Impaired oxidative stress in Thalassemia-Hemoglobin E traits after acute exhaustive exercise

Author(s):  
Natthaphon Nanakorn ◽  
Saikaew Chuechan
Proteomes ◽  
2019 ◽  
Vol 7 (1) ◽  
pp. 8 ◽  
Author(s):  
Saranyoo Ponnikorn ◽  
Rungrawee Mongkolrob ◽  
Suwit Klongthalay ◽  
Sittiruk Roytrakul ◽  
Kitima Srisanga ◽  
...  

β-thalassemia/Hb E is a global health issue, which is characterized by a range of clinical symptoms from a mild and asymptomatic anemia to severe disorders that require transfusions from infancy. Pathological mechanisms of the disease involve the excess of unmatched alpha globin and iron overload, leading to ineffective erythropoiesis and ultimately to the premature death of erythroid precursors in bone marrow (BM) and peripheral organs. However, it is unclear as to how BM microenvironment factors contribute to the defective erythropoiesis in β-thalassemia/Hb E patients. Here, we employed mass spectrometry-based comparative proteomics to analyze BM plasma that was collected from six β-thalassemia/Hb E patients and four healthy donors. We identified that the differentially expressed proteins are enriched in secretory or exosome-associated proteins, many of which have putative functions in the oxidative stress response. Using Western blot assay, we confirmed that atypical lipoprotein, Apolipoprotein D (APOD), belonging to the Lipocalin transporter superfamily, was significantly decreased in BM plasma of the tested pediatric β-thalassemia/Hb E patients. Our results highlight that the disease condition of ineffective erythropoiesis and oxidative stress found in BM microenvironment of β-thalassemia/Hb E patients is associated with the impaired expression of APOD protein.


2011 ◽  
Vol 668 (3) ◽  
pp. 407-413 ◽  
Author(s):  
Elif Şıktar ◽  
Deniz Ekinci ◽  
Erdinç Şıktar ◽  
Şükrü Beydemir ◽  
İlhami Gülçin ◽  
...  

2007 ◽  
Vol 333 (6) ◽  
pp. 346-353 ◽  
Author(s):  
Einat Gochman ◽  
Abraham Z. Reznick ◽  
Ophir Avizohar ◽  
Ami Ben-Amotz ◽  
Yishai Levy

2005 ◽  
Vol 94 (4) ◽  
pp. 595-601 ◽  
Author(s):  
Chieh-Chung Liu ◽  
Chi-Chang Huang ◽  
Wan-Teng Lin ◽  
Chin-Cheng Hsieh ◽  
Shih-Yi Huang ◽  
...  

Strenuous exercise is known to induce oxidative stress leading to the generation of free radicals. The purpose of the present study was to investigate the effects of lycopene, an antioxidant nutrient, at a relatively low dose (2·6 mg/kg per d) and a relatively high dose (7·8 mg/kg per d) on the antioxidant status of blood and skeletal muscle tissues in rats after exhaustive exercise. Rats were divided into six groups: sedentary control (C); sedentary control with low-dose lycopene (CLL); sedentary control with high-dose lycopene (CHL); exhaustive exercise (E); exhaustive exercise with low-dose lycopene (ELL); exhaustive exercise with high-dose lycopene (EHL). After 30 d, the rats in the three C groups were killed without exercise, but the rats in the three E groups were killed immediately after an exhaustive running test on a motorised treadmill. The results showed that xanthine oxidase (XO) activities of plasma and muscle, and muscular myeloperoxidase (MPO) activity in group E were significantly increased compared with group C. Compared with group E, the elevations of XO and MPO activities of muscle were significantly decreased in group EHL. The malondialdehyde concentrations of plasma and tissues in group E were significantly increased by 72 and 114 %, respectively, compared with those in group C. However, this phenomenon was prevented in rats of the ELL and EHL groups. There was no significant difference in the GSH concentrations of erythrocytes in each group; however, exhaustive exercise resulted in a significant decrease in the GSH content of muscle. In conclusion, these results suggested that lycopene protected muscle tissue from oxidative stress after exhaustive exercise.


2007 ◽  
Vol 2 (1) ◽  
pp. 56-70 ◽  
Author(s):  
Antoni Sureda ◽  
Pedro Tauler ◽  
Antoni Aguiló ◽  
Nuria Cases ◽  
Isabel Llompart ◽  
...  

AbstractIntense exercise induces inflammatory-like changes and oxidative stress in immune cells. Our aim was to study the effects of antioxidant diet supplementation on the neutrophil inflammatory response and on the tocopherol associated protein (TAP) expression after exhaustive exercise. Fourteen male-trained amateur runners were randomly divided in two placebo and supplemented groups. Vitamins C (152 mg/d) and E (50 mg/d) supplementation were administrated to the athletes for a month, using an almond based isotonic and energetic beverage. Non-enriched beverage was given to the placebo group. After one month, the subjects participated in a half-marathon race (21 km-run). Neutrophil TAP mRNA expression and markers of the inflammatory response were determined before, immediately after, and 3 h after finishing the half-marathon race. TAP expression increased after exercise mainly in the neutrophils of the placebo group. Exercise induced an inflammatory response in both placebo and supplemented groups, manifested with neutrophilia, increased creatine kinase and lactate dehydrogenase serum activities, neutrophil luminol chemiluminescence and myeloperoxidase release. Plasma malondialdehyde only increased in the placebo group after exercise. Diet supplementation with moderate levels of antioxidant vitamins avoids plasma damage in response to exhaustive exercise without the effects on the inflammatory process. Neutrophil degranulation and increased tocopherol associated protein could contribute to the neutrophil protection from the oxidative stress.


2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S109.2-S109
Author(s):  
A Olah ◽  
BT Nemeth ◽  
C Matyas ◽  
L Hidi ◽  
E Birtalan ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Yang Yuan ◽  
Shan-Shan Pan ◽  
Dong-Feng Wan ◽  
Jiao Lu ◽  
Yue Huang

Previous studies have shown that early exercise preconditioning (EEP) imparts a protective effect on acute cardiovascular stress. However, how mitophagy participates in exercise preconditioning- (EP-) induced cardioprotection remains unclear. EEP may involve mitochondrial protection, which presumably crosstalks with predominant H2O2 oxidative stress. Our EEP protocol involves four periods of 10 min running with 10 min recovery intervals. We added a period of exhaustive running and a pretreatment using phosphoinositide 3-kinase (PI3K)/autophagy inhibitor wortmannin to test this protective effect. By using transmission electron microscopy (TEM), laser scanning confocal microscopy, and other molecular biotechnology methods, we detected related markers and specifically analyzed the relationship between mitophagic proteins and mitochondrial translocation. We determined that exhaustive exercise associated with various elevated injuries targeted the myocardium, oxidative stress, hypoxia-ischemia, and mitochondrial ultrastructure. However, exhaustion induced limited mitochondrial protection through a H2O2-independent manner to inhibit voltage-dependent anion channel isoform 1 (VDAC1) instead of mitophagy. EEP was apparently safe to the heart. In EEP-induced cardioprotection, EEP provided suppression to exhaustive exercise (EE) injuries by translocating Bnip3 to the mitochondria by recruiting the autophagosome protein LC3 to induce mitophagy, which is potentially triggered by H2O2 and influenced by Beclin1-dependent autophagy. Pretreatment with the wortmannin further attenuated these effects induced by EEP and resulted in the expression of proapoptotic phenotypes such as oxidative injury, elevated Beclin1/Bcl-2 ratio, cytochrome c leakage, mitochondrial dynamin-1-like protein (Drp-1) expression, and VDAC1 dephosphorylation. These observations suggest that H2O2 generation regulates mitochondrial protection in EEP-induced cardioprotection.


2010 ◽  
Vol 42 ◽  
pp. 779
Author(s):  
Hsien-Tang Lin ◽  
Mallikarjuna Korivi ◽  
Chia-Chen Yang ◽  
Ming-Fen Hsu ◽  
Szu-Hsien Yu ◽  
...  

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