Reply #48: Medline: ApoE4 allele, Selenium Status & Prenatal Exposure

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Alzheimer disease: mercury as pathogenetic factor and apolipoprotein E as a moderator.

Neuro Endocrinol Lett. 2004 Oct;25(5):331-9.
Mutter J, Naumann J, Sadaghiani C, Schneider R, Walach H.

Institute for Environmental Medicine and Hospital Epidemiology, University Hospital Freiburg, Germany. [e-mail]

The etiology of most cases of Alzheimer's disease (AD) is as yet unknown. Epidemiological studies suggest that environmental factors may be involved beside genetic risk factors. Some studies have shown higher mercury concentrations in brains of deceased and in blood of living patients with Alzheimer's disease. Experimental studies have found that even smallest amounts of mercury but no other metals in low concentrations were able to cause all nerve cell changes, which are typical for Alzheimer's disease. The most important genetic risk factor for sporadic Alzheimer's disease is the presence of the apolipoprotein Ee4 allele whereas the apolipoprotein Ee2 allele reduces the risk of developing Alzheimer's disease. Some investigators have suggested that apolipoprotein Ee4 has a reduced ability to bind metals like mercury and therefore explain the higher risk for Alzheimer's disease. Therapeutic approaches embrace pharmaceuticals which bind metals in the brain of patients with Alzheimer's disease. In sum, both the findings from epidemiological and demographical studies, the frequency of amalgam application in industrialized countries, clinical studies, experimental studies and the dental state of AD patients in comparison to controls suggest a decisive role for inorganic mercury in the etiology of AD.

Publication Types:
Review

PMID: 15580166

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15580166&query_hl=15&itool=pubmed_docsum

Selenium status may also play a role:

The roles of serum selenium and selenoproteins on mercury toxicity in environmental and occupational exposure.

Environ Health Perspect. 2006 Feb;114(2):297-301.

Chen C, Yu H, Zhao J, Li B, Qu L, Liu S, Zhang P, Chai Z.

Laboratory of Nuclear Analytical Techniques and Laboratory for Nanoscale Materials and Related Bio-Environmental Sciences, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, People's Republic of China. [e-mail]

Many studies have found that mercury (Hg) exposure is associated with selenium (Se) accumulation in vivo. However, human studies are limited. To study the interaction between Se and Hg, we investigated the total Se and Hg concentrations in body fluids and serum Se-containing proteins in individuals exposed to high concentrations of Hg. Our objective was to elucidate the possible roles of serum Se and selenoproteins in transporting and binding Hg in human populations. We collected data from 72 subjects: 35 had very low Hg exposure as evidenced by mean Hg concentrations of 0.91 and 1.25 ng/mL measured in serum and urine, respectively; 37 had high exposure (mean Hg concentrations of 38.5 and 86.8 ng/mL measured in serum and urine, respectively). An association between Se and Hg was found in urine (r = 0.625; p < 0.001) but not in serum. Hg exposure may affect Se concentrations and selenoprotein distribution in human serum. Expression of both selenoprotein P and glutathione peroxidase (GSH-Px) was greatly increased in Hg miners. These increases were accompanied by elevated Se concentrations in serum. In addition, selenoprotein P bound more Hg at higher Hg exposure concentrations. Biochemical observations revealed that both GSH-Px activity and malondialdehyde concentrations increased in serum of the Hg-exposed group. This study aids in the understanding of the interaction between Se and Hg. Selenoproteins play two important roles in protecting against Hg toxicity. First, they may bind more Hg through their highly reactive selenol group, and second, their antioxidative properties help eliminate the reactive oxygen species induced by Hg in vivo.

PMID: 16451871

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16451871&query_hl=3&itool=pubmed_docsum

Early (in uterus and infant) exposure to mercury and lead.

Clin Nutr. 2005 Nov 21; Related Articles, Links

Dorea JG, Donangelo CM.

Laboratorio de Bioquimica Nutricional, Departamento de Nutricao, Universidade de Brasilia, C.P. 04322, 70919.970 Brasilia, Brazil.

Mercury and lead are toxic metals widely spread in the environment with bioaccumulative features that raises public health concerns. Both metals are equally dispersed in the human food chain but exposure and risk of toxicity during early human development are modulated by the diet and nutritional status. Understanding how Hg and Pb occur and interact with nutrients is fundamental to establish guidelines for diminishing exposure and the risk of toxicity. The risk of fetal and infant exposure to Hg can be influenced by maternal amalgam filling (inorganic Hg) and fish consumption (monomethyl Hg), whereas the risk of exposure to Pb is complex: maternal absorption depends on nutrient interactions (Ca and P); and maternal body Pb accumulation responds to all factors known to interact with bone and calcium metabolism. Maternal exposure to Hg and Pb is more important during fetal development than during breastfeeding. Moreover, these metals (especially Pb) are frequently higher in infant formulas which do not carry the nutritional and psychological advantages and protection of breastfeeding. Infant's reference dose is lower for Hg than for Pb, but risk of Pb contamination for fetuses and infant (breast- or formula-fed) is higher and lasts longer than Hg. Breastfeeding is essential to complete infant development. Interruption or suppression of breast-feeding with cow's milk-based formulas is not an option to environmental pollution.

PMID: 16307830


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16307830&query_hl=3&itool=pubmed_DocSum