Dietary selenium deficiency or selenomethionine excess drastically alters organ selenium contents without altering the expression of most selenoproteins in mice
Autor: | Yasumi Anan, Ki-ichi Shimada, Natsumi Tokoro, Isao Ishii, Noriyuki Akahoshi, Seiya Hayashi, Yuri Hashimoto, Ryoka Mizuno, Shotaro Kamata, Shingo Yamamoto |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
medicine.medical_specialty GPX1 GPX3 Endocrinology Diabetes and Metabolism Clinical Biochemistry Deiodinase chemistry.chemical_element Kidney Biochemistry Selenium 03 medical and health sciences Glutathione Peroxidase GPX1 Selenium deficiency Internal medicine medicine Animals Tissue Distribution Selenomethionine Selenoproteins Molecular Biology chemistry.chemical_classification Glutathione Peroxidase Nutrition and Dietetics integumentary system 030102 biochemistry & molecular biology biology Glutathione peroxidase Selenoprotein P food and beverages medicine.disease Diet Mice Inbred C57BL Oxidative Stress 030104 developmental biology Endocrinology Liver chemistry biology.protein Selenoprotein |
Zdroj: | The Journal of Nutritional Biochemistry. 69:120-129 |
ISSN: | 0955-2863 |
DOI: | 10.1016/j.jnutbio.2019.03.020 |
Popis: | Selenium is an essential trace element, and its deficiency can cause cardiomyopathy, arrhythmias and increased susceptibility to infection. Such clinical symptoms are considered primarily attributed to decreased expression of some of the 25 selenocysteine-containing selenoproteins in humans. Conversely, a selenium-excessive diet can cause acute poisoning and chronic symptoms with unknown mechanisms. To reveal the impact of selenium deficiency and excess on selenoprotein expression in vivo, mice (that possess 24 selenoproteins) were fed with selenium-deficient or selenomethionine-excessive diets for up to 4 weeks, and the expression levels of nine representative selenoproteins [glutathione peroxidase (Gpx) 1/2/3/4, thioredoxin reductase 1/2, deiodinase 1, and selenoprotein P/S] were measured in 10 organs (brain, heart, liver, lung, kidney, pancreas, spleen, testis, skeletal muscle and thymus). We observed a time-dependent decrease in the selenium content of most organs (except testis) of selenium-deficient mice but not in the expression levels of the nine selenoproteins, with the exceptions of Gpx1/2 in the heart/liver/kidney/pancreas/spleen and Gpx3 in the pancreas/spleen. Serum lipid peroxidation levels were up-regulated in response to Se deficiency because of the decreased expression/activity of Gpx3, a plasma-type Gpx. In contrast, a time-dependent increase was observed in the selenium content of all organs but not the expression levels of the nine selenoproteins in most organs of selenomethionine-excessive mice; however, markedly elevated protein-bound selenium levels were observed in the liver/kidney. These results suggest that the systemic response to selenium deficiency and selenomethionine excess involves the down-regulation of some selenoproteins such as Gpx1/Gpx3 and up-regulation of selenium-containing proteins (not selenoproteins), respectively. |
Databáze: | OpenAIRE |
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