Serum selenium

There is very little evidence relating to the role of ROMs in cholestatic liver disease. Serum selenium and glutathione peroxidase activity are decreased in humans with intrahepatic cholestasis of pregnancy (Kauppila et al., 1987). Low levels of vitamin E have been reported in patients with primary biliary cirrhosis, and in children with Alagille s syndrome or biliary atresia (Knight et al., 1986 Jeffrey etal., 1987 Lemonnier etal., 1987 Babin etal., 1988 Kaplan et al., 1988 Sokol etal., 1989). Serum levels of Mn-SOD are increased in patients with all stages of primary biliary cirrhosis compared with patients with other forms of chronic liver disease, although whether this causes or results from the disease process is unclear (Ono etal., 1991). 

Aaseth, J., Alexander, J., Thomassen, Y., Blomhoff, J.P. and Skrede, S. (1983). Serum selenium levels in liver diseases. Clin. Biochem. 15, 281-283. 

Kauppila, A., Korpela, H., Makila, U-M. and Yrjanheikki, E. (1987). Low serum selenium concentration and glutathione peroxidase activity in intrahepatic cholestasis of pregnancy. Br. Med. J. 294, 150-152. 

Korpela, H., Kumpulainen, J., Luoma, P.V., Arranto, A.J. and Sotaniemi, E.A. (1985). Decreased serum selenium in alcoholics as related to liver structure and function. Am. J. Clin. Nutr. 42, 147-151. 

Valimaki, M.J., Harju, K.J. and Ylikahri, R.H. (1983). Decreased serum selenium in alcoholics - a consequence of liver dysfunction. Clin. Chim. Acta 130, 291-296. 

Essential hypertension, whose prevalence is increased nearly two-fold in the diabetic population, may be another source of free-radical activity. The vascular lesions of hypertension can be produced by free-radical reactions (Selwign, 1983). In the recent Kuopio Ischaemic Heart Risk Factor Study in Finnish men, a marked elevation of blood pressure was associated with low levels of both plasma ascorbate and serum selenium (Salonen etal., 1988). A few studies report a hypotensive effect of supplementary ascorbate in patients with hypertension, but the actual changes in both systolic and diastolic pressure after ascorbate were not statistically significant in comparison with placebo (Trout, 1991). 

Necheles et al. (N4) first reported a genetically determined homozygous GSH-Px deficiency associated with neonatal jaundice and mild hemolysis. Spontaneous recovery from hemolysis was noted 3 months after birth. Thereafter, several cases with GSH-Px deficiency were reported. Newborn infants exhibit significantly lower red blood cell GSH-Px activity and serum selenium concentrations than adult control subjects, and a significantly positive correlation between selenium concentration and GSH-Px activity has been observed. Furthermore, the addition of selenium stimulates, both in vivo and in vitro, the GSH-Px activity. The neonatal red blood cell GSH-Px deficiency may be partially due to insufficient availability of selenium during pregnancy (P9). Therefore, the diagnosis of GSH-Px deficiency in newborn infants must be made carefully. 

The possible involvement of free radicals in the development of hypertension has been suspected for a long time. In 1988, Salonen et al. [73] demonstrated the marked elevation of blood pressure for persons with the lowest levels of plasma ascorbic acid and serum selenium concentrations. In subsequent studies these authors confirmed their first observations and showed that the supplementation with antioxidant combination of ascorbic acid, selenium, vitamin E, and carotene resulted in a significant decrease in diastonic blood pressure [74] and enhanced the resistance of atherogenic lipoproteins in human plasma to oxidative stress [75]. Kristal et al. [76] demonstrated that hypertention is accompanied by priming of PMNs although the enhancement of superoxide release was not correlated with the levels of blood pressure. Russo et al. [77] showed that essential hypertension patients are characterized by higher MDA levels and decreased SOD activities. 

Knekt B Aromaa A, Maatela J, et al, Serum selenium and subsequent risk of cancer among Finnish men and women. J Natl Cancer Inst 1990 82 864-868. 

Willet WC, Polk BF Morris JS, et al, Prediagnostic serum selenium and risk of cancer Lancet I 983 2 130-134. 

Nomura A, Heilbrun LK, Morris JS, Stemmermann GN. Serum selenium and the risk of cancer, by specific sites case-control analysis of prospective data, J Natl Cancer Inst 1987 79 103-108. 

S. Bro, H. Berendtsen, J. Norgaard, P. J. Jorgensen, Serum selenium concentration in maternal and umbilical cord blood. Relation to course and outcome of pregnancy, J. Trace Elem. Electrol. Health Dis., 2 (1988), 165-169. 

Early animal studies and human population surveys used whole blood as the main indicator of selenium status. Whole blood selenium can be determined after acid digestion using a fluorometric method. The more convenient carbon furnace atomic absorption spectroscopy (CFAAS) assay for plasma and/or serum selenium is now the most widely used procedure. The main components of plasma selenium are extracellular glutathione peroxidase (GSHPx 3) and selenoprotein P. 

Selenium, as selenocysteine, is incorporated into glutathione peroxidase (antioxidant), iodothyronine deiodinase (thyroid hormone regulation), and selenoprotein P (vitamin C metabolism). Prematurity, acute illness, chronic GI losses, and long-term selenium-free parenteral nutrition are associated with low serum selenium concentrations and decreased glutathione peroxidase activity. " The... 

An association between alcoholism and low serum selenium concentrations has been reported. Because selenium is important in... 

In a study of 68 male Latvian fish consumers (Hagmar et al. 1998), a significant inverse correlation was found between serum levels of selenium and TSH. No correlation was found between serum selenium concentration and the serum concentrations of T3 or T4. No measurements were made of dietary selenium intake. 

Ocular Effects. A case control study using a hospital discharge register indicated there was no correlation between serum selenium concentrations and cataract occurrence in humans (Knekt et al. 1992). Since this is a case control study, it does not provide information on the potential dietary factors, exposure to specific selenium compounds, or duration of exposure. 

Low serum selenium levels have been associated with an increased incidence of cancer in some prospective epidemiological studies (Salonen et al. 1984, 1985 Willet et al. 1983). In the United States, Willet et al. (1983) found that the risk of cancer for subjects in the lowest quintile (fifth) of serum... 

Although the age-specific risk of fatal cancers in the two populations cannot be calculated from the data reported, the overall incidence of cancer in the 4-year Finnish study was less than half that in the 5-year U.S. study. In addition, other prospective studies of Americans have found no correlation between fatal cancer and blood selenium concentrations (Coates et al. 1988). Thus, one cannot predict relative cancer risks with serum selenium levels in one population based on data from another population. 

A 9-year prospective follow-up study was conducted by Virtamo et al. (1987) on a group of men in Finland. At the beginning of the study, blood samples were taken as part of a study of coronary heart disease and other atherosclerotic diseases. Cancer data were collected from central registries for the years 1976 through 1983. The results indicated no association between low serum selenium levels (<0.045 mg selenium/L) and an increased risk of cancer. Evidence suggests that combined dietary deficiencies of vitamin E and selenium may be associated with increased cancer risk (Salonen et al. 

Dermal absorption was tested in eight women at a maximum dose of 0.0029 mg selenium/kg as selenomethionine (0.05% L-selenomethionine in a lotion). No detectable increase in serum selenium concentrations was observed but because the concentrations tested were so low, absorption cannot be ruled out (Burke et al. 1992a). Absorption of selenium disulfide was examined using a monthly 24-hour urine specimen in 16 persons who washed their hair weekly with a 1% selenium disulfide shampoo. No differences were found from control urinary selenium levels over the 1-year exposure period (Cummins and Kimura 1971). No absorption of selenium from selenium sulfide was seen in 15 persons who applied a 2.5% selenium sulfide suspension to their torsos and allowed it to remain on the body overnight (Kalivas 1993). 

There is a rapid decline in serum selenium levels 1 hour after intravenous administration of sodium selenite or sodium selenate to humans (Burk 1974 Nelp and Blumberg 1965). Burk (1974) found that 50% of the plasma selenium was protein-bound within the first 2 hours after administration 85% was bound within 4-6 hours after administration and 95% was bound after 24 hours. Circulating alpha-2 globulins have been reported to have the greatest affinity for selenium (Hirooka and Galambos 1966a). Burk (1974) found that lipoproteins, primarily the very low density lipoprotein (VLDL) and the low-density lipoprotein (LDL) fractions, were also involved in selenium binding. 

An examination of elimination data from 44 pigs exposed to excess selenium as sodium selenite in feed was found to fit a one-compartment model of selenium elimination (Davidson-York et al. 1999). Serum selenium levels were monitored over a period of 46 days beginning 1-14 days after termination of exposure to the feed containing excess selenium. Data were not adequate to depict the initial distribution phase, but a geometric mean elimination half-life of 12 days was calculated. It is likely that the period of elimination included in this study corresponds to the second phase described by Thomson and Stewart (1974). 

At blood levels of from 0.06 to 0.20 mg selenium/L, Deguchi (1985) found selenium to be positively correlated with grasping power and blood pressure in normal men and women and with hematocrit and hemoglobin concentrations in normal women. Similar correlations were not found in subjects with proteinuria or hypertension. In addition, Gebre-Medhin et al. (1988) found that in healthy children, serum selenium levels of 0.055-0.082 mg selenium/L were positively correlated with serum cholesterol, serum triglycerides, low and very low density lipoproteins, and apolipoproteins. Similar correlations were not found in diabetic children, who have slightly elevated serum selenium levels. 

A deficiency of selenium is also associated with cardiomyopathy (Johnson et al. 1981 Oster et al. 1983). Salonen et al. (1982) noted a statistically significant association between serum selenium concentrations of less than 0.045 mg selenium/L and the adjusted relative risk of coronary death, cardiovascular death, and myocardial infarction. Hojo (1981a) noted that patients with epilepsy had significantly lower urinary selenium levels than controls. 

Al-Saleh I, Al-Doush I, Ibrahim M, et al. 1998. Serum selenium levels in Saudi new-boms. IntJ Environ Health Res 8 269-275. 

Beguin Y, Bours V, Delbrouck JM, et al. 1989. Relationship of serum selenium levels to tumor activity in acute non-lymphocytic leukemia. Carcinogenesis 10(11) 2089-2091. 

Broghamer WLJ, McConnell KP, Grimaldi M, et al. 1978. Serum selenium and reticuloendothelial tumors. Cancer 41 1462-1466. 

Gebre-Medhin M, Ewald U, Tuvemo T. 1988. Serum selenium is related to low density lipoproteins in healthy children but not in children with diabetes. Upsula Journal of Medical Sciences 93 57-62. 

Kalivas J. 1993. Lack of serum selenium rise after overnight application of selenium sulfide. Arch Dermatol 129 646-648. 

Kallistratos G, Evangelou A, Seferiadis K, et al. 1985. Selenium and haemodialysis Serum selenium levels in healthy persons, non-cancer and cancer patients with chronic renal failure. Nephron 41 217-222. 

Kok FJ, DeBruijn AM, Hofman A, et al. 1987b. Is serum selenium a risk factor for cancer in men only Am J Epidemiol 125 12-16. 

Kok et al. 1987c. Serum selenium vitamin antioxidants, and cardiovascular mortality A 9-year followup study in the Netherlands. Am J Clin Nutr 45 462-468. 

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