Lipid peroxidation and myeloperoxidase activity of neutrophils in Turner's syndrome

Davidenkova, E. F.; Григорьева, В. В.; Shafran, M. G.; Verlinskaya, D. K.; Prozorova, M. V.

doi:10.1007/bf00830725

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…One such protein that has gained attention in the field of lipid peroxidation is the mitochondrial electron transport chain complex protein, cytochrome c. Upon pro-apoptotic stimulation, cytochrome c selectively oxidizes the anionic phospholipid cardiolipin in mitochondria and phosphatidylserine in the plasma membrane (Bayir et al, 2007b; Ji et al, 2012b; Kagan et al, 2005a; Tyurina et al, 2006). Similar to cytochrome c, a number of other membrane proteins with heme catalytic centers have been implicated in lipid peroxidation: myeloperoxidase (Davidenkova et al, 1982; Goldman et al, 1999), cytoglobin (Reeder et al, 2011), myoglobin (Grisham, 1985) and hemoglobin (Szebeni et al, 1984). …”

Section: Mechanism Of Lipid Peroxidationmentioning

confidence: 99%

Therapies targeting lipid peroxidation in traumatic brain injury

2016

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Lipid peroxidation can be broadly defined as the process of inserting a hydroperoxy group into a lipid. Polyunsaturated fatty acids present in the phospholipids are often the targets for peroxidation. Phospholipids are indispensable for normal structure of membranes. The other important function of phospholipids stems from their role as a source of lipid mediators – oxygenated free fatty acids that are derived from lipid peroxidation. In the CNS, excessive accumulation of either oxidized phospholipids or oxygenated free fatty acids may be associated with damage occurring during acute brain injury and subsequent inflammatory responses. There is a growing body of evidence that lipid peroxidation occurs after severe traumatic brain injury in humans and correlates with the injury severity and mortality. Identification of the products and sources of lipid peroxidation and its enzymatic or non-enzymatic nature is essential for the design of mechanism-based therapies. Recent progress in mass spectrometry-based lipidomics/oxidative lipidomics offers remarkable opportunities for quantitative characterization of lipid peroxidation products, providing guidance for targeted development of specific therapeutic modalities. In this review, we critically evaluate previous attempts to use non-specific antioxidants as neuroprotectors and emphasize new approaches based on recent breakthroughs in understanding of enzymatic mechanisms of lipid peroxidation associated with specific death pathways, particularly apoptosis. We also emphasize the role of different phospholipases (calcium-dependent and -independent) in hydrolysis of peroxidized phospholipids and generation of pro- and anti-inflammatory lipid mediators.

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Section: Mechanism Of Lipid Peroxidationmentioning

confidence: 99%

Therapies targeting lipid peroxidation in traumatic brain injury

2016

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“…The role of oxidative stress in aortic damage progression in some pathologies has already been described [ 7 , 36 ]; however, in others, human tissues are scarce [ 37 , 38 ]. Therefore, a study of oxidative stress and antioxidants in the aorta from patients with aortic damage is justified.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Oxidative Stress Enzymes and Structural and Functional Proteins on Human Aortic Tissue from Different Aortopathies

Soto

Soria-Castro

Guarner-Lans

et al. 2014

Oxidative Medicine and Cellular Longevity

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The role of oxidative stress in different aortopathies is evaluated. Thirty-two tissue samples from 18 men and 14 women were divided into: 4 control (C) subjects, 11 patients with systemic arterial hypertension (SAH), 4 with variants of Marfan's syndrome (MV), 9 with Marfan's syndrome (M), 2 with Turner's syndrome, and 2 with Takayasu's arteritis (TA). Aorta fragments were homogenized. Lipoperoxidation (LPO), copper-zinc and manganese superoxide dismutase (Mn and Cu-Zn-SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), endothelial nitric oxide synthase (eNOS), nitrates and nitrites (NO3 −/NO2 −), and type IV collagen, and laminin were evaluated. There was an increase in Mn- and Cu-Zn-SOD activity in SAH, MV, M, and Turner's syndrome. There was also an increase in CAT activity in M and Turner' syndrome. GPx and GST activity decreased and LPO increased in all groups. eNOS was decreased in SAH, MV, and M and NO3 −/NO2 − were increased in SAH and TA. Type IV collagen was decreased in Turner's syndrome and TA. Laminin γ-1 was decreased in MV and increased in M. In conclusion, similarities and differences in oxidative stress in the different aortopathies studied including pathologies with aneurysms were found with alterations in SOD, CAT, GPx, GST, and eNOS activity that modify subendothelial basement membrane proteins.

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Lipid peroxidation and myeloperoxidase activity of neutrophils in Turner's syndrome

Cited by 2 publications

References 7 publications

Therapies targeting lipid peroxidation in traumatic brain injury

Therapies targeting lipid peroxidation in traumatic brain injury

Analysis of Oxidative Stress Enzymes and Structural and Functional Proteins on Human Aortic Tissue from Different Aortopathies

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