Selenium Deficiency as a Cause of Overload of Iron and Unbalanced Distribution of Other Minerals

Chareonpong-Kawamoto, Nawarath; Yasumoto, Kyoden

doi:10.1271/bbb.59.302

Cited by 37 publications

(17 citation statements)

References 8 publications

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“…15,16 A selenium-deficient diet can induce oxidative injury, which may lead to myocardial injury and subsequent cardiac dysfunction, 17 and evidence shows that selenium deficiency can increase calcium overload. 18,19 Furthermore, myocardial calcium overload may cause myocardial Oxidative stress, calcium channels and selenium deficiency failure. 20,21 Oxidative stress leads to lipid peroxidation, and sulphydryl group oxidation seems to be among the mechanisms that may produce membrane defects, causing intracellular calcium overload and cardiac contractile dysfunction in the myocardium.…”

Section: Discussionmentioning

confidence: 99%

Correlation between Oxidative Stress and L-type Calcium Channel Expression in the Ventricular Myocardia of Selenium-deficient Mice

et al. 2012

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OBJECTIVE: Expression of the Cacna1c(calcium channel, voltage-dependent, Ltype, a1C subunit) gene was studied to investigate the relationship between oxidative stress and L-type calcium channels in the myocardium of seleniumdeficient mice. METHODS: Selenium levels in liver and heart tissue samples from mice fed normal or selenium-deficient diets were evaluated by fluorometry. In the same mice, glutathione peroxidase (GPx) and Cacna1c gene expression were analysed, malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured, oxidoreductase gene expression profiles were analysed (by DNA microarray), and myocardial structural changes were studied. RESULTS: In selenium-deficient versus control mice, Research has shown that deregulation of calcium through L-type calcium channels plays a crucial role in the pathogenesis of cell death, which results in calcium overload and eventually leads to cardiomyocyte injury. 5 Nevertheless, considerable uncertainty remains about whether L-type calcium channels are involved in cardiomyocyte damage induced by oxidative stress, and the degree to which the abundance and function of the L-type calcium channels are affected by oxidative stress. The present study assessed the relationship between oxidative stress and Ltype calcium channel levels in the myocardium, using a selenium-deficient mouse model. Materials and methods EXPERIMENTAL ANIMAL MODEL OF SELENIUM DEFICIENCYThe animal model of selenium deficiency was established according to the method of Vanderlelie et al. 6 , with slight modifications. The basal diet of the mice was low in selenium, containing 47% low-selenium yeast, 42% sucrose, 5% coconut oil, 5% premixed minerals and 1% premixed vitamins. Adult male and female C57BL/6 mice weighing 20 -25 g (10 weeks old) were housed in a pathogen-free environment at room temperature (22 -25°C) and maintained on the basal diet and tap water ad libitum before the selenium-deficient state was achieved. Animals were divided into six groups (n = 6 per group). Mice in seleniumdeficient groups were then fed a special mouse food that contained 4.5 µg/kg total selenium for 4, 12 or 24 weeks (groups SD-4w, SD-12w and SD-24w, respectively); control mice were fed standard mouse food containing 219 µg/kg total selenium for 4, 12 or 24 weeks (groups Ctr-4w, Ctr-12w and Ctr24w, respectively). At 4, 12 or 24 weeks, mice were sacrificed by severing the spinal cord. The heart, liver, brain and kidneys were perfused with ice-cold physiological saline (0.9% NaCl) until the blood was sufficiently removed; These organs were retained (and stored in ice-cold conditions) for use in the following experiments.Animal protocols were reviewed and approved by the Animal Care and Ethics

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Section: Discussionmentioning

confidence: 99%

Correlation between Oxidative Stress and L-type Calcium Channel Expression in the Ventricular Myocardia of Selenium-deficient Mice

et al. 2012

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“…For example, previous papers have reported an enhanced accumulation of iron (Fe) in the liver, kidney, and spleen of Se-deficient (SeD) rats. 5,6 The pathological phenomena of Se-deficiency are very similar to those caused by an Fe-overload. 7 Inversely, it has also been reported that Fe-deficiency causes a decrease of GSH-Px activities in red blood cells and liver.…”

Section: Introductionmentioning

confidence: 97%

Contents and Uptake Rates of Mn, Fe, Co, Zn, and Se in Se-Deficient Rat Liver Cell Fractions

et al. 2001

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“…9) In this study, Each specimen was fixed with osmium tetroxide and contrast was enhanced with uranyl acetate. large electron-dense bodies are distributed in the Iysosomes of the See -) rats.…”

Section: Discussionmentioning

confidence: 99%

“…8 ) Previous studies in our laboratory have shown that Se deficiency is associated with marked increases in the levels of iron in the serum and in various organs. 9 ) Increases in serum iron concentrations are accompanied by decreased serum levels of transferrin, with resultant higher transferrin saturation in Se-deficient [Se( -)] rats. A higher proportion of serum transferrin is, therefore, saturated with iron in Se( -) rats and, as a consequence, there appears to be a considerable increase in the amount of non-transferrin-bound iron.…”

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confidence: 99%

Histological Study of Iron Deposits in Selenium-deficient Rats

Chareonpong-Kawamoto

Higasa

Yasumoto

1995

Bioscience, Biotechnology, and Biochemistry

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Selenium Deficiency as a Cause of Overload of Iron and Unbalanced Distribution of Other Minerals

Cited by 37 publications

References 8 publications

Correlation between Oxidative Stress and L-type Calcium Channel Expression in the Ventricular Myocardia of Selenium-deficient Mice

Correlation between Oxidative Stress and L-type Calcium Channel Expression in the Ventricular Myocardia of Selenium-deficient Mice

Contents and Uptake Rates of Mn, Fe, Co, Zn, and Se in Se-Deficient Rat Liver Cell Fractions

Histological Study of Iron Deposits in Selenium-deficient Rats

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