The Role of Oxidative Stress in Diabetic Neuropathy: Generation of Free Radical Species in the Glycation Reaction and Gene Polymorphisms Encoding Antioxidant Enzymes to Genetic Susceptibility to Diabetic Neuropathy in Population of Type I Diabetic Patients

Background and Aims. Diabetic neuropathy is a frequent complication of type 2 diabetes mellitus (T2DM). Genetic susceptibility and oxidative stress may play a role in the appearance of T2DM and diabetic neuropathy. We investigated the relation between polymorphism in genes related to oxidative stress such asGSTM1,GSTT1, andGSTP1and the presence of T2DM and diabetic neuropathy (DN).Methods. Samples were collected from 84 patients with T2DM (42 patients with DN and 42 patients without DN) and 98 healthy controls and genotyped by using polymerase chain reaction and restriction fragment length polymorphism method.Results.GSTP1Ile105Val polymorphism was associated with the risk of developing T2DM (p=0.05) but not with the risk of developing DN in diabetic cases.GSTM1andGSTT1gene polymorphisms were associated with neither the risk of developing T2DM nor the risk of DN occurrence in diabetic patients. No association was observed between the patients with T2DM and DSPN (diabetic sensorimotor peripheral neuropathy) and T2DM without DSPN regarding investigated polymorphism.Conclusion. Our data suggest thatGSTP1gene polymorphisms may contribute to the development of T2DM in Romanian population.GSTM1,GSTT1, andGSTP1gene polymorphisms are not associated with susceptibility of developing diabetic neuropathy in T2DM patients.

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Role of Oxidative Stress and Mitochondrial Dysfunction in Skeletal Muscle in Type 2 Diabetic Patients

Current Pharmaceutical Design ◽

10.2174/1381612822666160217142949 ◽

2016 ◽

Vol 22 (18) ◽

pp. 2650-2656 ◽

Cited By ~ 5

Author(s):

Noelia Diaz-Morales ◽

Susana Rovira-Llopis ◽

Irene Escribano-Lopez ◽

Celia Bañuls ◽

Sandra Lopez-Domenech ◽

...

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Mitochondrial Dysfunction ◽

Diabetic Patients ◽

Type 2 Diabetic Patients ◽

Type 2 Diabetic

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Effects of Caloric Restriction on Cardiac Oxidative Stress and Mitochondrial Bioenergetics: Potential Role of Cardiac Sirtuins

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/528935 ◽

2013 ◽

Vol 2013 ◽

pp. 1-11 ◽

Cited By ~ 29

Author(s):

Ken Shinmura

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Oxidative Damage ◽

Caloric Restriction ◽

Functional Decline ◽

Cellular Damage ◽

Free Radical Theory ◽

Radical Theory ◽

Stress Theory

The biology of aging has not been fully clarified, but the free radical theory of aging is one of the strongest aging theories proposed to date. The free radical theory has been expanded to the oxidative stress theory, in which mitochondria play a central role in the development of the aging process because of their critical roles in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function associated with the accumulation of oxidative damage might be responsible, at least in part, for the decline in cardiac performance with age. In contrast, lifelong caloric restriction can attenuate functional decline with age, delay the onset of morbidity, and extend lifespan in various species. The effect of caloric restriction appears to be related to a reduction in cellular damage induced by reactive oxygen species. There is increasing evidence that sirtuins play an essential role in the reduction of mitochondrial oxidative stress during caloric restriction. We speculate that cardiac sirtuins attenuate the accumulation of oxidative damage associated with age by modifying specific mitochondrial proteins posttranscriptionally. Therefore, the distinct role of each sirtuin in the heart subjected to caloric restriction should be clarified to translate sirtuin biology into clinical practice.

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The protective role of CsNPs and CurNPs against DNA damage, oxidative stress, and histopathological and immunohistochemical alterations induced by hydroxyapatite nanoparticles in male rat kidney

Toxicology Research ◽

10.1039/c9tx00138g ◽

2019 ◽

Vol 8 (5) ◽

pp. 741-753 ◽

Cited By ~ 3

Author(s):

Israa F. Mosa ◽

Mokhtar I. Yousef ◽

Maher Kamel ◽

Osama F. Mosa ◽

Yasser Helmy

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Biological Effects ◽

Male Rats ◽

Nuclear Antigen ◽

Male Rat ◽

Control Group ◽

Renal Tubules ◽

Hydroxyapatite Nanoparticles

Abstract Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs.

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Advanced oxidation protein products in serum of patients with myotonic disease type I: association with serum γ-glutamyltransferase and disease severity

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm.2005.127 ◽

2005 ◽

Vol 43 (7) ◽

Cited By ~ 8

Author(s):

Gabriele Siciliano ◽

Livia Pasquali ◽

Anna Rocchi ◽

Michela Falorni ◽

Fabio Galluzzi ◽

...

Keyword(s):

Oxidative Stress ◽

Characteristic Curve ◽

Advanced Oxidation ◽

Clinical Severity ◽

Total Serum ◽

Type I ◽

Advanced Oxidation Protein Products ◽

Severity Scores

AbstractSteinert's disease (myotonic dystrophy type 1; MD) is caused by a CTG trinucleotide expansion on 19q13.3. Although the pathogenic mechanism underlying multisystem involvement in MD is still unclear, a role of oxidative stress in this disease has been suggested. We investigated 39 MD patients to assess the plasma concentration of advanced oxidation protein products (AOPPs) and γ-glutamyltransferase (GGT) and related them to clinical severity scores. Plasma AOPP levels (p=0.021), total serum GGT activity (p=0.0005) and GGT activity associated with low-density lipoprotein (p=0.0021) were significantly higher in patients than in controls. There was significant correlation between serum GGT levels and AOPPs (r=0.5831; p=0.0022). A statistically significant increase in serum GGT with age was found in MD patients (p=0.0193). Receiver operating characteristic curve analysis showed that higher AOPP levels were significantly associated with extra-muscular signs of the disease, i.e., cataracts and heart involvement (area under the curve±SE=0.908±0.083), but not with muscular involvement. The concomitant increment in GGT and AOPPs indicates a possible role of oxidative stress in the pathogenesis of MD type 1, while the association of increased AOPP levels with extra-muscular signs of the disease suggests that individual susceptibility to oxidative stress can modulate the extra-muscular phenotype of the disease.

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