Oxidative Stress in Type II Diabetes Mellitus and the Role of the Endogenous Antioxidant Glutathione

Whillier, Stephney; Kuchel, Philip W.; Raftos, Julia E.

doi:10.5772/21218

Cited by 3 publications

(3 citation statements)

References 104 publications

(128 reference statements)

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“…Depletion of GSH decreases the antioxidant capacity and leads to oxidative stress [94, 95]. Rats treated with K 2 Cr 2 O 7 presented low GSH levels in comparison with control, probably due to the oxidative stress induced for the K 2 Cr 2 O 7 exposition.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, K 2 Cr 2 O 7 decreased the activity of SOD, CAT, GPx, GR, and GST mainly 48 h after treatment. This effect may be secondary to decreased enzyme levels (secondary to changes in synthesis or degradation of enzymes) or decreased activity (e.g., by oxidative damage) without changes in enzymes levels [95]. In this context, Kalayarasan et al [73] postulated that K 2 Cr 2 O 7 produces high levels of O 2 •− which override enzymatic activity in liver tissues.…”

Section: Discussionmentioning

confidence: 99%

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Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

García-Niño

Tapia

Zazueta

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Curcumin is a polyphenol derived from turmeric with recognized antioxidant properties. Hexavalent chromium is an environmental toxic and carcinogen compound that induces oxidative stress. The objective of this study was to evaluate the potential protective effect of curcumin on the hepatic damage generated by potassium dichromate (K2Cr2O7) in rats. Animals were pretreated daily by 9-10 days with curcumin (400 mg/kg b.w.) before the injection of a single intraperitoneal of K2Cr2O7 (15 mg/kg b.w.). Groups of animals were sacrificed 24 and 48 h later. K2Cr2O7-induced damage to the liver was evident by histological alterations and increase in the liver weight and in the activity of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase in plasma. In addition, K2Cr2O7 induced oxidative damage in liver and isolated mitochondria, which was evident by the increase in the content of malondialdehyde and protein carbonyl and decrease in the glutathione content and in the activity of several antioxidant enzymes. Moreover, K2Cr2O7 induced decrease in mitochondrial oxygen consumption, in the activity of respiratory complex I, and permeability transition pore opening. All the above-mentioned alterations were prevented by curcumin pretreatment. The beneficial effects of curcumin against K2Cr2O7-induced liver oxidative damage were associated with prevention of mitochondrial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

García-Niño

Tapia

Zazueta

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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“…The excessive amount of free radical formed in this situation requires a protective response against oxidative stress-decreased entry of glucose into the cell to avoid more free radical formation by glucose metabolism. Thus, indirectly, whole body adiposity inhibit the phosphorylation of tyrosine in insulin receptor substrate 1 (IRS-1) as a 'protective mechanism' that down-regulates insulin sensitivity in the muscle [7]. In the same direction, fat accumulation inside muscle cells may lead to the entry of fatty acids into the mitochondria where they are prone to ROS production [1].…”

Section: Lifestylementioning

confidence: 99%

Lifestyle and Aging Effects in the Development of Insulin Resistance — Activating the Muscle as Strategy Against Insulin Resistance by Modulating Cytokines and HSP70

Heck¹,

Ludwig²,

Santos³

et al. 2015

Muscle Cell and Tissue

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This chapter discusses about subclinical processes related to insulin resistance development that worsen the muscle metabolic functions, generated by factors such as lifestyle bad quality food intake and sedentary behavior and aging. "lso discussed are the effects of regular physical exercise as a strategy to prevent the metabolic impairment in organisms, approaching since muscle subclinical molecular processes to the whole body s integrative physiology. Insulin resistance development includes modification in the pattern of inflammatory cytokines, heat shock proteins, tissuespecific defects in insulin action and signaling, oxidative stress and ectopic lipid deposition. The exercise is a known modulator of all parameters listed above and has important role in the regulation of immune-metabolic homeostasis from the muscle to the whole body. This chapter aims to present a new molecular approach related to the control of metabolism and encourage scientists and students to propose new strategies against insulin resistance and diabetes type developments.

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Oral administration of γ-glutamylcysteine increases intracellular glutathione levels above homeostasis in a randomised human trial pilot study

Zarka

Bridge

2017

Redox Biology

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ObjectiveTo determine if orally dosed γ-glutamylcysteine (γ-GC) can increase cellular glutathione (GSH) levels above homeostasis. Many chronic and age-related disorders are associated with down-regulation, or impairment, of glutamate cysteine ligase (GCL). This suggests that γ-GC supply may become limiting for the maintenance of cellular GSH at the normal levels required to effectively protect against oxidative stress and any resulting physiological damage.MethodsGSH levels were measured in lymphocytes of healthy, non-fasting participants before and after single oral doses (2 and 4 g) of γ-GC. Blood samples were immediately processed using high speed fluorescence-activated cell sorting to isolate 106 lymphocytes that were then assayed for GSH content.ResultsA single 2 g dose of γ-GC increased lymphocyte GSH content above basal levels (53±47%, p<0.01, n=14) within 90 min of administration. A randomized dosage (2 and 4 g γ-GC) crossover design was used to explore the pharmacokinetics of this GSH increase. In general, for both dose levels (n=9), GSH increased from initial basal levels over 3 h (tmax) before reaching maximum GSH concentrations (Cmax) that were near two (2 g γ-GC) to three (4 g γ-GC) fold basal levels (0.4 nmol/106 lymphocytes). Beyond tmax, GSH levels progressively declined reaching near basal levels by 5 h. The GSH half-life was between 2 and 3 h with exposure (AUC) to increased GSH levels of 0.7 (2 g γ-GC) and 1.8 (4 g γ-GC) nmol.h/106 lymphocytes.ConclusionsOral γ-GC is a non-toxic form of cysteine that can be directly taken up by cells and transiently increase lymphocyte GSH above homeostatic levels. Our findings that γ-GC can increase GSH levels in healthy subjects suggests that it may have potential as an adjunct for treating diseases associated with chronic GSH depletion. This trial was registered at anzctr.org.au as ACTRN12612000952842.

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Oxidative Stress in Type II Diabetes Mellitus and the Role of the Endogenous Antioxidant Glutathione

Cited by 3 publications

References 104 publications

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

Curcumin Pretreatment Prevents Potassium Dichromate-Induced Hepatotoxicity, Oxidative Stress, Decreased Respiratory Complex I Activity, and Membrane Permeability Transition Pore Opening

Lifestyle and Aging Effects in the Development of Insulin Resistance — Activating the Muscle as Strategy Against Insulin Resistance by Modulating Cytokines and HSP70

Oral administration of γ-glutamylcysteine increases intracellular glutathione levels above homeostasis in a randomised human trial pilot study

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