Selenium Deficiency-Induced Alterations in the Vascular System of the Rat

Qu, Xiaomei; Huang, Kaixun; Deng, Li-Qun; Xu, Huibi

doi:10.1385/bter:75:1-3:119

Cited by 27 publications

(8 citation statements)

References 38 publications

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“…The marginal effect of PCB 126 on LDL-C, consistent with other reports (Lind et al 2004), resulted in an increase in the HDL-C/LDL-C ratio which should be protective against cardiovascular disease if not disturbed otherwise, for example by oxidative stress. Se had no consistent effect on serum lipids, which is in agreement (Chen et al 1986; Crespo et al 1995; Panczenko-Kresowska and Ziemlanski 1987) or disagreement (Bleys et al 2008; Kaur and Bansal 2009; Qu et al 2000; Stranges et al 2010) with other reports. Differences in Se concentration and duration of feeding may be accountable for these discrepancies, since only a low Se level may increase the ‘good cholesterol’, while too much Se will elevate TC, LDL-C, and HDL-C (Laclaustra et al 2009b), and increase the risk of cardiovascular diseases (Laclaustra et al 2009a; Stranges et al 2010).…”

Section: Discussionsupporting

confidence: 77%

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Shen

Wang

et al. 2013

Environ Sci Pollut Res

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The environmental pollutants polychlorinated biphenyls (PCBs), especially dioxin-like PCBs, cause oxidative stress and associated toxic effects, including cancer and possibly atherosclerosis. We previously reported that PCB 126, the most potent dioxin-like PCB congener, decreases antioxidants such as hepatic selenium (Se), selenium-dependent glutathione peroxidase and glutathione (GSH), but also increases levels of the anti-atherosclerosis enzyme paraoxonase 1 (PON1) in liver and serum. To probe the interconnection of these three antioxidant systems, Se, GSH, and PON1, we examined the influence of varying levels of dietary Se and N-acetylcysteine (NAC), a scavenger of reactive oxygen species (ROS) and precursor for GSH synthesis, on PON1 in the absence and presence of PCB 126 exposure. Male Sprague Dawley rats, fed diets with differing Se levels (0.02, 0.2, or 2 ppm) or NAC (1%), were treated with a single intraperitoneal injection of corn oil or various doses of PCB 126 and euthanized 2 weeks later. PCB126 significantly increased liver PON1 mRNA, protein level and activity and serum PON1 activity in all dietary groups, but did not consistently increase thiobarbituric acid levels (TBARS), an indicator for lipid oxidation and oxidative stress, in liver or serum. Inadequate (high or low) dietary Se decreased baseline and PCB 126-induced aryl hydrocarbon receptor expression but further increased PCB 126-induced cytochrome P450 1A1 expression, the enzyme believed to be the cause for PCB 126-induced oxidative stress. In addition, a significant inverse relationship was observed between dietary Se levels and PON1 mRNA and PON1 activity, but also with TBARS levels in the liver, suggesting significant antioxidant protection from dietary Se. NAC lowered serum baseline TBARS levels in the controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 μmol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum. These results also show an unexpectedly predominantly inverse relationship between Se or NAC and PON1 during normal and PCB 126 exposure conditions. These interactions should to be further explored in the development of dietary protection regimens.

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Section: Discussionsupporting

confidence: 77%

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Shen

Wang

et al. 2013

Environ Sci Pollut Res

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“…For example, serum nitrite/nitrate content was found lower in male weanling C3H/HeJ mice fed a Se Ϫ diet for 5 wk than in Se ϩ controls (A. D. Smith, personal communication). Similar results were found in Wistar rats (35). Clearly, more studies are needed to clarify this point.…”

Section: Discussionsupporting

confidence: 80%

Reduced inotropic heart response in selenium-deficient mice relates with inducible nitric oxide synthase

Gómez

Levander

Sterin‐Borda

2003

American Journal of Physiology-Heart and Circulatory Physiology

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Atria from mice fed a selenium-deficient (Se(-)) diet have a diminished beta-adrenoceptor-inotropic cardiac response to isoproterenol or norepinephrine compared with atria from mice fed the same diet supplemented with 0.2 mg/kg Se as sodium selenite (Se(+)). This diminished response could be reversed by feeding Se(-) mice the Se(+) diet for 1 wk or by pretreatment with nitric oxide synthase (NOS) inhibitors such as N(G)-monomethyl-l-arginine or aminopyridine. Elevated serum concentrations of nitrite/nitrate as well as a threefold increase in the atrial NOS activity were seen in the Se(-) versus Se(+) mice. Western blotting and indirect immunofluorescence indicated an enhanced expression of inducible NOS in hearts from Se(-) mice. Increased expression and activity of NOS and increased nitrite/nitrate levels from Se(-) mice correlated with an impaired response to beta-adrenoceptor inotropic cardiac stimulation. Elevated nitric oxide levels may account for some of the pathophysiological effects of Se deficiency on the heart.

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“…On the other hand, feeding rats with Se-deficient diet increased the plasma levels of total cholesterol and LDL-c and decreased the HDL-c level. It down regulated the LDL-receptors that bind to LDL-c from the blood [28][29][30]. Spontaneously hypertensive (SHR) rats fed Se-deficient diet had higher plasma levels of triglycerides, total cholesterol and VLDL-c than SHR rats fed Se-sufficient diet.…”

Section: Discussionmentioning

confidence: 99%

Selenium decreases triglycerides and VLDL-c in diabetic rats exposed to electromagnetic radiation from mobile phone base stations

Ismaiil

Joumaa

Moustafa

2019

Journal of Taibah University for Science

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This study investigated the effects of exposure of diabetic rats to electromagnetic radiation (EMR) of 900 MHz from cell phone base stations antenna for four weeks on plasma triglycerides and cholesterol. We also examined whether selenium administration into these rats affects the levels of these parameters. Our results showed that the exposure of diabetic rats to this EMR increased the plasma triglycerides, total cholesterol and VLDL-c. The daily intraperitoneally injection of 2.0 μg selenium/kg body weight as sodium selenite into these rats decreased the triglycerides and VLDL-c levels compared to diabetic rats with EMR exposure. Selenium also restored the normal levels of plasma triglycerides, total cholesterol and HDL-c as compared to control rats. In conclusion, selenium decreased the elevated levels of triglycerides and cholesterol in diabetic rats exposed to EMR from cell phone base stations and hence it may decrease the development of some diabetic complications.

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Selenium Deficiency-Induced Alterations in the Vascular System of the Rat

Cited by 27 publications

References 38 publications

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Reduced inotropic heart response in selenium-deficient mice relates with inducible nitric oxide synthase

Selenium decreases triglycerides and VLDL-c in diabetic rats exposed to electromagnetic radiation from mobile phone base stations

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