Mitochondrial respiratory dysfunction-elicited oxidative stress and posttranslational protein modification in mitochondrial diseases

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.

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Identification of N7-(1-Carboxyethyl)-Arginine, a Novel Posttranslational Protein Modification of Arginine Formed at High Hydrostatic Pressure

Annals of the New York Academy of Sciences ◽

10.1196/annals.1333.006 ◽

2005 ◽

Vol 1043 (1) ◽

pp. 55-58 ◽

Cited By ~ 1

Author(s):

NADJA ALT ◽

PETER SCHIEBERLE

Keyword(s):

Hydrostatic Pressure ◽

High Hydrostatic Pressure ◽

Protein Modification ◽

Posttranslational Protein Modification

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Cardiac Mitochondrial Respiratory Function and Oxidative Stress: The Role of Exercise

International Journal of Sports Medicine ◽

10.1055/s-2005-837570 ◽

2005 ◽

Vol 26 (4) ◽

pp. 258-267 ◽

Cited By ~ 20

Author(s):

A. A. Ascensão ◽

J. F. Magalhães ◽

J. M. Soares ◽

R. M. Ferreira ◽

M. J. Neuparth ◽

...

Keyword(s):

Oxidative Stress ◽

Respiratory Function ◽

And Oxidative Stress ◽

Mitochondrial Respiratory

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Posttranslational Protein Modification: Biosynthetic Control Mechanisms in the Glycosylation of the Major Myelin Glycoprotein by Schwann Cells

Journal of Neurochemistry ◽

10.1111/j.1471-4159.1985.tb08743.x ◽

1985 ◽

Vol 44 (4) ◽

pp. 1194-1206 ◽

Cited By ~ 26

Author(s):

Joseph F. Poduslo

Keyword(s):

Schwann Cells ◽

Protein Modification ◽

Control Mechanisms ◽

Posttranslational Protein Modification

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Effects of antenatal melatonin therapy on lung structure in growth-restricted newborn lambs

Journal of Applied Physiology ◽

10.1152/japplphysiol.00783.2016 ◽

2017 ◽

Vol 123 (5) ◽

pp. 1195-1203 ◽

Cited By ~ 8

Author(s):

Graeme R. Polglase ◽

Jade Barbuto ◽

Beth J. Allison ◽

Tamara Yawno ◽

Amy E. Sutherland ◽

...

Keyword(s):

Oxidative Stress ◽

Fetal Growth ◽

Fetal Growth Restriction ◽

Lung Development ◽

Fetal Lung ◽

Growth Restriction ◽

Fetal Sheep ◽

Respiratory Dysfunction ◽

Melatonin Administration ◽

Lung Structure

Oxidative stress arising from suboptimal placental function contributes to a multitude of pathologies in infants compromised by fetal growth restriction (FGR). FGR infants are at high risk for respiratory dysfunction after birth and poor long-term lung function. Our objective was to investigate the contribution of oxidative stress to adverse lung development and the effects of melatonin administration, a powerful antioxidant, on lung structure in FGR lambs. Placental insufficiency and FGR was surgically induced in 13 fetal sheep at ∼105 days of gestation by ligation of a single umbilical artery. Maternal intravenous melatonin infusion was commenced in seven of the ewes 4 h after surgery and continued until birth. Lambs delivered normally at term and lungs were collected 24 h after birth for histological assessment of lung structure and injury and compared with appropriately grown control lambs ( n = 8). FGR fetuses were hypoxic and had lower glucose during gestation compared with controls. Melatonin administration prevented chronic hypoxia. Within the lung, FGR caused reduced secondary septal crest density and altered elastin deposition compared with controls. Melatonin administration had no effect on the changes to lung structure induced by FGR. We conclude that chronic FGR disrupts septation of the developing alveoli, which is not altered by melatonin administration. These findings suggest that oxidative stress is not the mechanism driving altered lung structure in FGR neonates. Melatonin administration did not prevent disrupted airway development but also had no apparent adverse effects on fetal lung development. NEW & NOTEWORTHY Fetal growth restriction (FGR) results in poor respiratory outcomes, which may be caused by oxidation in utero. We investigated the contribution of oxidative stress to adverse lung development and the effects of melatonin administration, a powerful antioxidant, on lung structure in FGR lambs. FGR disrupted septation of the developing alveoli, which is not altered by melatonin administration. Oxidative stress may not be the mechanism driving altered lung structure in FGR neonates.

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Protein carbonyls and protein thiols in rheumatoid arthritis

International Journal of Research in Medical Sciences ◽

10.18203/2320-6012.ijrms20181770 ◽

2018 ◽

Vol 6 (5) ◽

pp. 1738 ◽

Cited By ~ 1

Author(s):

Pullaiah P. ◽

Suchitra M. M. ◽

Siddhartha Kumar B.

Keyword(s):

Rheumatoid Arthritis ◽

Oxidative Stress ◽

Protein Modification ◽

Antioxidant Properties ◽

Protein Carbonyl ◽

Protein Carbonyls ◽

Carbonyl Content ◽

Protein Thiol ◽

Protein Carbonyl Content ◽

Protein Thiols

Background: Oxidative stress (OS) has an important role in the pathogenesis and progression of rheumatoid arthritis (RA). OS causes protein modification, thereby impairing the biological functions of the protein. This study was conducted to assess the oxidatively modified protein as protein carbonyl content and the antioxidant status as protein thiols, and to study the association between protein carbonyls and protein thiols in RA.Methods: Newly diagnosed RA patients who were not taking any disease modifying anti-rheumatic drugs were included into the study group (n=45) along with age and sex matched healthy controls (n=45). Serum protein carbonyl content and protein thiols were estimated.Results: Elevated protein carbonyl content and decreased protein thiol levels (p<0.001) were observed in RA. A significant negative correlation was observed between protein carbonyl content and protein thiol levels (p<0.001).Conclusions: Oxidative stress in RA is evidenced by enhanced protein oxidation and decreased antioxidant protein thiol levels. Decreased protein thiols may also reflect protein modifications leading to compromise in the antioxidant properties. This oxidant and antioxidant imbalance needs to be addressed by therapeutic interventions to prevent disease progression.

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