Dietary selenium- and vitamin E-induced alterations in some rabbit tissues

The effects of 10 weeks of dietary selenium and/or vitamin E deficiency (< 0.03 mg Se and 1.5 mg vitamin E per kg diet) on body Se and vitamin E stores and on the down-regulation of liver cellular glutathione peroxidase (GPx1) and plasma glutathione peroxidase (GPx3) were examined in growing female New Zealand White rabbits in comparison to Se (+ 0.40 mg Se/kg diet) and/or vitamin E (+ 150 I.U./kg diet) supplemented controls. Additionally plasma lactate dehydrogenase (LDH) activity, liver thiobarbituric acid-reactive substances (TBA-RS) and liver protein carbonyls were measured to assess the development of oxidative stress during an alimentary Se and/or vitamin E deficiency. Significantly decreased concentrations of Se and vitamin E in plasma (Se: - 70%; vitamin E: - 87%) and liver (Se: - 90%; vitamin E: - 95%) indicated an efficacious Se and vitamin E depletion of the rabbits within 10 weeks. GPx1 messenger RNA levels (GPx1 mRNA) in the livers of Se-depleted rabbits were down-regulated to 1/3-1/8 of the Se supplemented controls. GPx1 enzyme activity in the livers of Se-deficient rabbits declined to 10% of the Se-supplied control rabbits. A significantly elevated LDH activity in the blood plasma of Se- and vitamin E-deficient rabbits indicated a general impairment of tissues. Markedly increased TBA-RS concentrations and protein carbonyl contents in the livers of Se- and vitamin E-deficient rabbits gave further evidence for severe oxidative damage of cellular lipids and proteins during an alimentary Se and/or vitamin E deficiency. Both a full expresssion of GPx1 attained by dietary Se supplementation and dietary vitamin E supply effected an almost complete protection against oxidative cellular damage of the liver.

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“…In rats and mice, the liver is the main target organ of dietary Se deficiency (B URK 1987; B URK et al. 1995; T URAN et al. 1997; C HENG et al.…”

Section: Discussionmentioning

confidence: 99%

“…The preventive role of vitamin E against these diseases is uncontestable, whereas the role of single selenium supplementation is not yet clear (G OETTSCH and P APPENHEIMER 1931; H OVE et al. 1958; T URAN et al. 1997).…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium‐deficient rabbits

Müller

Pallauf

2002

Animal Physiology Nutrition

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“…Additionally, our previous data have shown also that further addition of high-affinity heavy metal Zn 2+ chelator, TPEN, following ZnPT (50 μM for 1 min), FluoZin-3 intensity decreased even below its initial value, representing its basal level in cardiomyocytes [27,18]. Of note, in all our experiments, the fluorescence loading and ZnPTinduced intracellular free Zn 2+ changes as well as intracellular free Zn 2+ chelation in the quiescent cells were confirmed to be homogenous by using confocal images of the loaded cells.…”

Section: Effect Of Intracellular Free Zn 2+ Increase ([Zn 2+ ] I ) Onmentioning

confidence: 90%

Intracellular Zn2+ Increase in Cardiomyocytes Induces both Electrical and Mechanical Dysfunction in Heart via Endogenous Generation of Reactive Nitrogen Species

Tuncay

Turan

2015

Biol Trace Elem Res

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Oxidants increase intracellular free Zn(2+) concentration ([Zn(2+)]i) in ventricular myocytes, which contributes to oxidant-induced alterations in excitation-contraction coupling (ECC). However, it is not clear whether increased [Zn(2+)]i in cardiomyocytes via increased reactive nitrogen species (RNS) has a role on heart function under pathological conditions, such as hyperglycemia. In this study, first we aimed to investigate the role of increased [Zn(2+)]i under in vitro condition in the development of both electrical and mechanical dysfunction of isolated papillary muscle strips from rat heart via exposed samples to a Zn(2+)-ionophore (Zn-pyrithione; 1 μM) for 20 min. Under simultaneous measurement of intracellular action potential and contractile activity in these preparations, Zn-pyrithione exposure caused marked prolongation in action potential repolarization phase and slowdown in both contraction and relaxation rates of twitch activity. Second, in order to demonstrate an association between increased [Zn(2+)]i and increased RNS, we monitored intracellular [Zn(2+)]i under an acute exposure of nitric oxide (NO) donor sodium nitroprusside, SNP, in freshly isolated quiescent cardiomyocytes loaded with FluoZin-3. Resting level of free Zn(2+) is significantly higher in cardiomyocytes under hyperglycemic condition compared to those of the controls, which seems to be associated with increased level of RNS production in hyperglycemic cardiomyocytes. Western blot analysis showed that Zn-pyrithione exposure induced a marked decrease in the activity of protein phosphatase 1 and 2A, member of macromolecular protein complex of cardiac ryanodine receptors, RyR2, besides significant increase in the phosphorylation level of extracellular signal-regulated kinase1/2 as a concentration-dependent manner. Overall, the present data demonstrated that there is a cross-relationship between increased RNS production and increased [Zn(2+)]i level in cardiomyocytes under pathological conditions such as hyperglycemia.

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Effect of dietary selenium and vitamin E on the biomechanical properties of rabbit bones

1997

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It is generally agreed that combined deficiency of selenium and vitamin E leads to several abnormalities including Kashin-Beck disease which is an endemic and chronic degenerative osteoarthrosis. The abnormalities can be reversed by the administration of various forms of selenium and vitamin E. The present study was designed to investigate the effects of dietary selenium and vitamin E on bone tissue and on the biomechanical properties of bone. Young rabbits of both sexes were fed with either a selenium- and vitamin E-adequate diet (control group), or a selenium- and vitamin E-deficient diet or a selenium-excess diet. The selenium-deficient diet resulted in a significant decrease in plasma selenium level and the selenium-excess diet resulted in a significant increase in the plasma selenium level with respect to the corresponding control values (p < 0.05). The diets did not affect the blood cell counts considerably but erythrocyte glutathione peroxidase activity increased (decreased) relatively when the plasma selenium level increased (decreased) (p < 0.05). The light microscopic investigations of the bone tissues of the two experimental groups indicate that the findings of the present work are compatible with osteomalacia. The biomechanical properties of the bones from the three groups were determined experimentally with bending tests. Both the Se- and vitamin E-deficient diet and the Se-excess diet decreased the biomechanical strength of the bones significantly while the bones belonging to the control group always had the largest modulus of elasticity (p < 0.05).

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Dietary selenium- and vitamin E-induced alterations in some rabbit tissues

Cited by 8 publications

References 51 publications

Down‐regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium‐deficient rabbits

Down‐regulation of GPx1 mRNA and the loss of GPx1 activity causes cellular damage in the liver of selenium‐deficient rabbits

Intracellular Zn2+ Increase in Cardiomyocytes Induces both Electrical and Mechanical Dysfunction in Heart via Endogenous Generation of Reactive Nitrogen Species

Effect of dietary selenium and vitamin E on the biomechanical properties of rabbit bones

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