Effect of triiodothyronine on reactive oxygen species generation by leukocytes, indices of oxidative damage, and antioxidant reserve

Metabolism ◽  
2000 ◽  
Vol 49 (6) ◽  
pp. 799-803 ◽  
Author(s):  
Cesar H. Magsino ◽  
Wael Hamouda ◽  
Husam Ghanim ◽  
Richard Browne ◽  
Ahmad Aljada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Reserve

scholarly journals Carvedilol Inhibits Reactive Oxygen Species Generation by Leukocytes and Oxidative Damage to Amino Acids

Circulation ◽  
2000 ◽  
Vol 101 (2) ◽  
pp. 122-124 ◽  
Author(s):  
Paresh Dandona ◽  
Rajaram Karne ◽  
Husam Ghanim ◽  
Wael Hamouda ◽  
Ahmad Aljada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Amino Acids ◽  
Oxidative Damage ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals The Suppressive Effect of Dietary Restriction and Weight Loss in the Obese on the Generation of Reactive Oxygen Species by Leukocytes, Lipid Peroxidation, and Protein Carbonylation1

2001 ◽  
Vol 86 (1) ◽  
pp. 355-362 ◽  
Author(s):  
Paresh Dandona ◽  
Priya Mohanty ◽  
Husam Ghanim ◽  
Ahmad Aljada ◽  
Richard Browne ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Amino Acids ◽  
Weight Loss ◽  
Oxidative Damage ◽  
Dietary Restriction ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Normal Subjects ◽  
Oxygen Species ◽  
Factor Α

Increased reactive oxygen species generation by the leukocytes of the obese may be responsible for increased oxidative injury to lipids and proteins and, hence, atherosclerosis. We have investigated whether reactive oxygen species generation by leukocytes and other indexes of oxidative damage in the body fall with short-term dietary restriction and weight loss. Nine nondiabetic obese subjects (body mass index, 32.5–64.4 kg/m2), not taking any antioxidants, were put on a 1000-Cal diet. Fasting blood samples were taken at 0, 1, 2, 3, and 4 weeks and at 12 weeks after the cessation of dietary restriction. Blood samples were also obtained at 1 and 2 h after administration of 75 g oral glucose at 0 and 4 weeks. Mononuclear cells (MNC) and polymorphonuclear leukocytes (PMN) were isolated, and reactive oxygen species generation was measured. Plasma concentrations of thiobarbituric acid-reactive species (TBARS), 13-hydroxyoctadecadienoic acid (13-HODE), 9-hydroxyoctadecadienoic acid (9-HODE), carbonylated proteins, o-tyrosine, and m-tyrosine as indexes of oxidative damage to lipids, proteins and amino acids, respectively, were measured. Antioxidant vitamins were measured as indexes of antioxidant reserves. Plasma tumor necrosis factor-α concentrations were also measured. Mean weight loss was 2.4 ± 0.6 kg at week 1, 2.5 ± 1.7 kg at week 2, 3.9 ± 0.8 kg at week 3, and 4.5 ± 2.8 kg at week 4 (P < 0.05). Reactive oxygen species generation by PMN fell from 236.4 ± 95.8 to 150.9 ± 69.0, 125.9 ± 24.3, 96.0 ± 39.9, and 103.1 ± 35.7 mV at weeks 1, 2, 3, and 4, respectively (P < 0.001). It increased 3 months after the cessation of dietary restriction to 270.0 ± 274.3 mV. Reactive oxygen species generation by MNC fell from 187.8 ± 75.0 to 101.7 ± 64.5, 86.9 ± 42.8, 63.8 ± 14.3, and 75.1± 32.2 mV and increased thereafter to 302.0 ± 175.5 mV at 1, 2, 3, 4, and 16 weeks, respectively (P < 0.005). Reactive oxygen species generation by PMN and MNC increased in response to glucose; the relative increase was greater at 4 weeks than that at week 0 due to a fall in the basal levels of reactive oxygen species generation. Consistent with the fall in reactive oxygen species generation, there was a reduction in plasma TBARS from 1.68 ± 0.17 μmol/L at week 0 to 1.47 μmol/L at 4 weeks (P < 0.05). The 13-HODE to linoleic acid ratio fell from a baseline of 100% to 56.4 ± 36.1% at 4 weeks (P < 0.05), and the 9-HODE to linoleic acid ratio fell from a baseline of 100% to 60.5 ± 37.7% at 4 weeks (P < 0.05). Carbonylated proteins fell from 1.39 ± 0.27 μg/mg protein at week 0 to 1.17 ± 0.12μ g/mg protein at week 4 (P < 0.05); o-tyrosine fell from 0.42 ± 0.03 mmol/mol phenylalanine at week 0 to 0.36 ± 0.02 mmol/mol phenylalanine at 4 weeks (P < 0.005), and m-tyrosine fell from 0.45 ± 0.04 mmol/mol phenylalanine at week 0 to 0.40 ± 0.03 mmol/mol phenylalanine at 4 weeks (P < 0.05). The basal concentrations of TBARS, 9-HODE, 13-HODE, carbonylated proteins, o-tyrosine, and m-tyrosine in the obese were significantly greater than those in normal subjects. On the other hand, tumor necrosis factor-α concentrations did not change during this 4-week period, nor was there any change in antioxidant vitamins. This is the first demonstration of 1) an increase in reactive oxygen species-induced damage in lipids, proteins, and amino acids in the obese compared with normal subjects; and 2) a decrease in reactive oxygen species generation by leukocytes and oxidative damage to lipids, proteins, and amino acids after dietary restriction and weight loss in the obese over a short period.

Роль оксида азота в реализации антиоксидантного эффекта неопиатного аналога лей-энкефалина в сердце новорожденных белых крыс

2019 ◽  
pp. 61-64
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Postnatal Period ◽  
Oxide System ◽  
No Synthase ◽  
Albino Rats ◽  
Oxygen Species ◽  
Control Parameters ◽  
Synthase Inhibitor

The eff ect of the non-opiate analog of leu-enkephalin (peptide NALE: Phe – D – Ala – Gly – Phe – Leu – Arg) on the reactive oxygen species generation in the heart of albino rats in the early postnatal period was studied. Peptide NALE was administered intraperitoneally in the dose of 100 μ/kg daily from 2 to 6 days of life. Reactive oxygen species generation was assessed by chemiluminescence in the heart homogenates of 7-day-old animals. Decreasing of reactive oxygen species generation nearly by 30 % and an increasing in antioxidant system activity by the 20-27 %, compared with the control parameters, were found. The antioxidant eff ect of peptide NALE is associated with the presence of the amino acid Arg in the structure of the peptide. An analogue of NALE peptide, devoid of Arg (peptide Phe – D – Ala – Gly – Phe – Leu – Gly), had a signifi cant lower antioxidant eff ect. The NO-synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the dose 50 mg/kg, administered with NALE peptide, reduced the severity of the NALE antioxidant eff ect. The results of the study suggest that the pronounced antioxidant eff ect of NALE peptide in the heart of albino rats, at least in part, is due to the interaction with the nitric oxide system.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

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