cataract, mascular degeneration, glaucoma

Life extension and
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Cataract, Macular degeneration, Glaucoma can be treated and prevented by caloric restriction.


Dietary caloric restriction may delay the development of cataract by attenuating the oxidative stress in the lenses of Brown Norway rats.
Exp Eye Res. 2004 Jan;78(1):151-8.
Wang K, Li D, Sun F.
Department of Ophthalmology, College of Physicians and Surgeons of Columbia University, New York, NY 10032-3702, USA.

Dietary caloric restriction (CR) is the only experimental intervention that can reliably retard the development of cataract in a normal animal model. Here we have studied the possible mechanisms by which CR retards the age-related degeneration of the lens of Brown Norway rats. We have found that CR slowed protein insolubilization and blunted declines of the total
soluble thiols, protein thiols, reduced glutathione and ascorbic acid levels in the lenses of old BN rats. From the lens protein point of view, the development of cataract in rat lenses has 3 stages: (1) the precipitation of gamma-crystallin, (2) the insolubilization of beta-crystallin, and (3) the final precipitation of alpha-crystallin which was saturated with other denatured lens proteins. A similar sequence is also observed when the lens proteins are subjected to oxidative stress in vitro. These data are the first to suggest that CR may retard the age-related degeneration of the lens by attenuating the oxidative stress in the lens. Since oxidative stress is likely a main cause of human cataract, CR intervention may be relevant to humans as well.

Normal mouse and rat strains as models for age-related cataract and the effect of caloric restriction on its development.
Exp Eye Res. 2000 May;70(5):683-92.
Wolf NS, Li Y, Pendergrass W, Schmeider C, Turturro A.
Department of Pathology, University of Washington, Seattle 98195-7470, USA.

The purpose of this study was to determine: (1) which of the commonly used strains of laboratory rats and mice provide good models for human age-related cataract, and (2) whether long term caloric restriction, a regimen that prolongs both median and maximum life span in rodents, would also delay the time of appearance of this age-related pathology. Three strains of mice and two rat strains commonly used in laboratory work and maintained on either ad libitum (AL) or calorically restricted (CR) diets in the National Institutes of Aging and Diet Restriction colony were examined by slit lamp for age-related cataracts at four or more time points during their life spans. These strains were Brown Norway and Fischer 344 rats, and C57BL/6, (C57BL6 x DBA/2)F1 and (C57BL/6 x C3H)F1 mice. None of these strains develop congenital cataracts. Various stages of cataract were found in the great majority of these animals in old age. In both rat strains and one mouse strain the cataracts occurred after mid-life, were most advanced late in life, and were similar in locations and appearance to those in humans. In the two mouse strains in which some cataracts appeared as early as 10-14 months of age, previously identified genetic defects affecting the eye were probably involved in the early appearances. CR extended life spain in all five rat and mouse strains and also delayed both the time of first appearances and the subsequent increase in cataract severity over time in the four dark-eyed strains. CR did not delay cataract formation in the single albino rat strain studied. In summation: (1) commonly used strains of laboratory rats and mice that are free of congenital or early appearing cataracts due to genetic defects would appear to serve as appropriate models for human age-related cataract, (2) caloric restriction (CR) provides a protective effect, delaying development of cataracts in the dark-eyed mouse and rat strains, while also extending their life spans, (3) CR did not delay the development of lens damage in the nonpigmented eye of the single albino strain studied, although it extended life span.

Cataract incidence and analysis of lens crystallins in the water-, urea- and SDS-soluble fractions of Emory mice fed a diet restricted by 40% in calories.Curr Eye Res. 1993 Dec;12(12):1081-91.
Mura CV, Roh S, Smith D, Palmer V, Padhye N, Taylor A.
Laboratory for Nutrition and Vision Research, USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111.

Restriction of dietary calorie intake is associated with life extension and with the delay of age-related disorders. Preliminary studies demonstrated that by feeding the Emory mouse a diet restricted by 21% in calories cataract and insolubilization of protein could also be delayed. To observe the effects of calorie restriction over prolonged portions of adulthood, Emory mice were fed the control diet (C) or a diet restricted by 40% in calories (R). Feeding the R diet was associated with delayed formation or progress of cataract over virtually the entire second half of life. At 11 months of age, bilateral grade 5 cataracts were present in 17% and 2% of C and R lenses, respectively. At 22 months of age, bilateral grade 5 cataracts were present in 90% and 18% of C and R lenses, respectively. The distribution of alpha-, beta-, and gamma- crystallins in the water-soluble, urea-soluble, and SDS-soluble fractions indicates more similarities than differences between C and R lenses with a specific grade of cataract or of a given age. However, there were significant and abrupt (after grade 4 cataract) losses of particular gamma-crystallins; gamma-crystallins which were not prominent at earlier stages became the major gamma-crystallin moieties. Losses of alpha-crystallins were also noted upon cataract formation or aging in most of the fractions. Aggregates including gamma- and alpha-crystallins also accumulate faster in the C group.

Moderate caloric restriction delays cataract formation in the Emory mouse.
FASEB J. 1989 Apr;3(6):1741-6.
Taylor A, Zuliani AM, Hopkins RE, Dallal GE, Treglia P, Kuck JF, Kuck K.
U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts 02111.

Eye lens senile cataract is a major cause of blindness, affecting the elderly in particular. The etiology of the disorder has been elusive, and attempts to delay the onset of senile cataracts have been unsuccessful. The need for more information is underscored by epidemiologists who estimate that the ability to delay cataract formation in humans by only 10 years would eliminate the need for 50% of the cataract extractions performed annually in the United States. The Emory mouse provides the best model for human senile cataracts. Feeding Emory mice a diet that was restricted in calories by approximately 21% delayed the onset of cataracts. This is the first study that demonstrates in vivo the delay of senile-type cataracts. In these animals, aging and cataracts are associated with diverse changes in the proportion of various proteins (particularly 21, 22, 31-34 kDa) and with transformation of proteins from a soluble to an insoluble state. In advanced cataracts, there is a loss of total protein. Within a cataract grade, there is no difference between restricted and nonrestricted animals in relative proportion of specific lens proteins or in amounts of total or soluble proteins. The transition from a clear to cataractous lens appears when the soluble-to-total protein ratio falls below about 0.58. The exclusive use of gamma-crystallin as an indicator of lens viability is questioned. To the extent that cataract formation is due to lens protein oxidation and/or an inability to proteolytically remove damaged protein, it would appear that caloric restriction results in enhanced protection against lens oxidative stress or in prolonged proteolytic function.

Macular degeneration

Caloric restriction retards age-related changes in rat retina.Biochem Biophys Res Commun. 2003 Sep 19;309(2):457-63.
Li D, Sun F, Wang K.
Department of Ophthalmology, College of Physicians and Surgeons of Columbia University, New York, NY, USA.
The neural retina of mammals consists of light sensitive photoreceptors and connecting neural cells that receive and send visual signal to the brain. Dietary caloric restriction (CR) is the only experimental intervention that can reliably retard the age-related degeneration of the retina in a normal mammalian model. Here, we studied the effect of CR on various biochemical parameters in the retina of male Brown Norway rats at different ages. We found that CR slowed the age-dependent protein insolubilization, blunted the declines in the total soluble thiols, and reduced glutathione and ascorbic acid levels in neural retina. We also observed that CR retarded the age-related decline in the levels of taurine, a vital amino acid in neural retina. These data are the first to implicate that CR may retard the age-related degeneration of retina by attenuating the oxidative stress and/or by sustaining the pool of protective factors in the neural retina.


Effects of age and long-term caloric restriction on the aqueous collecting channel in the mouse eye.
J Glaucoma. 1997 Feb;6(1):18-22.
Li Y, Wolf NS.
Department of Pathology, University of Washington, Seattle 98195-7470, USA.
PURPOSE: The mouse aqueous collecting channel, part of the mouse aqueous outflow pathway, was measured using a computer-assisted image analysis system. We used ad libitum-fed and calorie-restricted mice to investigate the effects of age and long-term caloric restriction on the lumen size of the channel.
RESULTS: The ad libitum-fed mice showed a significant age-related reduction in the lumen area. In the ad libitum-fed group, the lumen area of the channel decreased  by 30% at 30-35 months of age (p < 0.01), and the anteroposterior width declined by 21% (p < 0.001) as compared with mice 3-5 months of age. The calorie-restricted mice did not display any reduction with age in the lumen area or the anteroposterior width of the channel. When compared with the age-matched calorie-restricted mice, the lumen area of the  channel of the ad libitum-fed mice measured less by 34%, and anteroposterior width less by 21% at 30-35 months of age (p < 0.01).
CONCLUSIONS: These results indicate that an age-related morphological alteration in the mouse aqueous collecting channel occurred and that it is delayed by long-term caloric restriction. This suggests a possible role of life-long caloric restriction in reducing glaucomatous damages and perhaps delaying glaucoma development.

Tag Cloud: aging plan., grade, protein, macular, mouse, glaucoma, degeneration, oxidative, caloric, cataract, lenses, caloric restriction, lumen, retina, aqueous, libitumfed, neural, University, antiaging

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