Erythrocyte membrane lipid peroxidation and glycosylated hemoglobin in diabetes

Jain, S. K.; McVie, Robert; Duett, John; Herbst, John J.

doi:10.2337/diabetes.38.12.1539

Cited by 233 publications

(101 citation statements)

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“…None of Baker et al [13] MDA was determined as the these subjects were alcoholics or chronic measure of thio barbituric acid reactive smokers, and none of them suffered from any substances (TBARS). [14] SOD (EC 1.15.1.1) systematic diseases like hypertension or any activity was measured in the hemolysate by diabetic complication. Patients suffering from the method of Misra and Fridovich [15] disease of any origin other than osteoarthritis on inhibition of auto-oxidation of epinephrine were excluded from the study.…”

Section: Discussionmentioning

confidence: 99%

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with osteoarthritis

2007

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Section: Discussionmentioning

confidence: 99%

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with osteoarthritis

2007

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“…MDA (as an important indicator of lipid peroxidation) levels were measured according to a method of Jain et al [16]. The principle of the method was based on the spectrophotometric measurement of the color that occurred during the reaction of thiobarbituric acid with MDA.…”

Section: Mda Assaymentioning

confidence: 99%

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

et al. 2009

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The aim of this experimental study was to investigate the possible protective effect of dexmedetomidine (DEX) on traumatic spinal cord injury (SCI). Twentytwo New Zealand rabbits were divided into three groups: sham (no drug or operation, n = 6), Control [SCI ? single dose of 1 mL saline intraperitoneally (i.p), after trauma; n = 8] and DEX (SCI ? 1 lg/kg dexmedetomidine in 1 mL, i.p, after trauma, n = 8). Laminectomy was performed at T10 and balloon angioplasty catheter was applied extradurally. Four and 24 h after surgery, rabbits were evaluated by an independent observer according to the Tarlov scoring system. Blood, cerebrospinal fluid (CSF), tissue samples from spinal cord were taken for biochemical and histopathological evaluations. After 4 h of SCI, all animals in control or DEX treated groups became paraparesic. On the other hand, 24 h after SCI, partial improvements were observed in both control and DEX treated groups. Traumatic SCI leads to increase in the lipid peroxidation and decreases enzymatic or nonenzymatic endogenous antioxidative defense systems. Again, SCI leads to apoptosis in spinal cord. DEX treatment slightly prevented lipid peroxidation and augmented endogenous antioxidative defense systems in CSF or spinal cord tissue, but failed to prevent apoptosis or neurodeficit after traumatic SCI. Therefore, it could be suggested that treatment with dexmedetomidine does not produce beneficial results in SCI.

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“…Tissues were homogenized in 10 mmol/l Tris containing 50 mmol/l butylated hydroxy toluene (BHT) and aliquots were saved for protein assay by the Bradford method (BioRad, Hercules, Calif., USA). Lipid peroxidation was assessed by measuring malondialdehyde (MDA), an end-product of fatty acid peroxidation which can be used to estimate the extent of lipid peroxidation [35]. Briefly, 0.2 ml protein extracts were diluted in 0.8 ml PBS plus 0.025 ml BHT (50 mmol/l) and reacted with 0.5 ml of 30% thiobarbituric acid (TBA).…”

Section: Relative Quantitative (Real Time) Rt-pcr Of Pax-3 Mrnamentioning

confidence: 99%

Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural tube defects

et al. 2003

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Aims/hypothesis. Maternal diabetes increases oxidative stress in embryos. Maternal diabetes also inhibits expression of embryonic genes, most notably, Pax-3, which is required for neural tube closure. Here we tested the hypothesis that oxidative stress inhibits expression of Pax-3, thereby providing a molecular basis for neural tube defects induced by diabetic pregnancy. Methods. Maternal diabetes-induced oxidative stress was blocked with α-tocopherol (vitamin E), and oxidative stress was induced with the complex III electron transport inhibitor, antimycin A, using pregnant diabetic or non-diabetic mice, primary cultures of neurulating mouse embryo tissues, or differentiating P19 embryonal carcinoma cells. Pax-3 expression was assayed by quantitative RT-PCR, and neural tube defects were scored by visual inspection. Oxidation-induced DNA fragmentation in P19 cells was assayed by electrophoretic analysis.Results. Maternal diabetes inhibited Pax-3 expression and increased neural tube defects, and α-tocopherol blocked these effects. In addition, induction of oxidative stress with antimycin A inhibited Pax-3 expression and increased neural tube defects. In cultured embryo tissues, high glucose-inhibited Pax-3 expression, and this effect was blocked by α-tocopherol and GSHethyl ester, and Pax-3 expression was inhibited by culture with antimycin A. In differentiating P19 cells, antimycin A inhibited Pax-3 induction but did not induce DNA strand breaks. Conclusion/interpretation. Oxidative stress inhibits expression of Pax-3, a gene that is essential for neural tube closure. Impaired expression of essential developmental control genes could be the central mechanism by which neural tube defects occur during diabetic pregnancy, as well as other sources of oxidative stress. [Diabetologia (2003) 46:538-545]

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Erythrocyte membrane lipid peroxidation and glycosylated hemoglobin in diabetes

Cited by 233 publications

References 0 publications

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with osteoarthritis

Status of lipid peroxidation, glutathione, ascorbic acid, vitamin E and antioxidant enzymes in patients with osteoarthritis

Does dexmedetomidine reduce secondary damage after spinal cord injury? An experimental study

Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural tube defects

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