Serum selenium concentration related to myocardial infarction and fatty acid content of serum lipids.

Miettinen, Tatu A.; Alfthan, Georg; Huttunen, Jukka; Pikkarainen, J; Naukkarinen, V; Mattila, S; Kumlin, T

doi:10.1136/bmj.287.6391.517

Cited by 75 publications

(22 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In several prospective (3)(4)(5) and case-control (6) studies, low serum selenium levels were associated with increased risk of coronary heart disease. However, in other studies, this association could not be confirmed (7)(8)(9)(10). Antioxidant defense is achieved by additive or synergistic action of enzymes and antiox-idant nutrients (11,12).…”

mentioning

confidence: 93%

See 1 more Smart Citation

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Kardinaal

Kok

Kohlmeier

et al. 1997

American Journal of Epidemiology

View full text Add to dashboard Cite

The association between selenium status and risk of acute myocardial infarction was examined in a multicenter case-control study in 10 centers from Europe and Israel in 1991-1992. Selenium in toenails was assessed for 683 nonfatal male cases with first acute myocardial infarction and 729 controls less than 70 years of age. Median toenail selenium content was 0.553 /xg/g for cases and 0.590 jxg/g for controls. After adjustment for age, center, and smoking, the odds ratio for myocardial infarction in the highest quintile of selenium as compared with the lowest was 0.63 (95 percent confidence interval 0.37-1.07, p for trend = 0.08). The observed inverse trend was somewhat stronger when the authors adjusted for vitamin E status (p = 0.05). Analysis stratified for smoking habits showed an inverse association in former smokers (odds ratio for the 75th-25th percentile contrast = 0.63 (95 percent confidence interval 0.43-0.94)), but not in current smokers (odds ratio = 0.97 ( 0.71-1.32)) or in those who had never smoked (odds ratio = 1.55 (0.87-2.76)). Analysis stratified by center showed a significant inverse association between selenium levels and risk of myocardial infarction for Germany (Berlin) only (75th to 25th percentile odds ratio = 0.62 (95 percent confidence interval 0.42-0.91)), which was the center with the lowest selenium levels. It appears that the increased risk of acute myocardial infarction at low levels of selenium intake is largely explained by cigarette smoking; selenium status does not appear to be an important determinant of risk of myocardial infarction at the levels observed in a large part of Europe. Am J Epidemiol 1997;145:373-9. antioxidants; case-control studies; myocardial infarction; selenium Evidence is accumulating that oxidation of low density lipoprotein particles and cytotoxic effects of lipid peroxides enhance the formation of foam cells and atherosclerotic lesions (1, 2). Selenium is part of the enzyme glutathione peroxidase, which plays an important role in the antioxidant defense of the body against the deleterious actions of free radicals and lipid per-

show abstract

mentioning

confidence: 93%

“…The question of whether low selenium status predisposes to cardiovascular disease has been addressed in a number of studies in the past decade (3)(4)(5)(6)(7)(8)(9)(10). In several prospective (3)(4)(5) and case-control (6) studies, low serum selenium levels were associated with increased risk of coronary heart disease.…”

mentioning

confidence: 99%

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Kardinaal

Kok

Kohlmeier

et al. 1997

American Journal of Epidemiology

View full text Add to dashboard Cite

show abstract

“…Feeding was conducted daily for 10 weeks. An additional 2 weeks of behavioral testing was conducted after BSSG feeding ended (total 12 weeks of testing) to allow blood sterol content to become normalized (Sanders et al 2000;Miettinen et al 1983). At this stage, half the mice were sacrificed.…”

Section: Feeding Of Bssgmentioning

confidence: 99%

Chronic Exposure to Dietary Sterol Glucosides is Neurotoxic to Motor Neurons and Induces an ALS–PDC Phenotype

Tabata

Wilson

et al. 2008

Neuromol Med

View full text Add to dashboard Cite

Epidemiological studies of the Guamanian variants of amyotrophic lateral sclerosis (ALS) and parkinsonism, amyotrophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC), have shown a positive correlation between consumption of washed cycad seed flour and disease occurrence. Previous in vivo studies by our group have shown that the same seed flour induces ALS and PDC phenotypes in out bred adult male mice. In vitro studies using isolated cycad compounds have also demonstrated that several of these are neurotoxic, specifically, a number of water insoluble phytosterol glucosides of which β-sitosterol β-D-glucoside (BSSG) forms the largest fraction. BSSG is neurotoxic to motor neurons and other neuronal populations in culture. The present study shows that an in vitro hybrid motor neuron (NSC-34) culture treated with BSSG undergoes a dose-dependent cell loss. Surviving cells show increased expression of HSP70, decreased cytosolic heavy neurofilament expression, and have various morphological abnormalities. CD-1 mice fed mouse NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript chow pellets containing BSSG for 15 weeks showed motor deficits and motor neuron loss in the lumbar and thoracic spinal cord, along with decreased glutamate transporter labelling, and increased glial fibrillary acid protein reactivity. Other pathological outcomes included increased caspase-3 labelling in the striatum and decreased tyrosine-hydroxylase labelling in the striatum and substantia nigra. C57BL/6 mice fed BSSG-treated pellets for 10 weeks exhibited progressive loss of motor neurons in the lumbar spinal cord that continued to worsen even after the BSSG exposure ended. These results provide further support implicating sterol glucosides as one potential causal factor in the motor neuron pathology previously associated with cycad consumption and ALS-PDC.

show abstract

“…It was reported that approximately 60% of selenium in plasma is present as selenoprotein P (Satia et al, 2005;Stranges et al, 2006). This protein differs from other selenoproteins in that it incorporates up to 10 Se atoms per molecule in the form of selenocysteine as opposed to the single selenocysteine incorporated in other selenoproteins (Miettinen et al, 1983). Selenoprotein P is abundant throughout the body suggesting that one function is to serve as a primary transporter in systemic selenium delivery (Rayman, 2000;2005).…”

Section: Ajesmentioning

confidence: 99%

Selenium Effect on Hyperoxia-Induced Glutathione Peroxidase Activity and Free Radicals Production in the Brain

Bin-Jaliah¹

2013

American Journal of Environmental Sciences

View full text Add to dashboard Cite

The purpose of this study was to examine the behavior of Glutathione Peroxidase (GPx) activity and Free Radicals (FR) production in the brain during graded hyperoxia exposure with and without selenium preventive intake. Forty two adult male rats were assigned to seven groups, six animals each. The first group served as control and the second, third and fourth groups were exposed to hyperoxia for 24, 48 and 72 h, respectively. The fifth, six and seventh groups were exposed to hyperoxia for 24, 48 and 72 h with selenium treatment. Following the exposure period for each group animals were sacrificed and brain tissues were homogenized for GPx and FR analysis. The results of 2-way ANOVA showed that the main effects of both selenium and hyperoxia were significant (p<0.05) for GPx. However, FR production was significantly (p<0.05) affected by hyperoxia only. Pair-wise means comparisons showed that the corresponding means (±) SD of GPx activity decreased significantly (p<0.05), from baseline non-selenium values of 13841.72±1245.67 and 14594.89±6711.50 to 5741.72±949.31 and 4829.98±775.52 following 24 and 48 h of hyperoxia exposure respectively, then increased to 7846.19±2467.69, following 72 h of hyperoxia exposure, as compared with non-selenium mean value of 4346.38±349.14. These differences were attributed to the ability of brain tissue to use selenium to reduce the requirements for GPx during 24 and 48 h as such to spare the integrity of its antioxidant mechanism during 72 h. Based on the results of the present study selenium's supplement and diet rich selenium are recommended for TBI patients.

show abstract

Serum selenium concentration related to myocardial infarction and fatty acid content of serum lipids.

Cited by 75 publications

References 9 publications

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Association Between Toenail Selenium and Risk of Acute Myocardial Infarction in European Men: The EURAMIC Study

Chronic Exposure to Dietary Sterol Glucosides is Neurotoxic to Motor Neurons and Induces an ALS–PDC Phenotype

Selenium Effect on Hyperoxia-Induced Glutathione Peroxidase Activity and Free Radicals Production in the Brain

Contact Info

Product

Resources

About