Oxidative Damage to Proteins and Abnormal Concentration of Pentosidine during Haemodyalysis and after Renal Transplantation

This study is the first to assess the diagnostic utility of redox biomarkers in patients with colorectal cancer (CRC). Antioxidant barrier (Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), uric acid (UA), reduced glutathione (GSH)), redox status (total antioxidant (TAC)/oxidant status (TOS), ferric reducing ability (FRAP)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA)) were measured in serum/plasma samples of 50 CRC patients. The activity of SOD was significantly higher whereas the activity of CAT, GPx and GR was considerably lower in CRC patients compared to the control group (p < 0.0001). Levels of UA, TOS, and OSI and concentrations of AGE, AOPP, and MDA were significantly higher, and the levels of GSH, TAC, and FRAP were considerably lower in CRC patients compared to the healthy controls (p < 0.0001). AUC for CAT with respect to presence of lymph node metastasis was 0.7450 (p = 0.0036), whereas AUC for MDA according to the depth of tumour invasion was 0.7457 (p = 0.0118). CRC is associated with enzymatic/non-enzymatic redox imbalance as well as increased oxidative damage to proteins and lipids. Redox biomarkers can be potential diagnostic indicators of CRC advancement.

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Evolution of oxidation dynamics of histidine: non-reactivity in the gas phase, peroxides in hydrated clusters, and pH dependence in solution

Physical Chemistry Chemical Physics ◽

10.1039/c4cp03550j ◽

2014 ◽

Vol 16 (40) ◽

pp. 22179-22191 ◽

Cited By ~ 19

Author(s):

Fangwei Liu ◽

Wenchao Lu ◽

Yigang Fang ◽

Jianbo Liu

Keyword(s):

Photodynamic Therapy ◽

Oxidative Damage ◽

Gas Phase ◽

Ph Dependence ◽

Biological Species ◽

Important Process ◽

Photochemical Transformations ◽

Oxidative Damage To Proteins ◽

Hydrated Clusters

Oxidation of histidine by 1O2 is an important process associated with oxidative damage to proteins during aging, diseases and photodynamic therapy of tumors and jaundice, and photochemical transformations of biological species in the troposphere.

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Salivary Gland Function, Antioxidant Defence and Oxidative Damage in the Saliva of Patients with Breast Cancer: Does the BRCA1 Mutation Disturb the Salivary Redox Profile?

Cancers ◽

10.3390/cancers11101501 ◽

2019 ◽

Vol 11 (10) ◽

pp. 1501 ◽

Cited By ~ 14

Author(s):

Sawczuk ◽

Maciejczyk ◽

Sawczuk-Siemieniuk ◽

Posmyk ◽

Zalewska ◽

...

Keyword(s):

Breast Cancer ◽

Salivary Gland ◽

Oxidative Damage ◽

Cancer Progression ◽

Brca1 Mutation ◽

Total Antioxidant Status ◽

Redox Balance ◽

Breast Cancer Patients ◽

Total Antioxidant ◽

Oxidative Damage To Proteins

: Oxidative stress plays a key role in breast cancer progression. However, little is still known about the relationship between the BRCA1 mutation, the incidence of breast cancer and oral homeostasis. This is the first study to evaluate the secretory function of salivary glands, biomarkers of redox balance, and oxidative damage to proteins and lipids in the saliva of subjects with the BRCA1 mutation. Ninety eight women were enrolled in the study and allocated to four groups based on molecular DNA testing: generally healthy patients without the BRCA1 mutation, patients with breast cancer but without the BRCA1 mutation, generally healthy patients with the BRCA1 mutation, and patients with both breast cancer and the BRCA1 mutation. We demonstrated that saliva from breast cancer patients with the BRCA1 mutation is characterized by enhanced antioxidant capacity and a higher degree of oxidative damage to proteins and lipids. The BRCA1 mutation can cause a predisposition to early salivary gland dysfunction, both in patients with breast cancer and in healthy individuals, leading to a decrease in salivary proteins. Using cluster analysis, we showed that salivary peroxidase, advanced glycation end-products (AGE), total antioxidant status (TAS) and malondialdehyde (MDA) may have particular clinical significance in non-invasive diagnostics of breast cancer.

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Oxidative Damage to Proteins

Aging at the Molecular Level ◽

10.1007/978-94-017-0667-4_3 ◽

2003 ◽

pp. 27-45 ◽

Cited By ~ 1

Author(s):

Nicolle Sitte

Keyword(s):

Oxidative Damage ◽

Oxidative Damage To Proteins

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A Longitudinal Study of the Antioxidant Barrier and Oxidative Stress in Morbidly Obese Patients after Bariatric Surgery. Does the Metabolic Syndrome Affect the Redox Homeostasis of Obese People?

Journal of Clinical Medicine ◽

10.3390/jcm9040976 ◽

2020 ◽

Vol 9 (4) ◽

pp. 976 ◽

Cited By ~ 5

Author(s):

Barbara Choromańska ◽

Piotr Myśliwiec ◽

Magdalena Łuba ◽

Piotr Wojskowicz ◽

Jacek Dadan ◽

...

Keyword(s):

Bariatric Surgery ◽

Metabolic Syndrome ◽

Superoxide Dismutase ◽

Uric Acid ◽

Oxidative Damage ◽

Redox Homeostasis ◽

Morbidly Obese ◽

Obese Patients ◽

Obese People ◽

Oxidative Damage To Proteins

This is the first study to evaluate both the antioxidant barrier, glutathione metabolism, and oxidative damage to proteins and lipids in morbidly obese patients undergoing bariatric treatment. The study included 65 patients with class 3 obesity divided into two subgroups: morbidly obese patients without metabolic syndrome (OB) and obese patients with metabolic syndrome (OB + MS). Blood samples were collected before surgery as well as one, three, six, and twelve months after the bariatric treatment. Superoxide dismutase and reduced glutathione (GSH) were significantly decreased, whereas glutathione reductase and uric acid were enhanced in morbidly obese patients before bariatric surgery as compared to lean control. Moreover, in the OB group, we observed the increase of superoxide dismutase (SOD) and the decrease of uric acid (UA) after the bariatric treatment; however, these changes were not observed in the OB + MS group. The oxidative damage to proteins (advanced glycation end products, AGE; advanced oxidation protein products, AOPP) and lipids (8-isoprostanes, 8-isop; 4-hydroxynoneal) was higher in OB as well as OB + MS patients. We noticed that AGE and AOPP levels diminished after the bariatric treatment, whereas redox status (ratio of GSH to oxidized glutathione) was still reduced in the OB + MS group. Summarizing, morbid obesity is associated with disturbances in the antioxidant barrier and enhanced oxidative damage to proteins and lipids. Although bariatric surgery improves redox homeostasis in obese patients, those with metabolic syndrome show a continuous decrease in the antioxidant status. In patients undergoing bariatric treatment, antioxidant supplementation may be considered.

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Normoxic ventilatory resuscitation following controlled cortical impact reduces peroxynitrite-mediated protein nitration in the hippocampus

Journal of Neurosurgery ◽

10.3171/jns/2008/108/01/0124 ◽

2008 ◽

Vol 108 (1) ◽

pp. 124-131 ◽

Cited By ~ 25

Author(s):

Edward S. Ahn ◽

Courtney L. Robertson ◽

Viktoria Vereczki ◽

Gloria E. Hoffman ◽

Gary Fiskum

Keyword(s):

Oxidative Damage ◽

Sprague Dawley ◽

Controlled Cortical Impact ◽

Neuronal Nuclei ◽

Ca1 Region ◽

Significant Difference ◽

Cortical Impact ◽

Fraction Of Inspired Oxygen ◽

Oxidative Damage To Proteins ◽

Hyperoxic Ventilation

Object Ventilatory resuscitation with 100% O2 after severe traumatic brain injury (TBI) raises concerns about the increased production of reactive oxygen species (ROS). The product of peroxynitrite-meditated tyrosine residue nitration, 3-nitrotyrosine (3-NT), is a marker for oxidative damage to proteins. The authors hypothesized that posttraumatic resuscitation with hyperoxia (100% fraction of inspired oxygen [FiO2] concentration) results in increased ROS-induced damage to proteins compared with resuscitation using normoxia (21% FiO2 concentration). Methods Male Sprague–Dawley rats underwent controlled cortical impact (CCI) injury and resuscitation with either normoxic or hyperoxic ventilation for 1 hour (5 rats per group). Twenty-four hours after injury, rat hippocampi were evaluated using 3-NT immunostaining. In a second experiment, animals similarly underwent CCI injury and normoxic or hyperoxic ventilation for 1 hour (4 rats per group). One week after injury, neuronal counts were performed after neuronal nuclei immunostaining. Results The 3-NT staining was significantly increased in the hippocampi of the hyperoxic group. The normoxic group showed a 51.0% reduction of staining in the CA1 region compared with the hyperoxic group and a 50.8% reduction in the CA3 region (p < 0.05, both regions). There was no significant difference in staining between the injured normoxic group and sham-operated control groups. In the delayed analysis of neuronal survival (neuronal counts), there was no significant difference between the hyperoxic and normoxic groups. Conclusions In this clinically relevant model of TBI, normoxic resuscitation significantly reduced oxidative damage to proteins compared with hyperoxic resuscitation. Neuronal counts showed no benefit from hyperoxic resuscitation. These findings indicate that hyperoxic ventilation in the early stages after severe TBI may exacerbate oxidative damage to proteins.

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