March 1994
Volume 35, Issue 3
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Articles  |   March 1994
Galactose-induced cataract formation in guinea pigs: morphologic changes and accumulation of galactitol.
Author Affiliations
  • J B Mackic
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • F N Ross-Cisneros
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • J G McComb
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • I Bekhor
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • M H Weiss
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • R Kannan
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
  • B V Zlokovic
    Department of Neurological Surgery, Children's Hospital of Los Angeles, University of Southern California School of Medicine 90033.
Investigative Ophthalmology & Visual Science March 1994, Vol.35, 804-810. doi:
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      J B Mackic, F N Ross-Cisneros, J G McComb, I Bekhor, M H Weiss, R Kannan, B V Zlokovic; Galactose-induced cataract formation in guinea pigs: morphologic changes and accumulation of galactitol.. Invest. Ophthalmol. Vis. Sci. 1994;35(3):804-810.

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Abstract

PURPOSE: To develop and characterize a new model of galactose-induced cataract formation in young, 3- to 4-week-old Hartley guinea pigs. METHODS: Experimental animals were fed 50% galactose in powdered guinea pig chow containing 0.5 g ascorbate/kg diet. Control animals were fed normal powdered guinea pig chow (0.5 g ascorbate/kg diet). Lenses from all animals were subjected to photo-slit-lamp examination, light microscopic analysis, and high-pressure liquid chromatography (HPLC) analysis of polyol content. RESULTS: Photo-slit-lamp examination indicated initial opacities in equatorial subcapsular region between 3 and 5 days in all galactose-fed animals (20/20); opacities progressed toward the anterior pole when diet was extended to 14 days. Histologic analysis of the equatorial changes confirmed progressive cataract formation consisting of small intra-fibrillar vacuoles in the pre-equatorial region (3 days), an increased number of enlarged and coalesced vacuoles (6 days), and progressive tissue swellings with cellular disruption and signs of epithelial multilayering (14 days). The anterior epithelium showed increased cell height and swelling after 3 days of the galactose diet. HPLC analysis of lens tissue indicated progressive accumulation of galactitol, 18 mM after 3 days, which plateaued to about 30 mM between 6 and 14 days. The level of myo-inositol dropped from a control value of 2.8 +/- 0.7 mM to 1.5 +/- 0.7 mM after 3 days, and was nearly undetectable after 14 days of the galactose diet. CONCLUSIONS: The current study suggests that the guinea pig model may serve as a valuable new tool to study sugar-induced cataract formation and to characterize the early morphologic and biochemical events in cataractogenesis.

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