In vitro effect of gliclazide on DNA damage and repair in patients with type 2 diabetes mellitus (T2DM)

Śliwińska, Agnieszka; Błasiak, Janusz; Kasznicki, Jacek; Drzewoski, Józef

doi:10.1016/j.cbi.2008.03.017

Cited by 52 publications

(24 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies have utilised the Comet assay to investigate oxidative damage in relation to various conditions including diabetes [28] and obesity, where an association between DNA damage, BMI, antioxidant status and MDA concentration was observed [29]. Our study showed a significant difference in Comet intensity, head intensity and tail intensity in the ODM group compared to O group.…”

Section: Discussionsupporting

confidence: 53%

Changes in markers of oxidative stress and DNA damage in human visceral adipose tissue from subjects with obesity and type 2 diabetes

Jones

Prior

Barry

et al. 2014

Diabetes Research and Clinical Practice

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 53%

Changes in markers of oxidative stress and DNA damage in human visceral adipose tissue from subjects with obesity and type 2 diabetes

Jones

Prior

Barry

et al. 2014

Diabetes Research and Clinical Practice

View full text Add to dashboard Cite

“…It has been suggested that it decreases hyperglycemia and hyperinsulinemia and inhibits oxidative stress. It is also a promising therapeutic candidate for the prevention of vascular complications of diabetes, by decreasing the level of DNA damage induced by reactive oxygen species [13, 40]. Also it has been found that gliclazide reduced oxidative stress in liver and kidney tissues of diabetic rats [11, 41].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Beta Glucan and Gliclazide on Brain Tissue and Sciatic Nerve of Diabetic Rats Induced by Streptozosin

Alp

Varol

Çelik

et al. 2012

Experimental Diabetes Research

View full text Add to dashboard Cite

There have not been yet enough studies about effects of beta glucan and gliclazide on oxidative stress created by streptozotocin in the brain and sciatic nerve of diabetic rats. The aim of this paper was to investigate the antioxidant effects of gliclazide and beta glucan on oxidative stress and lipid peroxidation created by streptozotosin in brain and sciatic nerve. Total of 42 rats were divided into 6 groups including control, diabetic untreated (DM) (only STZ, diabetic), STZ (DM) + beta glucan, STZ (DM) + gliclazide, only beta glucan treated (no diabetic), and only gliclazide treated (no diabetic). The brain and sciatic nerve tissue samples were analyzed for malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and paraoxonase (PON-1) levels. We found a significant increase in MDA, TOS, and OSI along with a reduction in TAS level, catalase, and PON-1 activities in brain and sciatic nerve of streptozotocin-induced diabetic rats. Also, this study shows that in terms of these parameters both gliclazide and beta glucan have a neuroprotective effect on the brain and sciatic nerve of the streptozotocin-induced diabetic rat. Our conclusion was that gliclazide and beta glucan have antioxidant effects on the brain and sciatic nerve of the streptozotocin-induced diabetic rat.

show abstract

“…These agents are reported to benefit the diabetic patients in reducing both hyperglycemia and also the mutagenic complications associated with enhanced oxidative stress. [27][28][29][30] In this study, following 4 weeks of insulin (regular) treatment to NA-STZ diabetic animals, although reduction in the elevated blood glucose was observed [ Figure 1], the incidences of MN frequency and sperm abnormalities as well as the diminished antioxidant status was not altered [Tables 1-3]. These observations indicated that the tested doses of insulin did not protect the bone marrow erythrocytes and spermatozoa cells against the reactive oxygen species induced lesion in diabetic condition.…”

Section: Discussionmentioning

confidence: 99%

Failure to detect the anti-mutagenic effect of insulin in experimental type-2 diabetic rats

Rabbani¹,

Devi²,

Khanam³

2010

J Pharm Negative Results

View full text Add to dashboard Cite

Background:The oxidative stress is known to cause mutation-related disorders in diabetic patients. Materials and Methods: The present study was designed to investigate the anti-mutagenic effect of insulin in nicotinamide (NA: 230 mg/kg, i.p.) and streptozotocin (STZ: 65 mg/kg, i.p.) induced nuclear defects. Bone marrow micronucleus (MN) test and caudal epididymal sperm abnormalities were detected to find the somatic and germinal cell mutations, respectively. The antioxidant status was determined by estimating serum lipid peroxidation, catalase, superoxide dismutase and glutathione peroxidase levels. Results: The experimental type diabetes significantly (P < 0.001) reduced the antioxidant status and enhanced MN frequency and sperm defects compared to control animals. Although administration of insulin (1, 3, 5 and 7 IU/kg, s.c. for 4 weeks) significantly (P < 0.001) reduced hyperglycemia, it did not alter the antioxidant status, and somatic and germinal cell defects in diabetic rats. Conclusion:The results suggest that insulin did not have protective effect against the genotoxicity induced by NA-STZ diabetes.

show abstract

In vitro effect of gliclazide on DNA damage and repair in patients with type 2 diabetes mellitus (T2DM)

Cited by 52 publications

References 46 publications

Changes in markers of oxidative stress and DNA damage in human visceral adipose tissue from subjects with obesity and type 2 diabetes

Changes in markers of oxidative stress and DNA damage in human visceral adipose tissue from subjects with obesity and type 2 diabetes

Protective Effects of Beta Glucan and Gliclazide on Brain Tissue and Sciatic Nerve of Diabetic Rats Induced by Streptozosin

Failure to detect the anti-mutagenic effect of insulin in experimental type-2 diabetic rats

Contact Info

Product

Resources

About