  • Increased unmyelinated axons, myelin destruction, and glial cell proliferation were observed in the optic nerves of zinc-deficient rats.

Conclusions:

  • Zinc is essential for maintaining the structural integrity of the optic nerve.
  • Optic nerve damage due to zinc deficiency may be irreversible even with zinc repletion.
  • Drug-induced optic neuropathies, such as ethambutol neuropathy, might be secondary to zinc deficiency.