N-Acetyl-ß-D-Glucosaminidase Activity in Serum, Kidney and
Liver of Streptozotocin-Induced Diabetic Rat

Takumi, Toru; Kodama, Satoru; Takahashi, Tomohiro; Matsuo, Tamotsu

doi:10.1159/000469379

Cited by 3 publications

(2 citation statements)

References 10 publications

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“…13 Elevated urinary NAG excretion has been reported in renal damage produced by various causes, including diabetic humans and rats. 12,14,15 Conversely, NAG activity in the urine is correlated with an increase in urinary microalbumin and other parameters relevant to diabetes. Furthermore, some non-diabetic clinical and experimental studies have demonstrated a relationship between urinary NAG excretion and renal oxidative damage.…”

Section: Introductionmentioning

confidence: 99%

“…Urinary NAG excretion has been recommended as a useful marker for the detection of changes in proximal tubular function long before elevations in other markers, such as proteinuria and an increase in serum creatinine 13 . Elevated urinary NAG excretion has been reported in renal damage produced by various causes, including diabetic humans and rats 12,14,15 . Conversely, NAG activity in the urine is correlated with an increase in urinary microalbumin and other parameters relevant to diabetes.…”

Section: Introductionmentioning

confidence: 99%

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MELATONIN REDUCES URINARY EXCRETION OF N‐ACETYL‐β‐d‐GLUCOSAMINIDASE, ALBUMIN AND RENAL OXIDATIVE MARKERS IN DIABETIC RATS

Öktem

Özgüner

Yilmaz³

et al. 2006

Clin Exp Pharma Physio

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1. Increased oxidative stress has an important role in the pathogenesis of diabetic nephropathy. The aim of the present study was to evaluate diabetic nephropathy by determining markers of oxidative stress and the urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), albumin and to investigate the possible protective effects of in vivo melatonin on renal tubular oxidative damage in diabetic rats. 2. Twenty-six rats were randomly divided into three groups: (i) group I, control, non-diabetic rats (n = 9); (ii) group II, untreated diabetic rats (n = 8); and (iii) group III, melatonin-treated diabetic rats (n = 9). In groups II and III, diabetes developed 3 days after administration of a single dose of streptozotocin (35 mg/kg, i.p.). Thereafter, whereas the rats in group II received no treatment, rats in group III began to receive 10 mg/kg per day, i.p., melatonin for 8 weeks. Malondialdehyde (MDA), an index of lipid peroxidation, NAG and microalbumin in the urine, markers of renal tubular damage, were the parameters used for oxidative stress-induced renal injury. Superoxide dismutase (SOD), xanthine oxidase (XO) and glutathione peroxidase (GSH-Px) activities were determined to evaluate changes in the anti-oxidant status of kidney tissue. 3. In untreated diabetic rats, urinary NAG, albumin and renal MDA levels were markedly increased compared with control rats (P < 0.0001). However, these parameters were reduced in diabetic rats by melatonin treatment (P < 0.0001). Urinary excretion of NAG was positively correlated with the microalbuminuria and renal MDA levels (r = 0.8; P < 0.0001). The SOD and XO activities in the untreated diabetic group were found to be significantly higher than those of the control group (P < 0.0001). Superoxide dismutase and XO activities decreased in melatonin-treated rats compared with untreated diabetic rats (P < 0.002 and P < 0.023, respectively). However, the decrease did reach levels seen in control rats. There were no significant differences in GSH-Px activity between the three groups. 4. Therefore, on the basis of these data, we suggest that urinary NAG, albumin excretion, XO activity and MDA levels are more valuable parameters showing the degree of renal tubular injury than classical markers of oxidative stress, including SOD and GSH-Px, in diabetic rat kidneys. Melatonin has an ameliorating effect on oxidative stress-induced renal tubular damage via its anti-oxidant properties. Thus, it may be suggested that urinary NAG excretion and microalbuminuria may be important markers showing the degree of renal changes and the success of long-term treatment of renal impairment with melatonin.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MELATONIN REDUCES URINARY EXCRETION OF N‐ACETYL‐β‐d‐GLUCOSAMINIDASE, ALBUMIN AND RENAL OXIDATIVE MARKERS IN DIABETIC RATS

Öktem

Özgüner

Yilmaz³

et al. 2006

Clin Exp Pharma Physio

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Activities of Lysosomal Enzymes in Alloxan-Induced Diabetes in the Mouse

Witek

Rochon-Szmejchel²,

Stanisławska³

et al. 2017

Advances in Experimental Medicine and Biology

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The study investigated a panel of lysosomal enzymes in the liver and kidney tissues in alloxan-induced diabetes in the mouse. The mice were divided into six experimental groups receiving 10% alloxan at a dose of 50 and 75 mg/kg over a period of four, eight, and twelve days; each group was compared with controls receiving 0.9% NaCl. The findings were that diabetes induced by both doses of alloxan was accompanied by significant increases in the lysosomal activities of acid phosphatase and the glycosidases investigated: β-glucuronidase, β-galactosidase, β-glucosidase, and N-acetyl-hexosaminidase. The lysosomal enzyme activity in both liver and kidney cells peaked 12 days after onset of diabetes for most enzymes, at the time when hyperglycemia and hyperinsulinemia already started abating after their peak at 8 days into the course of diabetes. The enzyme activity was in most cases higher with the higher dose of alloxan and thus higher level of glycemia. Lysosomal enzymes degrade glycoconjugates, the molecules that are present in the basement membrane of endothelial cells where they contribute to capillary wall stability. Thus, enhanced activity of these enzymes could presage the progression of diabetic microangiopathy, atherosclerosis, and the development of microvascular complications.

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Effect of dietary fiber and butyric acid on lysosomal enzyme activities in streptozotocin-induced diabetic rats

Kumar

Shetty

Salimath

2005

Eur Food Res Technol

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N-Acetyl-ß-D-Glucosaminidase Activity in Serum, Kidney and Liver of Streptozotocin-Induced Diabetic Rat

Cited by 3 publications

References 10 publications

MELATONIN REDUCES URINARY EXCRETION OF N‐ACETYL‐β‐d‐GLUCOSAMINIDASE, ALBUMIN AND RENAL OXIDATIVE MARKERS IN DIABETIC RATS

MELATONIN REDUCES URINARY EXCRETION OF N‐ACETYL‐β‐d‐GLUCOSAMINIDASE, ALBUMIN AND RENAL OXIDATIVE MARKERS IN DIABETIC RATS

Activities of Lysosomal Enzymes in Alloxan-Induced Diabetes in the Mouse

Effect of dietary fiber and butyric acid on lysosomal enzyme activities in streptozotocin-induced diabetic rats

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