Cardiac myoglobin participates in the metabolic pathway of selenium in rats. Issue 4 (26th March 2018)
- Record Type:
- Journal Article
- Title:
- Cardiac myoglobin participates in the metabolic pathway of selenium in rats. Issue 4 (26th March 2018)
- Main Title:
- Cardiac myoglobin participates in the metabolic pathway of selenium in rats
- Authors:
- Hori, Eriko
Yoshida, Sakura
Fuchigami, Takeshi
Haratake, Mamoru
Nakayama, Morio - Abstract:
- Abstract : We demonstrated that cardiac myoglobin participates in the selenium metabolism in rat hearts. Abstract : As an essential micronutrient, selenium deficiency is a leading cause of cardiovascular diseases. The heart is continuously beating to deliver blood to the entire body, and this requires a high amount of energy. An adult heart normally obtains 50–70% of its adenosine 5′-triphosphate from fatty acid β-oxidation. An increase in fatty acid oxidation activity induces the generation of larger amounts of by-products (reactive oxygen species, ROS) from mitochondrial oxidative phosphorylation. Selenium-dependent glutathione peroxidases play a critical role in the removal of these ROS, especially organic hydroperoxides, from the heart. The definitive transport and/or detailed metabolic pathways from the selenium-source compounds to the selenoproteins in the heart still remain unclear. We explored the selenium-binding proteins in a rat cardiac cell lysate using its reactive metabolic intermediate, selenotrisulfide (STS), and MALDI TOF-mass spectrometry. Several proteins with a free cysteine (Cys) thiol were found to be reactive with STS through a thiol-exchange reaction. The most distinctive Cys-containing protein in the cardiac cell lysate was identified as myoglobin (Mb) from a rat protein database search and tryptic fragmentation experiments. When separately examined in selenium adequate rats, selenium-binding to the cardiac Mb was verified using selenium-specificAbstract : We demonstrated that cardiac myoglobin participates in the selenium metabolism in rat hearts. Abstract : As an essential micronutrient, selenium deficiency is a leading cause of cardiovascular diseases. The heart is continuously beating to deliver blood to the entire body, and this requires a high amount of energy. An adult heart normally obtains 50–70% of its adenosine 5′-triphosphate from fatty acid β-oxidation. An increase in fatty acid oxidation activity induces the generation of larger amounts of by-products (reactive oxygen species, ROS) from mitochondrial oxidative phosphorylation. Selenium-dependent glutathione peroxidases play a critical role in the removal of these ROS, especially organic hydroperoxides, from the heart. The definitive transport and/or detailed metabolic pathways from the selenium-source compounds to the selenoproteins in the heart still remain unclear. We explored the selenium-binding proteins in a rat cardiac cell lysate using its reactive metabolic intermediate, selenotrisulfide (STS), and MALDI TOF-mass spectrometry. Several proteins with a free cysteine (Cys) thiol were found to be reactive with STS through a thiol-exchange reaction. The most distinctive Cys-containing protein in the cardiac cell lysate was identified as myoglobin (Mb) from a rat protein database search and tryptic fragmentation experiments. When separately examined in selenium adequate rats, selenium-binding to the cardiac Mb was verified using selenium-specific fluorometry. Cardiac Mb is thought to participate in the selenium metabolic pathway in the heart. … (more)
- Is Part Of:
- Metallomics. Volume 10:Issue 4(2018)
- Journal:
- Metallomics
- Issue:
- Volume 10:Issue 4(2018)
- Issue Display:
- Volume 10, Issue 4 (2018)
- Year:
- 2018
- Volume:
- 10
- Issue:
- 4
- Issue Sort Value:
- 2018-0010-0004-0000
- Page Start:
- 614
- Page End:
- 622
- Publication Date:
- 2018-03-26
- Subjects:
- Metals -- Physiological effect -- Periodicals
572.51 - Journal URLs:
- https://academic.oup.com/metallomics/issue ↗
http://www.rsc.org/ ↗
http://www.rsc.org/Publishing/Journals/mt/index.asp ↗ - DOI:
- 10.1039/c8mt00011e ↗
- Languages:
- English
- ISSNs:
- 1756-5901
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5694.710000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 6349.xml