The increase in lipid peroxidation in diabetic rat lens can be reversed by oral sorbinil

Yeh, Li-An; Ashton, Michael A.

doi:10.1016/0026-0495(90)90029-c

Cited by 35 publications

(18 citation statements)

References 26 publications

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“…One likely explanation for the lower levels is, increased oxidation of pyrraline in diabetes because of enhanced oxidative stress. Several studies have shown an enhancement in oxidative stress in diabetic lenses [21]. This may result in pyrraline ether crosslinking [16], leading to decreased levels of unmodified pyrraline.…”

Section: Discussionmentioning

confidence: 99%

The presence of a glucose‐derived Maillard reaction product in the human lens

Nagaraj

Sady

1996

FEBS Letters

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Pyrraline is an advanced Maillard reaction product formed by the non-enzymatic reaction initiated by glucose with lysine residues on proteins. This reaction involves an intermediate, 3-deoxyglucosone, concentration of which is shown to be elevated in plasma and lenses during diabetes. Bovine lens alpha crystallins incubated with 3-deoxyglucosone showed that pyrraline formation was a major modification and its quantification by two different methods revealed time-dependent accumulation. Pyrraline was quantified in normal, senile cataractous and diabetic lenses. Although a wide variation was observed, the mean value in cataractous lenses (mean_+S.E.: 48.4+12.67 pmol/mg protein) was higher than in age-matched normal lenses (30.9 + 10.26 pmol). Surprisingly, in diabetic lenses, the mean value was lower than normal lenses (28.4+ 15.3 pmol). These results suggest that glucose-specific advanced Maillard products occur in the human lens and such modifications may play a role in lens aging and cataract formation.

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Section: Discussionmentioning

confidence: 99%

The presence of a glucose‐derived Maillard reaction product in the human lens

Nagaraj

Sady

1996

FEBS Letters

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“…As NADPH is used in several critical reductive metabolic steps, a large drain on the NADPH pool could compromise the ability of the cell to protect itself from oxidative stress. NADPH is also required for GSH reductase to regenerate GSH [37][38][39][40]. Considering the importance of oxidative stress in the pathophysiology of diabetic state and development of cognitive impairment, reduction of oxidative stress by EPS may produce a beneficial effect on diabeticinduced cognitive impairment.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Epalrestat on Memory Impairment in Streptozotocin-Induced Type-2 Diabetic Rats Using Different Behavioral Models.

Jaiswal

Mishra

2018

Asian J Pharm Clin Res

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Objective: The present study was designed to evaluate the protective effects of epalrestat (EPS) on memory and learning in type-2 diabetes.Methods: Sixty percent high-fat diet for 2 weeks and a single dose of streptozotocin (35 mg/kg, ip) was used to induce memory impairment in rats. Once the diabetes is confirmed, test drug (EPS -13.5, 27, and 54 mg/kg, oral) and donepezil (1 mg/kg, oral) were administered to different groups of rats for 4 weeks followed by an assessment of memory and learning deficit using behavioral paradigms: Elevated plus maze (EPM), Morris water maze (MWM), and passive avoidance test.Results: EPS and donepezil showed significant improvement in learning and memory of rats, as indicated by markedly decreased escape latency to reach a hidden platform and increased time spent in target quadrant using MWM task, reduced transfer latency in EPM, and also there is a significant increase in the transfer latencies using passive avoidance test were noted. Memory-enhancing activity of EPS (13.5, 27, and 54 mg/kg) was comparable with the diabetic control group. Conclusion:The study findings suggest that memory-enhancing effect of EPS may be mediated by its antioxidant and anti-inflammatory activities. This recommends the potential effect of EPS therapy as a useful memory restorative agent in the treatment of neurodegenerative disease seen in type-2 diabetes rat.

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“…Because NADPH is used in several critical reductive metabolic steps, such as detoxification of ROS and hydroperoxide, a large drain on the NADPH pool could compromise the ability of the cell to protect itself from oxidative stress. NADPH is also required for glutathione reductase to regenerate GSH, and glutathione peroxidase reduces lipid hydroperoxides level at the expense of GSH [15,[23][24][25]. AR has a K m for NADPH 10-fold lower than glutathione reductase.…”

Section: Discussionmentioning

confidence: 99%

“…AR has a K m for NADPH 10-fold lower than glutathione reductase. AR could steal NADPH from glutathione reductase and cause decrease in the GSH level [24]. Other investigators reported that oxidation of sorbitol to fructose by SDH causes oxidative stress because its co-factor NAD+ is converted to NADH in the process, and NADH is the substrate for NAD(P)H oxidase to generate ROS [26].…”

Section: Discussionmentioning

confidence: 99%

Aldose Reductase Inhibitor, Epalrestat, Reduces Lipid Hydroperoxides in Type 2 Diabetes

et al. 2009

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Abstract. The increased flux of polyol pathway induced by hyperglycemia is implicated in the pathogenesis of various complications associated with diabetic, which results in increased oxidative stress. Because oxidative stress causes tissue damage in patients with diabetes, searching for an effective strategy to reduce oxidative stress in clinical setting is important in order to prevent diabetic complications. The aim of this study was to evaluate the effects of aldose reductase inhibition on oxidative stress in patients with type 2 diabetes mellitus. The subjects of this study were 21 patients with type 2 diabetes. We compared the levels of various oxidative stress markers and antioxidants including plasma thiobarbituric acid-reactive substances, malondialdehyde-modified low-density lipoprotein, vitamin E, β-carotene and lipid hydroperoxides in erythrocytes at baseline with those measured after a 3-month course of epalrestat (150 mg/day), an aldose reductase inhibitor. While administration of epalrestat did not result in significant changes in plasma thiobarbituric acid-reactive substances, malondialdehyde-modified low-density lipoprotein, vitamin E, or β-carotene, it significantly reduced lipid hydroperoxides in erythrocytes. Given the importance of measuring lipid hydroperoxides in erythrocytes as an index of oxidative stress, these results highlight the potential usefulness of epalrestat in reducing oxidative stress in type 2 diabetes mellitus.

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The increase in lipid peroxidation in diabetic rat lens can be reversed by oral sorbinil

Cited by 35 publications

References 26 publications

The presence of a glucose‐derived Maillard reaction product in the human lens

The presence of a glucose‐derived Maillard reaction product in the human lens

Neuroprotective Effect of Epalrestat on Memory Impairment in Streptozotocin-Induced Type-2 Diabetic Rats Using Different Behavioral Models.

Aldose Reductase Inhibitor, Epalrestat, Reduces Lipid Hydroperoxides in Type 2 Diabetes

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