October 1994
Volume 35, Issue 11
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Articles  |   October 1994
Decreased rhodopsin regeneration in diabetic mouse eyes.
Author Affiliations
  • S E Ostroy
    Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.
  • S M Frede
    Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.
  • E F Wagner
    Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.
  • C G Gaitatzes
    Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.
  • E M Janle
    Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.
Investigative Ophthalmology & Visual Science October 1994, Vol.35, 3905-3909. doi:
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    • Get Citation

      S E Ostroy, S M Frede, E F Wagner, C G Gaitatzes, E M Janle; Decreased rhodopsin regeneration in diabetic mouse eyes.. Invest. Ophthalmol. Vis. Sci. 1994;35(11):3905-3909.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To evaluate the effect of diabetes on rhodopsin regeneration in the excised mouse eye. METHODS: A superfused excised mouse eye preparation that exhibits rhodopsin regeneration after moderate bleaches and that is responsive to the composition of the perfusate was used. Diabetes was induced in albino mice (BALB/c) with the diabetogenic agent streptozotocin. Absorption spectrophotometry of the excised eye was used to monitor rhodopsin concentrations. RESULTS: Significant reductions in rhodopsin regeneration were observed in diabetic mice. Severely diabetic mice exhibited only 64% and 55% regeneration (at perfusate glucose levels of 5.1 mM and 10 mM, respectively), and moderately diabetic mice exhibited 74% and 73% regeneration, compared to the greater than 100% regeneration observed in nondiabetic mice. Glucose perfusate concentration has a major effect on rhodopsin regeneration. Lower concentrations of perfusate glucose (3 mM) reduced the amount of rhodopsin regeneration in both nondiabetic mice and diabetic mice. The diabetic mice seemed to tolerate higher concentrations of perfusate glucose (20 mM) better than the nondiabetic mice. Neither correction for osmolarity nor substitution with a nonglycolytic substrate increased the amount of rhodopsin regeneration in the diabetic mice. CONCLUSIONS: Diabetes reduced the amount of rhodopsin regeneration that followed moderate bleaches in excised mouse eyes. The data suggest that some process or processes associated with rhodopsin regeneration have been affected in the diabetic.

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