Selenium

Selenium
© 1996 - 2004 PFPC

   Selenium is an essential component of the three deiodinases which regulate conversion from T4 into T3 .

   Selenium deficiency caused by fluorides is well acknowledged in China. As a result of this well-known fact, entire villages formerly suffering from Kashin-Beck disease as a result of fluoride contamination (and a disease established to involve selenium deficiency) have been relocated under extensive government programs such as "Project 2000".

   Some Chines studies have shown that selenium supplementation may reduce the effects of "fluorosis" (Wang et al, 2004; Bian et al, 2000;1999). Effects are more pronounced when selenium is given together with zinc (Chen et al, 2000; Yu et al, 2002; Xue et al, 2001).

   However, at high doses, selenium has been found to enhance fluoride effects, and to act synergistically with fluoride (Zhang et al, 2001).

   It is recommended to first correct thryoid status. The
selenoenzymes (glutathione peroxidase, deiodinases) are under control of the Ca2+/phosphoinositol second-messenger cascade (Regulated by TSH -> G q/11). In humans, serum TSH levels are inversely correlated with plasma selenium levels (Hagbar et al, 1998).

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Bian J, Liu Y, Yang Xa,et al - “Experimental study on effects of selenium in rats with fluorosis” CHINESE JOURNAL OF ENDEMIOLOGY, No.2, vol.18 (1999)

Abstract:

Objective:Study on effects of selenium(Se) on fluorine (F), anti-oxidation enzymes and lipid metabolism in rats with fluorosis.

Methods: Wistar rats with chronic fluorosis which were duplicated with 2.63mmol/L F in drinking water for 10 months divied into 4 groups(1) high F water (2.63mmol/L);(2)high F water and Se-supplementation (2.0mg/kg) in fodder; (3)normal water; (4)normal water and Se for 10 months.The contents of F in urine were observed tendentiously, F in bones, liver, kidneys and serum were tested.The activities of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) in erythrocyte, liver and kidneys, the contents of total cholesterol (TC), high density lipoproteincholesterol (HDL-C) and low density lipoproteincholesterol (LDL-C) in serum were determined.

Results:There was an increase of urine F and a decrease of liver, kidneys and bones F, anti-oxidation enzymes and lipid metabolism improved in high F and Se group compared with high F group.The function of promoting excretion of F and decreasing tissue and bones F in normal water and Se group had the advantage of that in normal water group, at the same time, the level of anti-oxidation enzymes and lipid approached it in control group.

Conclusions: Se in the range of certain concentration had the role of excreting high F, adjusting disorder of free radicals and lipid metablism, and prompting the recovery of fluorosis in rats with fluorosis.

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Bian J, Li HX, Liu Y, et al - "Dynamically observed skeletal X-ray in rats with chronic fluorosis and effects of selenium" Chinese Journal of Endemiology  19(4)260-261 (2000)
(Shandong Institute for Prevention and Treatment of  Endemic Disease, Jinan 250014, China)

Abstract:

Objective: To observe trend of skeletal radiography in rats with chronic fluorosis and effect of selenium.

Methods:Two groups of Wistar rats were fed with normal fodder and high concentration of NaF water (1.58,2.63 mmol/L fluorine,F) and two groups with selenite fodder (2.0 mg/kg selenium,Se) and high F for 14 months.The rats were photographed by means of radiography with molybdenum target tubes biomonthly total 6 times and the contents of urine,serum and bone F in the rats were examined in 14 months.

Results: Urine,serum and bone F in rats with fluorosis increased. Concerning bone X-ray changes,abnormalities were observed first in pelvis,then in lumbar vertebrae,finally in thoracic and pectoral limbes. Early skeletal fluorosis was found in 8 months. There was a positive correlation between
concentration of F in drinking water and degree skeletal fluorosis and of abnormal bone struture. After supplement of Se, serum and bone F decreased.Abnormal bone structure and skeletal fluorosis were reduced.

Conclusions: Pelvie could be referred as essential observation section by radiography and skeletal fluorosis appeared in the middle and late period of fluorosis.Certain concentration of Se could antagonize high F, delay and decrease the occurrence of skeletal fluorosis in rats with fluorosis.

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Bian J, Xian S, Ye P, Wang X, Liu C, Liu Y - "Effect of
Na2SeO3-supplementation on fluorine content, anti-oxidative
enzymes activities and lipid peroxidation of the patients with fluorosis" Acta Nutrimenta Sinica  16 (1):56-60 (1994)

BIOSIS COPYRIGHT: BIOL ABS. The contents of selenium (Se) and fluorine (F) in serum, urine and hair, the activity of glutathione peroxidase (GSH-Px) in erythrocyte, the activity and content of superoxide dismutase (SOD) in red blood cells, the activity of SOD in serum and the content of lipid peroxide (LPO) in serum of 40 patients with dental fluorosis and 78 patients with skeletal fluorosis were determined in an area with a high concentration of F in the drinking water and a low concentration of Se in the environment before and after Na2SeO3-supplementation. The results showed that the level of Se in the serum, urine and hair of the patients of both groups was higher after Se-supplementation. At the same time, the content of F in urine increased and in serum decreased. Increases of the activities of GSH-Px, SOD in RBC and of the rate of GSH-Px, SOD/LPO, decrease of the content of LPO in serum of the patients were observed. Se might be able to improve the function of anti-oxidative enzymes.

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Chen J, Chen X, Yang K - "Effects of selenium and zinc on the DNA damage caused by fluoride in pallium neural cells of rats."  Wei Sheng Yan Jiu 29(4):216-7 (2000)

To investigate the effects of fluoride on DNA damage as well as the effects of selenium and zinc against fluoride respectively or jointly in pallium neural cells of rats, single cell gel electrophoresis was used to detect the DNA damage of neural cells prepared in vitro. The results showed that the degree of DNA damage in the fluoride group and the selenium group were significantly greater than that in control group(P < 0.01). The damage in the fluoride group was even more serious. The damage in the fluoride + selenium group and fluoride + zinc group was slighter than that in the fluoride group but with no significant difference. The extent of DNA damage in the fluoride + selenium + zinc group was significantly slighter than that in the fluoride group(P < 0.05). It suggested that fluoride and selenium could induce DNA damage in pallium neural cells of rats respectively. Moreover, the joint antagonistic effect of selenium and zinc against fluoride was more obvious.

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Wang A, Xia T, Ru R, Yuan J, Chen X, Yang K - "Antagonistic effect of selenium on oxidative stress, DNA, and apoptosis induced by fluoride in human hepatocytes" Fluoride 37(2): 107-116 (2004)
http://www.fluorideresearch.org/372/files/FJ2004_v37_n2_p107-116.pdf

Yu R, Xia T, Wang A, Chen X - "Effects of selenium and zinc on rat renal apoptosis and change of cell cycle induced by fluoride" Zhonghua Yu Fang Yi Xue Za Zhi 36(4):219-21 (2002)

OBJECTIVE: This study was conducted to study the effects of sodium fluoride (NaF) on rat renal apoptosis and proliferation, the antagonistic effect of selenium-zinc preparation (Se-Zn) to NaF. METHODS: Wistar rats were provided with distilled water containing NaF (50 mg/L) and administered by gavage with different dosed of Se-Zn for six months. Kidney cell apoptosis and the cell cycle of proliferation were detected by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry. RESULTS: NaF caused rat renal apoptosis, reduce the cell number of G(2)/M period in cell cycle and decrease the relative content of DNA significantly. Se-Zn inhibited the effects of NaF on apoptosis and increased the cell number of G(2)/M period in cell cycle, but failed to increase relative content of DNA. CONCLUSION: It was suggested that NaF could induce apoptosis and change the cell cycle in rat renal cells and Se-Zn could antagonize apoptosis and the changes of cell cycle induced by NaF.

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Xue C, Chen X, Yang K - "Study on antagonistic effects of selenium and zinc on the renal impairments induced by fluoride in rats" Wei Sheng Yan Jiu 29(1):21-3 (2000)

Wistar rats were provided with distilled water containing NaF(100 mg/L), and were administered through gavage with Na2SeO3[0.1 mg/(kgBW.d)] and/or ZnSO4[14.8 mg/(kg BW.d)]. The results of biochemical, pathological and ultrastructural examinations showed that fluoride could cause serious renal impairments. The major damage induced by fluoride was epithelia of proximal renal tubules. The lipid peroxidation might be one of the mechanisms of fluoride toxicity. Na2SeO3 and ZnSO4 could antagonize the renal impairments induced by fluoride through their antioxidation. The cooperative effect of Na2SeO3 and ZnSO4 was more powerful than either Na2SeO3 or ZnSO4 alone.

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Zhang Z, Shen X, Xu X - Effects of selenium on the damage of learning-memory ability of mice induced by fluoride" Wei Sheng Yan Jiu 30(3):144-6 (2001)

Sodium fluoride added with or without sodium selenite in deionized water was administered to male mice for 8 weeks. The influences of fluoride on learning-memory behavior were tested on Y-maze, and the ultrastructure of Gray I synaptic interface in the CA3 area hippocampus was quantitatively analyzed by electron microscopy and computer image processing appliance. The main results showed that the learning capability of mice drinking higher concentration of fluoride presented remarkable deterioration. The thickness of post-synaptic density (PSD) was decreased. The width of the synaptic cleft was remarkably increased. It was found that combined administration of fluoride and proper concentration of selenium could decrease the toxic effect of fluoride. There were synergetic toxicities if the concentration of selenium was too high. The results suggested that selenium might antagonize the neurotoxicity of fluoride on behavior and morphology.

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Zhang Z, Xu X, Shen X, Xu X - "Effect of fluoride exposure on synaptic structure of brain areas related to learning-memory in mice" Wei Sheng Yan Jiu. 1999 Jul;28(4):210-2 (1999)

The learning-memory behavior was tested in mice on a Y-maze after drinking different concentration of sodium fluoride. The impairment on the structure of Gray 1 synaptic interface in the CA3 area of mice hippocampus were quantitatively analyzed by electron microscopy and computer image processing appliance. The main results are as follows: the learning ability of mice drinking high concentration of fluoride presented remarkable deterioration, the thickness of post-synaptic density (PSD) was decreased, and the width of synaptic cleft was remarkably increased. The results suggested that the
impairment on the learning capability induced by fluorosis may be closely related with the pathological changes of synaptic structure in the brain of mice.

SELENIUM:

Hagmar L, Persson-Moschos M, Akesson B, Schutz A - "Plasma levels of selenium, selenoprotein P and glutathione peroxidase and their correlations to fish intake and serum levels of thyrotropin and thyroid hormones: a study on Latvian fish consumers" Eur J Clin Nutr 52(11):796-800 (1998)

    "TSH in serum was inversely correlated with plasma selenium and selenoprotein P."

Savaskan NE, Brauer AU, Kuhbacher M, Eyupoglu IY, Kyriakopoulos A, Ninnemann O, Behne D, Nitsch R - “Selenium deficiency increases susceptibility to glutamate-induced excitotoxicity” FASEB J 17(1):112-4  (2003)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1242422 0