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Tuesday, 24 December 2013

Dietary Minerals - Calcium (2)

Calcium, a trace mineral plays an important role in build and maintain strong bones and teeth, found abundantly in meat, poultry, fish,  nut, seeds, bean, etc. As we age, calcium is absorbed less effectively.
8. Calcium and S100 proteins
S100 proteins play a crucial role in multiple important biological processes in vertebrate organisms acting predominantly as calcium signal transmitters.According to the study by the Polish Academy of Sciences, after four Ca(2+) ions bind, it undergoes a dramatic conformational change, resulting in exposure, in each of its two identical subunits, a large hydrophobic cleft that binds to target proteins. It has been shown that abnormal expression of S100A1 is strongly correlated with a number of severe human diseases: cardiomyopathy and neurodegenerative disorders(8).

9. Calcium and aluminum salt
Most humans living in industrialized societies are routinely exposed to bioavailable aluminum salts in the form of additives-in commercially-prepared foods, alum-clarified drinking water, certain pharmaceuticals, sunscreens, and other topical applications. Minute amounts of this aluminum are absorbed into the circulation. Trace aluminum levels cross the blood-brain barrier and progressively accumulate in large pyramidal neurons of the hippocampus, cortex, and other brain regions vulnerable in Alzheimer's disease. According to the study by the St George Hospital Campus,  intraneuronal aluminum interferes with Ca2+ metabolism in the aged brain and describes a way to test this hypothesis. This paper reviews: 1) major changes that occur in brain Ca2+ homeostasis and Ca2+ signaling, subtly with aging and more overtly in Alzheimer's disease; and 2) evidence from the scientific literature that aluminum causes these same changes in neurons(9).

10. calcium and aluminum in Neurodegenerative disorders
Both calcium and aluminum have been implicated in the cell damage and death that occurs in several neurodegenerative disorders including Alzheimer's disease (AD). In the study to examine the effects of experimentally elevated intraneuronal levels of aluminum ([Al]i) and/or calcium ([Ca2+]i) on neuronal degeneration and antigenic alterations in the microtubule-associated protein tau in cell cultures of rat hippocampus and human cerebral cortex, showed that Exposure of cultures to Al3+ alone (200 microM) for up to 6 d did not result in neuronal degeneration. Neurons exposed to the divalent cation ionophore A23187 degenerated within 4 h when Ca2+ was present in the culture medium whether or not Al3+ was present. Measurements of [Ca2+]i using the calcium indicator dye fura-2 demonstrated a direct relationship between increased [Ca2+]i and neuronal degeneration. In contrast, neurons did not degenerate when exposed to A23187 in the presence of Al3+ and the absence of Ca2+, despite a 10-fold elevation in [Al]i as measured by laser microprobe mass spectrometry. Calcium influx, but not aluminum influx, elicited antigenic changes in tau similar to those seen in AD neurofibrillary tangles. Neurons exposed to glutamate in the presence of Al3+ but in the absence of Ca2+ were not vulnerable to injury. Finally, increased [Al]i occurred in neurons that degenerated as the result of exposure to glutamate indicating that aluminum associates with degenerating neurons(10).

11. Neuronal calcium homeostasis in the aging nervous system
Maintenance of the cellular calcium homeostasis plays an important role for neuronal cell function and interneuronal cell to cell communication. Therefore, alterations of the neuronal Ca2+ homeostasis may play a crucial role for brain aging in general and for age-related deficits in cognitive functions particularly.
Numerous studies indicate various disturbances of the Ca2+ homeostasis on different levels like Ca2+ channel properties, 45Ca2+ uptake, or Ca2+ binding proteins. Investigations on alterations of the free intracellular calcium concentration ([Ca2+]i) in presynaptic synaptosomal preparations led to inconsistent results reporting increased or unchanged [Ca2+]i in aged animals, according to the Central Institute of Mental Health, Dept. Psychopharmacology(11).

12. Disruption of calcium homeostasis and Alzheimer's disease (AD)
Oligomerization, conformational changes, and the consequent neurodegeneration of Alzheimer's β-amyloid protein (AβP) play crucial roles in the pathogenesis of Alzheimer's disease (AD). Mounting evidence suggests that oligomeric AβPs cause the disruption of calcium homeostasis, eventually leading to neuronal death, according to the School of Pharmaceutical Sciences, Kyushu University of Health and Welfare(12).

13. BK Channels in Cardiovascular Diseases and Aging
Aging is a major risk factor for cardiovascular diseases, one of the main world-wide causes of death. Several structural and functional changes occur in the cardiovascular system during the aging process and the mechanisms. BK channels are transmembrane proteins that play a key role in many physiological processes, including regulation of vascular tone.In vascular smooth muscle cells, BK opening and the consequent efflux of potassium (K(+)) leads to membrane hyperpolarization, which is followed by the closure of voltage-dependent Ca(2+) channels, reduction of Ca(2+) entry and vasodilatation. BK regulates nitric oxide-mediated vasodilatation and thus is crucial for normal endothelial function(13).

14. Ca(2+) waves regulate blood vessel tone and vasomotion
Agonist-stimulated smooth muscle Ca(2+) waves regulate blood vessel tone and vasomotion.The Pharmacology, and Therapeutics, University of British Columbia, present a first report of endothelin-1 stimulated waves of Ca(2+) depletion from the sarcoplasmic reticulum of vascular smooth muscle cells using a calsequestrin-targeted Ca(2+) indicator and confirmed that these waves are due to regenerative Ca(2+)-induced Ca(2+) release by the receptors for inositol 1,4,5-trisphosphate(14).

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Sources
(8) http://www.ncbi.nlm.nih.gov/pubmed/23351007
(9) http://www.ncbi.nlm.nih.gov/pubmed/22330830
(10) http://www.ncbi.nlm.nih.gov/pubmed/8448655
(11) http://www.ncbi.nlm.nih.gov/pubmed/7997060
(12) http://www.ncbi.nlm.nih.gov/pubmed/21547225
(13) http://www.ncbi.nlm.nih.gov/pubmed/23423545
(14) http://www.ncbi.nlm.nih.gov/pubmed/23408969