Effect of Sorbitol Dehydrogenase Inhibition on Sugar Cataract Formation in Galactose-fed and Diabetic Rats

Kador, Peter F.; Inoue, Jun; Secchi, E.Fillipo; Lizak, Martin J.; Rodriguez, Libaniel; Mori, Kazuhiko; Greentree, William; Blessing, K.; Lackner, Petra A.; Sato, Sanai

doi:10.1006/exer.1998.0502

Cited by 35 publications

(19 citation statements)

References 15 publications

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“…The fact that cataract induction by galactose in the cultured monkey lens follows a similar course (not shown) to that found with xylose argues against SDH as the major factor, since galactitol is not a substrate for SDH. Inhibition of SDH potentiates cataract in diabetic rats and has no effect in galactose fed rats (Kador et al, 1996). These findings are consistent with the fact that sorbitol is a substrate for SDH while galactose is not, and with the polyol hypothesis.…”

Section: Discussionsupporting

confidence: 71%

Effects of Xylose on Monkey Lenses in Organ Culture: A Model for Study of Sugar Cataracts in a Primate

Jernigan

Zigler

Liu

et al. 1998

Experimental Eye Research

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Section: Discussionsupporting

confidence: 71%

Effects of Xylose on Monkey Lenses in Organ Culture: A Model for Study of Sugar Cataracts in a Primate

Jernigan

Zigler

Liu

et al. 1998

Experimental Eye Research

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“…This has been explored in rodent models using sorbitol dehydrogenase inhibitors (SDIs) [163][164][165] as well as SDH-deficient and SDH-knockout mouse models [166,167]. In the peripheral nervous system there have been conflicting results.…”

Section: Oxidative Stress and The Polyol Pathway In Diabetic Neuropathymentioning

confidence: 98%

Diabetic neuropathy and oxidative stress

Pop‐Busui

Sima

Stevens

2006

Diabetes Metab. Res. Rev.

240

154

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This review will focus on the impact of hyperglycemia-induced oxidative stress in the development of diabetes-related neural dysfunction. Oxidative stress occurs when the balance between the production of reactive oxygen species (ROS) and the ability of cells or tissues to detoxify the free radicals produced during metabolic activity is tilted in the favor of the former. Although hyperglycemia plays a key role in inducing oxidative stress in the diabetic nerve, the contribution of other factors, such as endoneurial hypoxia, transition metal imbalances, and hyperlipidemia have been also suggested. The possible sources for the overproduction of ROS in diabetes are widespread and include enzymatic pathways, auto-oxidation of glucose, and mitochondrial superoxide production. Increase in oxidative stress has clearly been shown to contribute to the pathology of neural and vascular dysfunction in diabetes. Potential therapies for preventing increased oxidative stress in diabetic nerve dysfunction will be discussed.

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“…The hyperosmotic theory of the etiology of sugar cataract identifies aldose reductase (AR) as the primary factor responsible for this pathological alteration induced by hyperglycemic or hypergalactosemic conditions. In diabetic conditions, the enzyme AR converts excess glucose to sorbitol in a nicotinamide adenine dinucleotide phosphate (NADPH) dependent manner (Kador et al, 1998;Obrosova et al, 2001). Due to its poor membrane permeability, sorbitol accumulates in the cells, resulting in the lens fiber degeneration and opacification (Kinoshita, 1974).…”

Section: Introductionmentioning

confidence: 98%

Inhibitory effects of chlorogenic acid on aldose reductase activity in vitro and cataractogenesis in galactose-fed rats

Kim

Lee

et al. 2011

Arch. Pharm. Res.

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Chlorogenic acid (5-O-caffeoylquinic acid, CA), a phenolic compound found ubiquitously in plants, has antidiabetic effect in diabetic animal models. In this study, we investigated the inhibitory effect of CA on diabetic cataractogenesis. We evaluated the aldose reductase (AR) activity during cataract development in 50% galactose-fed rats, an animal model of sugar cataract. Galactose-fed rats were treated orally with CA (10 and 50 mg/kg body weight) once a day for 2 weeks. In vehicle-treated galactose-fed rats, lens opacity was increased, and lens fiber swelling and membrane rupture were observed. In addition, AR protein was highly expressed in lens epithelial cells and lens cortical fibers of galactose-fed rats. However, CA inhibited the rat AR activity in vitro, and the administration of CA prevented the development of sugar cataract through the inhibition of AR activity. These observations suggest that CA is useful for the treatment of sugar cataract.

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Effect of Sorbitol Dehydrogenase Inhibition on Sugar Cataract Formation in Galactose-fed and Diabetic Rats

Cited by 35 publications

References 15 publications

Effects of Xylose on Monkey Lenses in Organ Culture: A Model for Study of Sugar Cataracts in a Primate

Effects of Xylose on Monkey Lenses in Organ Culture: A Model for Study of Sugar Cataracts in a Primate

Diabetic neuropathy and oxidative stress

Inhibitory effects of chlorogenic acid on aldose reductase activity in vitro and cataractogenesis in galactose-fed rats

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