Quantification of protein modification by oxidants

Hawkins, Clare L.; Morgan, Philip E.; Davies, Michael J.

doi:10.1016/j.freeradbiomed.2009.01.007

Cited by 428 publications

(328 citation statements)

References 159 publications

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“…Our observations demonstrate that a high proportion (83%) of children with NAFLD show signs of oxidative injury, as evaluated by elevated circulating levels of protein carbonyls. Protein-bound carbonyls arise from free radical-mediated protein oxidation and are a widely used generic marker of oxidative stress (29). Although protein carbonyls can also originate from protein glycoxidation, elevated serum protein carbonyls are unrelated to glycemia or insulin resistance, indicating that they are expression of oxidative injury (29).…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress parameters in paediatric non-alcoholic fatty liver disease

Nobili

Parola

Alisi³

et al. 2010

Int J Mol Med

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Abstract.We have investigated the presence and the possible clinical implications of oxidative stress in children with nonalcoholic fatty liver disease (NAFLD). The present study was an observational study of oxidative stress parameters in the progression of paediatric NAFLD. We observed the role of oxidative stress in children diagnosed with NAFLD by evaluating: serum protein carbonyls, hepatic expression of 8-hydroxy-2-deoxyguanosine (8-OHG), and circulating antibody against malondialdehyde adducted human serum albumin (MDA-HSA). Forty consecutive children with biopsy-proven NAFLD (27 male; 13 female) referred to Bambino Gesù Children's Hospital, Rome, Italy, from January 2007 to April 2008 were included in the study. Serum variations of protein carbonyls, 8-OHG, and circulating antibody against MDA-HSA were evaluated. Elevated protein carbonyls were evident in 33 subjects (83%) irrespective of obesity and insulin resistance. Moreover, liver biopsies of NAFLD patients positive for circulating protein carbonyls also showed a significant increase in the nuclear staining for 8-OHG (p=0.006; 95% CI 3.1-17.7). Anti-MDA-HSA IgG above control threshold was detected in 25 (63%) children. Although protein carbonyl levels were unrelated with disease severity, patients with elevated anti-MDA-HSA IgG had scores for lobular inflammation significantly higher (p=0.019) than subjects with antibodies within the control range, while steatosis, hepatocyte ballooning and fibrosis were similar. High anti-MDA-HSA reactivity was also associated with a 13-fold increased risk (OR=12.9; 95% CI 1.5-113.8; p=0.013) of a NAFLD activity score (NAS) ≥5. These results demonstrate that oxidative stress has an high prevalence in children with NAFLD and is associated with an increased severity of steatohepatitis.

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Section: Discussionmentioning

confidence: 99%

Oxidative stress parameters in paediatric non-alcoholic fatty liver disease

Nobili

Parola

Alisi³

et al. 2010

Int J Mol Med

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“…Pellets were washed with acetone, centrifuged (6000 g · 5 min) to remove acetone, dried under a stream of N 2(g) , resuspended in 6 M methanesulfonic acid containing 0.2% tryptamine, and finally hydrolyzed under vacuum at 110°C for *12 h, as described previously (27).…”

Section: Assessment Of Renal 3-chloro-tyrosine Levelsmentioning

confidence: 99%

Selenium Inhibits Renal Oxidation and Inflammation But Not Acute Kidney Injury in an Animal Model of Rhabdomyolysis

Shanu

Groebler

Kim

et al. 2013

Antioxidants & Redox Signaling

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Acute kidney injury (AKI) is a manifestation of rhabdomyolysis (RM). Extracellular myoglobin accumulating in the kidney after RM promotes oxidative damage, which is implicated in AKI. Aim: To test whether selenium (Se) supplementation diminishes AKI and improves renal function. Results: Dietary selenite increased Se in the renal cortex, as demonstrated by X-ray fluorescence microscopy. Experimental RM-stimulated AKI as judged by increased urinary protein/creatinine, clusterin, and kidney injury molecule-1 (KIM-1), decreased creatinine clearance (CCr), increased plasma urea, and damage to renal tubules. Concentrations of cholesterylester (hydro)peroxides and F 2 -isoprostanes increased in plasma and renal tissues after RM, while aortic and renal cyclic guanidine monophosphate (cGMP; marker of nitric oxide (NO) bioavailability) decreased. Renal superoxide dismutase-1, phospho-P65, TNFa gene, MCP-1 protein, and the 3-chloro-tyrosine/tyrosine ratio (Cl-Tyr/Tyr; marker of neutrophil activation) all increased after RM. Dietary Se significantly decreased renal lipid oxidation, phospho-P65, TNFa gene expression, MCP-1 and Cl-Tyr/Tyr, improved NO bioavailability in aorta but not in the renal microvasculature, and inhibited proteinuria. However, CCr, plasma urea and creatinine, urinary clusterin, and histopathological assessment of AKI remained unchanged. Except for the Se++ group, renal angiotensin-receptor-1/2 gene/protein expression increased after RM with parallel increases in MEK1/2 inhibitor-sensitive MAPkinase (ERK) activity. Innovation: We employed synchrotron radiation to identify Se distribution in kidneys, in addition to assessing reno-protection after RM. Conclusion: Se treatment has some potential as a therapeutic for AKI as it inhibits oxidative damage and inflammation and decreases proteinuria, albeit histopathological changes to the kidney and some plasma and urinary markers of AKI remain unaffected after RM. Antioxid Redox Signal. 18, 756-769.

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“…Protein carbonylation was detected spectrophotometrically by following the absorption band (370 nm) of the hydrazone generated by reaction of the protein carbonyls with 2,4-dinitrophenylhydrazine, according to the method described by Hawkins et al 79 siRNA transfection. Cells were transfected by adding 485 μL serum-free DMEM media with 10 μL Dharmafect 1 transfection reagent and a final concentration of 40 nM SiRNA to 10-cm dishes with 2 mL of DMEM media containing 1% FBS.…”

Section: Chemicalsmentioning

confidence: 99%

Spatiotemporal autophagic degradation of oxidatively damaged organelles after photodynamic stress is amplified by mitochondrial reactive oxygen species

et al. 2012

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Although reactive oxygen species (ROS) have been reported to evoke different autophagic pathways, how ROS or their secondary products modulate the selective clearance of oxidatively damaged organelles is less explored. To investigate the signaling role of ROS and the impact of their compartmentalization in autophagy pathways, we used murine fibrosarcoma L929 cells overexpressing different antioxidant enzymes targeted to the cytosol or mitochondria and subjected them to photodynamic (PD) stress with the endoplasmic reticulum (ER)-associated photosensitizer hypericin. We show that following apical ROS-mediated damage to the ER, predominantly cells overexpressing mitochondria-associated glutathione peroxidase 4 (GPX4) and manganese superoxide dismutase (SOD2) displayed attenuated kinetics of autophagosome formation and overall cell death, as detected by computerized time-lapse microscopy. Consistent with a primary ER photodamage, kinetics and colocalization studies revealed that photogenerated ROS induced an initial reticulophagy, followed by morphological changes in the mitochondrial network that preceded clearance of mitochondria by mitophagy. Overexpression of cytosolic and mitochondria-associated GPX4 retained the tubular mitochondrial network in response to PD stress and concomitantly blocked the progression toward mitophagy. Preventing the formation of phospholipid hydroperoxides and H2O2 in the cytosol as well as in the mitochondria significantly reduced cardiolipin peroxidation and apoptosis. All together, these results show that in response to apical ER photodamage ROS propagate to mitochondria, which in turn amplify ROS production, thereby contributing to two antagonizing processes, mitophagy and apoptosis

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Quantification of protein modification by oxidants

Cited by 428 publications

References 159 publications

Oxidative stress parameters in paediatric non-alcoholic fatty liver disease

Oxidative stress parameters in paediatric non-alcoholic fatty liver disease

Selenium Inhibits Renal Oxidation and Inflammation But Not Acute Kidney Injury in an Animal Model of Rhabdomyolysis

Spatiotemporal autophagic degradation of oxidatively damaged organelles after photodynamic stress is amplified by mitochondrial reactive oxygen species

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