Aspects of oxidative stress in children with Type 1 diabetes mellitus

Varvařovská, J; Ráček, Jaroslav; Štětina, Rudolf; Sýkora, Josef; Pomahačová, Renata; Rušavý, Zdeněk; Lacigová, S; Trefil, Ladislav; Siala, Konrad; Stožický, F

doi:10.1016/j.biopha.2004.09.011

Cited by 63 publications

(50 citation statements)

References 27 publications

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“…In the present study vitamin E attenuated the increase in lipid hydroperoxide, accompanied by a concomitant increase in the activities of GSH-Px and SOD, which modulated the concentration of ROS. These data were consistent with studies reporting that vitamin E exerted a beneficial effect on the antioxidant enzyme activity in type 1 diabetes (Varvarovská et al 2004;Musalmah et al 2002). Indeed, antioxidant therapy could prevent a disturbance in the mechanism of protection against the deleterious cellular and biomolecular effects that led to alterations in the cell function.…”

Section: Discussionsupporting

confidence: 81%

Evaluation of lipid profile and oxidative stress in STZ-induced rats treated with antioxidant vitamin

Almeida

Braga

Novelli

et al. 2012

Braz. arch. biol. technol.

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The present study investigated the effect of supplementation of vitamin E on streptozotocin (STZ)-induced diabetic rats by measuring blood glucose, changes in body weight, food and water intake, lipid profile, serum urea and creatinine level, and antioxidant enzyme activity. Male Wistar rats were divided into four groups: control rats (GI); rats receiving vitamin E (GII); STZ-induced diabetic rats (GIII) and STZ-induced diabetic rats treated with vitamin E (GIV). Vitamin E reduced (p<0.05) blood glucose and urea, improved the lipid profile (decreased the serum levels of total cholesterol, LDL cholesterol, VLDL cholesterol and triacylglycerols, and increased HDL cholesterol) and increased total protein in STZ-induced diabetic rats (GIV). Vitamin prevented changes in the activity of SOD and GSH-Px and in the concentration of lipid hydroperoxide. These results suggested that vitamin E improved hyperglycaemia and dyslipidaemia while inhibiting the progression of oxidative stress in STZ-induced diabetic rats.

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Section: Discussionsupporting

confidence: 81%

Evaluation of lipid profile and oxidative stress in STZ-induced rats treated with antioxidant vitamin

Almeida

Braga

Novelli

et al. 2012

Braz. arch. biol. technol.

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“…This suggestion would fit with the particular risk of RPE-dependent maculopathy in type 2 diabetes, and the independent association between retinopathy and adverse cardiovascular outcomes [55]. The observation of more effective DNA repair mechanisms in type 1 diabetes, with little evidence of increased oxidative DNA susceptibility compared with type 2 diabetes [31,32] could account for the earlier onset of a senescent retinal phenotype in type 2 diabetes compared with type 1 diabetes.…”

Section: Telomeres Replicative Senescence and Diabetic Retinopathymentioning

confidence: 92%

“…The poorer outcomes in type 2 diabetes patients for recurrence-free survival rates and median survival [12] could also be related to this hypothesis, with type 2 diabetes driving a progressive repopulation of carcinogenic genomically unstable epithelial cells [10,11,[25][26][27]. In this context, it is important to note that evidence of a substantially increased risk of epithelial cancers in type 1 diabetes is lacking [12], and that we and others have shown that increased DNA oxidative susceptibility is not a feature of type 1 diabetes [31], perhaps because of more effective DNA repair mechanisms in younger type 1 patients [32]. We also suggest, although the epidemiological evidence is lacking, that an adverse intrauterine environment could be one variable that predisposes towards both type 2 diabetes and an increased risk of epithelial malignancies through feto-placental pre-programming of epithelial and other cell types mediated through telomere attrition.…”

Section: Telomere Attrition and Increased Malignancy Risk In Type 2 Dmentioning

confidence: 97%

“…We also suggest that subjects with an antecedent history of IUGR, programmed towards reduced glomerular numbers [45,46], would be particularly prone to developing a senescent renal cortical phenotype if they developed type 2 diabetes. The observation of more effective DNA repair mechanisms in type 1 diabetes, with little evidence of increased oxidative DNA susceptibility compared with type 2 diabetes [31,32], could account for the earlier onset of a senescent renal phenotype and proteinuria in type 2 diabetes than in type 1 diabetes.…”

Section: Telomeres Replicative Senescence and Diabetic Nephropathymentioning

confidence: 98%

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Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes

Sampson

Hughes

2006

Diabetologia

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Telomeres are the repeat DNA sequences at the end of chromosomes necessary for successful DNA replication and chromosomal integrity. Telomeres shorten at cell division at a rate determined by oxidative DNA damage, and cells are triggered into replicative senescence once telomeres shorten to a critical length. Telomere-related chromosomal maintenance also has a role in carcinogenesis. Type 2 diabetes is characterised by increased oxidative stress, increased oxidative DNA damage, senescent retinal and renal phenotypes, and an increased risk of epithelial malignancy. We suggest that increased oxidative DNA damage and telomere attrition in type 2 diabetes leads to: (1) carcinogenic telomere-dependent chromosomal nonreciprocal translocations, genomic instability, and the development of epithelial cancers; (2) senescent retinal and renal phenotypes (expressed as diabetic retinopathy and nephropathy); and (3) senescent vascular endothelial, monocyte-macrophage and vascular smooth muscle cells (expressed as endothelial dysfunction and accelerated atherogenesis). An adverse intrauterine environment leads to increased feto-placental oxidative stress and feto-placental oxidative DNA damage. We also suggest that intrauterine oxidative DNA damage and telomere shortening is another point at which increased oxidative stress could contribute to a pre-programmed increased risk of senescent phenotypes in adult offspring, characterised by type 2 diabetes and epithelial malignancy. These suggestions can be used to understand early glucose intolerance in the young children of type 1 diabetes pregnancies, poor cancer outcomes in type 2 diabetes, beta cell fatigue in type 2 diabetes and the absence of increased epithelial cancer risk in type 1 diabetes.

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“…As an antioxidant, vitamin C can improve oxidative stress in diabetics (21), and it was therefore used as a positive control. Vitamin C (0.1 g/tablet) was purchased from Beijing Double-Crane Pharmaceutical Co., Ltd. (Beijing, China; lot no.…”

Section: Animalsmentioning

confidence: 99%

Jinmaitong decreases sciatic nerve DNA oxidative damage and apoptosis in a streptozotocin-induced diabetic rat model

Yin

Liang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Diabetic peripheral neuropathy (DPN) is a common chronic complication of diabetes. Jinmaitong (JMT), a Traditional Chinese Medicine, improves certain symptoms of DPN, such as limb pain and numbness. The aim of the present study was to investigate the effects of JMT on DNA oxidative damage and apoptosis in the sciatic nerve of diabetic rats. The rats were divided into a normal and a diabetic group. Diabetes was induced using streptozotocin (60 mg/kg). The diabetic model (DM) rats received vitamin C (0.05 g/kg/day) or JMT [low-dosage (L), 0.44 g/kg/day; medium-dosage (M), 0.88 g/kg/day or high-dosage (H), 1.75 g/kg/day]. After 16 weeks, the mechanical pain threshold of the rats was evaluated. The expression of 8-hydroxy-deoxyguanosine (8-OHdG), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase p22phox , B-cell lymphoma 2 (Bcl-2), caspase 3 and cleaved-poly(ADP-ribose) polymerase 1 (PARP-1) in the sciatic nerve tissues was measured using the reverse transcription-quantitative polymerase chain reaction, immunohistochemistry and western blotting. JMT had no effect on body weight and fasting blood glucose levels. Following treatment, the rats in the JMT groups had an improved pain threshold compared with the DM controls (JMT-L, 52.9±6.5 g; JMT-M, 74.7±9.3 g; and JMT-H, 61.7±2.0 g vs. DM control, 35.32±12.06 g; all P<0.01), while the threshold in the JMT-M rats was similar to that of normal controls (P>0.05). 8-OHdG and NADPH oxidase p22 phox expression was significantly decreased in the three JMT groups compared with that in the DM controls (all P<0.05). Following JMT treatment, Bcl-2 levels were increased, while caspase 3 and cleaved-PARP-1 levels were decreased compared with those in the DM controls (all P<0.01). In conclusion, JMT may reduce DNA oxidative damage to the sciatic nerve in diabetic rats, as well as regulate genes involved in peripheral neuronal cell apoptosis, suggesting that JMT could be used to prevent or treat DPN in diabetic patients.

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Aspects of oxidative stress in children with Type 1 diabetes mellitus

Cited by 63 publications

References 27 publications

Evaluation of lipid profile and oxidative stress in STZ-induced rats treated with antioxidant vitamin

Evaluation of lipid profile and oxidative stress in STZ-induced rats treated with antioxidant vitamin

Chromosomal telomere attrition as a mechanism for the increased risk of epithelial cancers and senescent phenotypes in type 2 diabetes

Jinmaitong decreases sciatic nerve DNA oxidative damage and apoptosis in a streptozotocin-induced diabetic rat model

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