Quantitative Analysis of Retinal Vessel Changes in Galactose-Fed Dogs

Takahashi, Yukio; Augustin, Wisly; Wyman, Milton; Kador, Peter F.

doi:10.1089/jop.1993.9.257

Cited by 18 publications

(16 citation statements)

References 14 publications

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“…6. Dose-dependent reduction of cataract severity observed when data from a 36 month prevention study utilizing 0n5 and 5 mg kg −" day −" of M79175 (Takahashi et al, 1993) is combined with the present data utilizing 10 and 16 mg kg −" day of M79175. 36-month values for 10 and 16 mg kg −" day −" were interpolated from Fig.…”

Section: Lens Changes In M79175-treated Galactose-fed Dogsmentioning

confidence: 53%

“…In the adult dog lens, aldose reductase activity is comparable to the lower levels observed in the human lens and studies indicate that sugar cataract formation in both the adult dog and humans is primarily limited to the formation of posterior superficial cortical opacities (Sato et al, 1991). While reduction of cataract formation by aldose reductase inhibitors has been reported in galactose-fed dogs, prevention of cataracts has not been obtained (Kador et al, 1990 ;Takahashi et al, 1993 ;Engerman and Kern, 1993). As a result, alternative mechanisms of sugar cataract formation such as non-enzymatic glycosylation, oxidative insult and redox changes have been evoked to occur in dog lenses where levels of aldose reductase is lower.…”

Section: Introductionmentioning

confidence: 99%

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Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Sato

Mori

Wyman

et al. 1998

Experimental Eye Research

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Section: Lens Changes In M79175-treated Galactose-fed Dogsmentioning

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Sato

Mori

Wyman

et al. 1998

Experimental Eye Research

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“…If the pathogenesis of the retinopathy were better understood, new therapies might be feasible by which retinopathy could be inhibited, even if control of glycemia were less than perfect. The finding that diabetic-like retinopathy can be produced in nondiabetic animals by feeding them a galactoserich diet (3)(4)(5)(6)(7)(8) has provided strong evidence that elevated hexose concentration is itself sufficient to initiate the retinopathy. Unfortunately, it has remained unclear which of the many biochemical sequelae of hyperglycemia contribute more directly to development of the retinopathy.…”

mentioning

confidence: 99%

Pharmacological Inhibition of Diabetic Retinopathy

2001

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Effects of aminoguanidine and aspirin on the development of retinopathy have been examined in 5-year studies of diabetic dogs. Either agent was administered daily in doses of 20 -25 mg ⅐ kg ؊1 ⅐ day ؊1 . Because severity of hyperglycemia greatly influences development of the retinopathy, special effort was devoted to maintaining comparable glycemia in experimental and control groups. The retinal vasculature was isolated by the trypsin digest method, and retinopathy was assessed by light microscopy. Diabetes for 5 years resulted, as expected, in saccular capillary aneurysms, pericyte ghosts, acellular capillaries, retinal hemorrhages, and other lesions. Administration of aminoguanidine essentially prevented the retinopathy, significantly inhibiting the development of retinal microaneurysms, acellular capillaries, and pericyte ghosts compared with diabetic controls. Aspirin significantly inhibited the development of retinal hemorrhages and acellular capillaries over the 5 years of study, but had less effect on other lesions. Although diabetes resulted in significantly increased levels of advanced glycation end products (AGEs) (namely, pentosidine in tail collagen and aorta, and Hb-AGE), aminoguanidine had no significant influence on these parameters of glycation. Nitration of a retinal protein was significantly increased in diabetes and inhibited by aminoguanidine. The biochemical mechanism by which aminoguanidine has inhibited retinopathy thus is not clear. Aminoguanidine (but not aspirin) inhibited a diabetesinduced defect in ulnar nerve conduction velocity, but neither agent was found to influence kidney structure or albumen excretion.

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“…[42][43][44] The development of retinal lesions follows with the degeneration of retinal capillary pericytes between 18 and 24 months, the histological development of microaneurysms (27-33 months), and the clinical appearance of dot and blot haemorrhages at 33-36 months. 37,38,45 At this time, morphological changes in corneal endothelial cells also occur. 46 Between 36 and 48 months, significant changes in retinal perfusion develop, which result in retinal hypoxia and the subsequent development of lesion association with the preproliferative and subsequently proliferative stage.…”

Section: The Galactose-fed Dogmentioning

confidence: 99%

Asteroid hyalosis: pathogenesis and prospects for prevention

Kador

Wyman

2008

Eye

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Asteroid hyalosis (AH) is a common degenerative process in which fatty calcium globules collect within the vitreous humour. The condition rarely causes visual disturbances, and surgical removal is only rarely required. The presence of AH has been associated with systemic diseases such as diabetes; however, research in this area has been hampered by the lack of an animal model of AH. Recently, we have reported that AH occurs in galactose-fed beagles that develop the advanced stages of diabetes-like retinopathy. Comparisons of vitreous humour containing asteroid bodies (ABs) collected from these galactose-fed beagles and vitreous samples from age-matched normal beagles without ABs indicate that ABs contain calcium and phosphorous. Subtraction analysis of chloroform extracts of the vitreous samples by electrospray mass spectroscopy resulted in the identification of the quasimolecular ion of 1,2-dipalmitoyl-glycero-3-phosphoethanolamine (DPPE) as the main component of ABs. Since several reports indicate that ABs are composed of lipid-calcium complexes, we have proposed that the main component of ABs in the galactose-fed dogs with AH is a quasimolecular ion of DPPE in which two molecules of DPPE are complexed through their phosphates groups with calcium. We suggest that these lipid components diffuse into the vitreous from the degenerating retinas of these dogs.

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Quantitative Analysis of Retinal Vessel Changes in Galactose-Fed Dogs

Cited by 18 publications

References 14 publications

Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Dose-Dependent Prevention of Sugar Cataracts in Galactose-fed Dogs by the Aldose Reductase Inhibitor M79175

Pharmacological Inhibition of Diabetic Retinopathy

Asteroid hyalosis: pathogenesis and prospects for prevention

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