Cataract development in 12-month-old rats fed a 25% galactose diet and its relation to osmotic stress and oxidative damage.
We attempted to clarify the pattern of cataract development in 12-month-old rats fed a 25% galactose diet and to assess the relation of cataract development with osmotic stress and oxidative damage. In lenses of 12-month-old male Wistar rats fed a 25% galactose diet over an 8-month period, suture accentuation appeared at 6 months of galactose feeding and then opacities developed from the anterior subcapsular cortex toward the posterior subcapsular cortex, reaching the nuclear region at 8 months of galactose feeding. Increases in lens galactitol and lipid peroxide contents and a decrease in lens reduced glutathione content occurred at 4, 6 and 8 months of galactose feeding. The increase in lens lipid peroxide content and the decrease in lens reduced glutathione content were accelerated with an increase in feeding period, while the increase in lens galactitol content was decelerated. An increase in lens water content and a decrease in lens protein content occurred at 6 and 8 months of galactose feeding. The lens vitamin E content increased at 6 months of galactose feeding and this increase was concomitant with increases in serum vitamin E and total cholesterol concentrations. The serum lipid peroxide concentration increased at 4 and 6 months of galactose feeding. The present results indicate that in lenses of 12-month-old rats fed a 25% galactose diet, suture accentuation appears initially and then opacities develop from the anterior subcapsular cortex toward the posterior subcapsular cortex, finally reaching the nuclear region. These results also suggest that in the galactosemic aged rats, osmotic stress would mainly contribute to cataract formation, while oxidative damage could be linked to both cataract formation and progression, although an increase in lens vitamin E content occurs during the cataract development.
Ohta
Y
Y
Department of Biochemistry, School of Medicine, Fujita Health University, Toyoake, Japan.
Yamasaki
T
T
Niwa
T
T
Goto
H
H
Majima
Y
Y
Ishiguro
I
I
D000818:Animals; D001834:Body Water / Q000378:metabolism*; D002386:Cataract / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D003459:Crystallins / Q000378:metabolism; D004032:Diet; D004376:Galactitol / Q000378:metabolism; D005690:Galactose / Q000009:adverse effects*; D005693:Galactosemias / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000378:metabolism; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D009997:Osmotic Pressure; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000097:blood
D003459:Crystallins; D008054:Lipid Peroxides; D004376:Galactitol; D014810:Vitamin E; D002784:Cholesterol; D005978:Glutathione; D005690:Galactose