Oxidative protein damage in early stage Type 1 diabetic patients

Telci, Ayşegül; Çakatay, Ufuk; Salman, Serpil; Satman, İlhan; Sıvas, Ahmet

doi:10.1016/s0168-8227(00)00197-2

Cited by 130 publications

(95 citation statements)

References 39 publications

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“…Protein thiols may preemptively scavenge oxidants which initiate peroxidation. Telci et al (2000) found that plasma thiols was significantly decreased between the diabetic groups than their age-matched controls. Wittenstein et al (2002) also found lower plasma thiol levels in type I diabetes compared to the controls.…”

Section: Discussionmentioning

confidence: 81%

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Paşaoğlu

Sancak

Bukan

2004

Tohoku J. Exp. Med.

101

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We investigated lipid peroxidation, resistance of plasma and red blood cells to oxidation, and antioxidant defense system in erythrocytes and sera in patients with type 2 diabetes mellitus. One group included newly diagnosed 20 patients and the other included 20 patients treated with oral antidiabetic agents (OAD). Twenty healthy subjects served as controls. Serum and red blood cell malondialdehyde (MDA), glutathione (GSH), resistance to oxidation, and plasma thiol (total -SH) levels were measured. In addition, glycated hemoglobin, serum fructosamine, uric acid, total protein, total cholesterol, triglyceride and glucose levels were determined. Although newly diagnosed patients had higher serum and erythrocyte MDA levels than those of controls, the highest levels of MDA were determined in patients treated with OAD. MDA levels after exposing to oxidation increased in OAD group more than in newly diagnosed patients. Total -SH and erythrocyte GSH levels of the both diabetic groups were lower than controls. These results show that serum and erythrocyte lipid peroxidation was increased in diabetic patients. The sera of the patients showed a decreased resistance against oxidation. We therefore suggest that the effect of increased free radicals may be prevented by antioxidant systems in early stages of type 2 diabetes but in advanced stages this relationship is impaired owing to decreased antioxidant activity. Decreased red blood cell GSH and serum total -SH levels may be due to a compensation mechanism of the antioxidants. diabetes mellitus; lipid peroxidation; antioxidants

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Section: Discussionmentioning

confidence: 81%

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Paşaoğlu

Sancak

Bukan

2004

Tohoku J. Exp. Med.

101

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“…Oxidative stress is known to play a significant role in the induction of these processes (Giugliano et al, 1996;Baynes and Thorpe, 1999). High levels of oxidative stress with excessive generation of free radicals and depleted levels of free radicals scavenging enzymes have been demonstrated in several studies, both in experimental animal models of diabetes and in human diabetic subjects (Bonnefont-Rousselot et al, 2000;Telci et al, 2000;Turk et al, 2002). In type 1 diabetes, reactive oxygen species (ROS) are involved in β-cell dysfunction initiated by autoimmune reactions and inflammatory cytokines (Cnop et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Antidiabetics in combination with hydroxychloroquine improve antioxidant and hepatoprotective activities in alloxan-induced diabetic rats

et al. 2015

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Hyperglycemia exerts toxic effects on the pancreatic β-cells. This study investigated the hypothesis that the antidiabetic drugs glibenclamide and metformin, in combination with hydroxychloroquine (HCQ) offer additional protection for the pancreas against oxidative stress and produce hepatoprotective effect in alloxan-induced diabetic rats. Diabetes was induced in male Long-Evans rats by a single dose of alloxan (120 mg/kg; i.p.). Different groups of diabetic animals were treated with glibenclamide (10 mg/70 kg, i.p.), metformin (850 mg/70 kg, i.p.), HCQ (300 mg/70 kg, i.p.) and combination of both glibenclamide and metformin with HCQ, separately for a period of 28 days. Diabetic rats had significantly elevated levels of serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT), while catalase (CAT) and superoxide dismutase (SOD) activity were significantly reduced. Glibenclamide and metformin produced no significant effects on antioxidant enzymes but both showed significant (p<0.05) result in reducing SGOT and SGPT level in diabetic rats. In contrast, the combination of glibenclamide or metformin with HCQ showed better effect on up-regulation of CAT and SOD activity and down-regulation of SGOT and SGPT activity in comparison with the antidiabetic drug alone. These findings suggest that, HCQ potentiates the effect of glibenclamide and metformin to protect pancreas against oxidative stress and produce hepatoprotective effect in diabetic rats.

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“…clinical manifestations of microvascular complications are rarely observed during the developmental age period; however, the biochemical markers of oxidative stress associated with chronic hyperglycemia are prevalent in this age group [3]. attempts to employ markers of oxidative stress as additional clinical manifestations to evaluate the metabolic status in diabetes or to predict the risk of developing late complications have been undertaken by numerous authors [4][5][6][7].…”

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confidence: 99%

Trace Elements, Magnesium, and the Efficacy of Antioxidant Systems in Children with Type 1 Diabetes Mellitus and in Their Siblings

Salmonowicz¹,

Krzystek−Korpacka²,

Noczyńska³

2014

Adv Clin Exp Med

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Background. Magnesium (Mg), selinium (Se), zinc (Zn), manganese (Mn), and copper (cu) are involved in the mechanisms of antioxidant defense. Mn and cu, which participate in the generation of reactive oxygen species (ROS), also have pro-oxidative properties. Objectives. To evaluate the levels of Mg, Se, Zn, Mn, and cu, as well as the effectiveness of antioxidant defense mechanisms in children with Type 1Diabetes Mellitus (T1DM) and in their siblings. The preliminary findings were originally reported in 2009 at the 35 th annual conference of the International Society for Pediatric and adolescent Diabetes (ISPaD) in Ljubljana, Slovenia. Material and Methods. The study involved 87 children with T1DM, 2-19 years old, treated for T1DM for an average of 3.5 years. The sibling and control groups comprised 27 and 41 children, aged 4.5-16.5 years and 10.5-18 years respectively. The parameters named above were assessed in relation to metabolic compensation levels (Hb a1c ) and disease duration. Results. compared with the control group, T1DM children had lower plasma levels of Mg and Zn and higher levels of cu; the siblings had lower levels of Zn; T1DM children had lower copper/zinc superoxide dismutase (cuZnSOD) activity; and both T1DM children and their siblings had higher catalase (caT) activity and lower total antioxidant status (TaS) levels. Conclusions. There may be a correlation between impaired antioxidant status and Mg and Zn deficiency and increased cu levels in T1DM children. Oxidative stress in T1DM is accompanied by alterations in enzymatic activity and non-enzymatic mechanisms of antioxidant defense. The decreased TaS levels noted in T1DM patients may impair the effectiveness of non-enzymatic antioxidant systems. The increased caT activity and unimpaired selenium-dependent glutathione peroxidase (Se-GSHPx) activity point indirectly to enhanced ROS generation in T1DM children. The impaired antioxidant defense found in the siblings of T1DM patients may indicate that genetic factors play a role (Adv Clin Exp Med 2014, 23, 2, 259-268).

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Oxidative protein damage in early stage Type 1 diabetic patients

Cited by 130 publications

References 39 publications

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Lipid Peroxidation and Resistance to Oxidation in Patients with Type 2 Diabetes Mellitus

Antidiabetics in combination with hydroxychloroquine improve antioxidant and hepatoprotective activities in alloxan-induced diabetic rats

Trace Elements, Magnesium, and the Efficacy of Antioxidant Systems in Children with Type 1 Diabetes Mellitus and in Their Siblings

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