Erythrocyte caspase-3 and antioxidant defense is activated in red blood cells and plasma of type 2 diabetes patients at first clinical onset

Savu, Octavian; Bradescu, Ovidiu Marius; Serafinceanu, Cristian; Iosif, Liviu; Tirgoviste, Constantin Ionescu; Stoian, Irina

doi:10.1179/1351000213y.0000000040

Cited by 9 publications

(5 citation statements)

References 40 publications

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“…An alternative study found DM patients to have higher PS exposure due to the suppression of flippase enzyme activity, the suppression of which was caused by higher levels of membrane tubulin [ 109 ]. RBC cell death in T2D patients was also documented and associated to be with increased RBC caspase 3 activation [ 110 , 111 ].…”

Section: Multifactorial Mechanisms Explaining Shortened Rbc Lifespan ...mentioning

confidence: 99%

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

et al. 2023

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Diabetes Mellitus (DM) is a complex metabolic disorder associated with multiple microvascular complications leading to nephropathy, retinopathy, and neuropathy. Mounting evidence suggests that red blood cell (RBC) alterations are both a cause and consequence of disturbances related to DM-associated complications. Importantly, a significant proportion of DM patients develop varying degrees of anemia of confounding etiology, leading to increased morbidity. In chronic hyperglycemia, RBCs display morphological, enzymatic, and biophysical changes, which in turn prime them for swift phagocytic clearance from circulation. A multitude of endogenous factors, such as oxidative and dicarbonyl stress, uremic toxins, extracellular hypertonicity, sorbitol accumulation, and deranged nitric oxide metabolism, have been implicated in pathological RBC changes in DM. This review collates clinical laboratory findings of changes in hematology indices in DM patients and discusses recent reports on the putative mechanisms underpinning shortened RBC survival and disturbed cell membrane architecture within the diabetic milieu. Specifically, RBC cell death signaling, RBC metabolism, procoagulant RBC phenotype, RBC-triggered endothelial cell dysfunction, and changes in RBC deformability and aggregation in the context of DM are discussed. Understanding the mechanisms of RBC alterations in DM provides valuable insights into the clinical significance of the crosstalk between RBCs and microangiopathy in DM.

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Section: Multifactorial Mechanisms Explaining Shortened Rbc Lifespan ...mentioning

confidence: 99%

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

et al. 2023

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“…Diabetes has been known to stimulate apoptosis by the activation of caspase-3 in affected tissues (Savu et al, 2013 ). Using an animal model of T2DM, Kim et al in their studies demonstrated an increased level of tau phosphorylation and cleavage in the brains of db/db mice which are models for diabetic dyslipidemia (Kim B. et al, 2013 ).…”

Section: Crosstalk Of T2dm and Tau Pathology In Admentioning

confidence: 99%

Alzheimer's Disease and Type 2 Diabetes: A Critical Assessment of the Shared Pathological Traits

2018

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Alzheimer's disease (AD) and Type 2 Diabetes Mellitus (T2DM) are two of the most prevalent diseases in the elderly population worldwide. A growing body of epidemiological studies suggest that people with T2DM are at a higher risk of developing AD. Likewise, AD brains are less capable of glucose uptake from the surroundings resembling a condition of brain insulin resistance. Pathologically AD is characterized by extracellular plaques of Aβ and intracellular neurofibrillary tangles of hyperphosphorylated tau. T2DM, on the other hand is a metabolic disorder characterized by hyperglycemia and insulin resistance. In this review we have discussed how Insulin resistance in T2DM directly exacerbates Aβ and tau pathologies and elucidated the pathophysiological traits of synaptic dysfunction, inflammation, and autophagic impairments that are common to both diseases and indirectly impact Aβ and tau functions in the neurons. Elucidation of the underlying pathways that connect these two diseases will be immensely valuable for designing novel drug targets for Alzheimer's disease.

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“…Kumar et al [68] also found increased plasma SOD activity in patients with RA, similarly to Mazzetti et al [69]. Similar results were found in early type 2 diabetes patients [70], where increased antioxidant defense in plasma and erythrocytes is explained as a potential mechanism that can overcome oxidative damage induced by ROS overproduction. There are some reports on erythrocyte SOD, CAT, and GPx activities in patients with RA or in rats with AA, but the results are controversial [71,72].…”

Section: Evaluation Of Results Of Administration Of Hyaluronans In Exmentioning

confidence: 57%

The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

Bauerová¹,

Kucharská²,

Poništ³

et al. 2019

Antioxidants

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The pathogenesis of rheumatoid arthritis is poorly understood; however, elevated oxidative stress has been described to be involved. In this chapter, we present experiments with endogenous molecules bearing antioxidative properties. In our studies, we used male Lewis rats, and the arthritis was induced with Mycobacterium butyricum. In the first experiment, we tested coenzyme Q 10 (CoQ 10) in the oral daily dose of 100 mg/kg b.w. Markers of inflammation and total antioxidant status were corrected in the group supplemented. CoQ 10 treatment significantly improved concentrations of the investigated endogenous antioxidants. Further as an important fact, we consider a good bioavailability of used CoQ 10 formulation which was confirmed by increased CoQ concentrations in plasma, tissue, and mitochondria from skeletal muscles. In the second study, we describe the results with hyaluronic acid (HA) administered in oral daily doses of 0.5 mg and 5 mg/kg b.w. and of different molecular weights (0.43, 0.99, and 1.73 MDa). A notable antioxidative effect of HA was assessed: its administration increased the activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) in erythrocytes and total antioxidant capacity of plasma and reduced the marker of oxidative damage to lipids-plasmatic lipid hydroperoxides. HA with the highest molecular weight showed the most significant effect.

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Erythrocyte caspase-3 and antioxidant defense is activated in red blood cells and plasma of type 2 diabetes patients at first clinical onset

Cited by 9 publications

References 40 publications

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications

Alzheimer's Disease and Type 2 Diabetes: A Critical Assessment of the Shared Pathological Traits

The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

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