Cardiac myoglobin participates in the metabolic pathway of selenium in rats

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.

Metabolism and Mechanism of Toxicity of Selenium-Containing Supplements Used for Optimizing Human Selenium Status

“…Высокая биологическая активность органических форм селена -аминокислот, их уникальная антиоксидантная активность, способность защиты от онкологических, кардиологических и нейрогенных заболеваний (болезнь Альцгеймера, болезнь Паркинсона) определяют важность исследования данных соединений [8][9][10].…”

Expression Profile Analysis of Selenium-Related Genes in Peripheral Blood Mononuclear Cells of Patients with Keshan Disease

“…Currently, KD is considered as a gene-environment interaction disease linked to selenium deficiency [2]. Selenium, an essential micronutrient, exerts its function through selenoproteins or small selenium metabolites in the human body [3]. It has been shown that all selenoproteins that have enzymic functions are selenium-dependent, generally with selenocysteine at the active site as a redox center to reduce oxidative damage to biomolecules.…”