Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Magnesium Deficiency”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources
PubMed2004

[Magnesium deficiency--benefits of "life salt nuti ma-su"].

One of essential minerals magnesium tastes bitter, so human love to remove magnesium from salt. But magnesium is also essential for cell functions in the body. Salts are getting purifying only NaCl from sea water. It means other minerals are gone out. So other essential minerals easily are getting to deficiency in the body. Recently the technique of purification of salt from sea water has developed. But the contents of magnesium other than [NaCl] is getting decrease. So deficiency symptom is easily occurred. The important role of magnesium is control of higher function of nervous system, behavior, memory and learning in the human. So we have to intake a lot of magnesium from many kinds of salts including sea water.

Animals↗
PubMed1989

[Magnesium deficiency caused by epirubicin/cisplatin].

In 19 patients receiving a cytostatic therapy with epirubicine and cisplatinum, 31 times in total the renal loss of magnesium was determined using the colorimetric xylidile-blue-method. 16 patients, whose magnesium input postoperatively was equally well known, served as a control. In all these patients a negative magnesium balance could be demonstrated being significantly higher (p less than 0.01) in those receiving cytostatic therapy.

Adult↗
PubMed1995

Mechanisms of the enhanced contractile response to a low concentration of phorbol 12,13-dibutyrate in thoracic aorta isolated from rats with dietary magnesium deficiency.

The mechanisms underlying the enhanced contractile response to phorbol 12,13-dibutyrate (PDBu) were examined in de-endothelialized thoracic aortas isolated from rats with dietary magnesium (Mg) deficiency. PDBu (1.0 nM)-induced contractions were significantly larger in Mg-deficient rats than in the controls. The contraction was completely inhibited by nifedipine, removal of external Ca2+ or by l-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0 microM) significantly decreased the KD value and increased the Bmax for the binding of [3H]PN200-110 to the aortas. The degree of the decrease in the KD value was significantly greater in Mg-deficient rats than in the controls. The PDBu-induced decrease in the KD value was abolished by H7. These results suggest that activation of protein kinase C by phorbol esters may participate in the activation of L-type Ca2+ channels, which increases both the affinity of [3H]PN200-110 binding and the magnitude of the external Ca(2+)-dependent contraction. Dietary Mg-deficiency may enhance these processes.

Animals↗
PubMed1990

Dementias: the role of magnesium deficiency and an hypothesis concerning the pathogenesis of Alzheimer's disease.

Evidence is presented indicating that dementias are associated with a relative insufficiency of Magnesium (Mg) in the brain. Such insufficiency may be attributable to low intake or retention of Mg; high intake of a neurotoxic metal, such as aluminum (Al), which inhibits activity of Mg-requiring enzymes; or impaired transport of Mg and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease (AD) involves a defective transport process, characterized by both an abnormally high incorporation of Al and an abnormally low incorporation of Mg into brain neurons. The hypothesis is advanced that an altered serum protein contributes to the progression of AD by having a greater affinity for Al than for Mg, in contrast to the normal protein, which binds Mg better than Al. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate Al uptake and impede Mg uptake. Evidence suggests that albumin is the serum protein that is altered.

Albumins↗