Experimental Calcium-Magnesium Deficiency in Rats: Chemical and Histochemical Study

Kumamoto, Tetsuzo; Nakagawa, Shiro; Suematsu, Chiharu; Shimizu, Eiichi; Yata, Y; Hirohata, Tajimi

doi:10.1267/ahc.8.294

Cited by 11 publications

(3 citation statements)

References 11 publications

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“…Several animal studies explored the influence of reduced dietary levels of Ca and Mg, and whether these deficiencies interact with environmental heavy metals. Kumamoto et al (1975) fed rats for 6 weeks on a diet that contained 0.4% of the normal Ca and 20% of the normal Mg. Kumamoto et al (1975) found increased Ca in spinal cord, kidney, and muscle tissues and decreased Ca in blood serum, cerebellum, liver and intestines. Nakagawa et al (1977) measured Ca levels in spinal cords of these rats by electron probe microanalysis and demonstrated a 6-fold rise in Ca in the Ca and Mg deficient rat spinal cords as well as a 6-fold elevation in number of motor neurons affected when compared with controls.…”

Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

“…Results demonstrated similar motor neuron pathology in all monkeys on the Ca deficient diet regardless of supplementation with the Al, Mn, or cycad flour although the animals were clinically normal at the end of the study. Evidence indicated that the Ca deficiency led to an abnormal absorption of toxic metals and neuropathology (Kumamoto et al 1975; Yase 1979; Yasui et al 1991b; Yoshimasu et al 1976). Yasui et al (1991b, 1997) evaluated the influence of a 90-day Ca-deficient diet in rats, where the treatment groups were either Ca deficient (0.24% of control), Ca and Mg deficient (0.67% of control for Mg), or Ca and Mg deficient and supplemented with Al (19.4-fold higher than controls).…”

Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

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A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Chernoff

Hill

Diggs

et al. 2017

Journal of Toxicology and Environmental Health, Part B

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The compound BMAA (β-N-methylamino-L-alanine) has been postulated to play a significant role in four serious neurological human diseases: Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) found on Guam, and ALS, Parkinsonism, and dementia that occur globally. ALS/PDC with symptoms of all three diseases first came to the attention of the scientific community during and after World War II. It was initially associated with cycad flour used for food because BMAA is a product of symbiotic cycad root-dwelling cyanobacteria. Human consumption of flying foxes that fed on cycad seeds was later suggested as a source of BMAA on Guam and a cause of ALS/PDC. Subsequently, the hypothesis was expanded to include a causative role for BMAA in other neurodegenerative diseases including Alzheimer's disease (AD) through exposures attributed to proximity to freshwaters and/or consumption of seafood due to its purported production by most species of cyanobacteria. The hypothesis that BMAA is the critical factor in the genesis of these neurodegenerative diseases received considerable attention in the medical, scientific, and public arenas. This review examines the history of ALS/PDC and the BMAA-human disease hypotheses; similarities and differences between ALS/PDC and the other diseases with similar symptomologies; the relationship of ALS/PDC to other similar diseases, studies of BMAA-mediated effects in lab animals, inconsistencies and data gaps in the hypothesis; and other compounds and agents that were suggested as the cause of ALS/PDC on Guam. The review concludes that the hypothesis of a causal BMAA neurodegenerative disease relationship is not supported by existing data.

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Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

Section: Alternate Hypotheses Of Causal Factors Related To Als/pdcmentioning

confidence: 99%

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Chernoff

Hill

Diggs

et al. 2017

Journal of Toxicology and Environmental Health, Part B

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show abstract

“…the experimental animals showed the following morphological changes in both CNS and muscle tissues [10. 11]: Ca deposition in anterior horn of the spinal cord, type 1 fiber atrophy and mild type 2 fiber hypertrophy: the Ca content in the spinal cord was higher than that in controls, while the Mg content showed slight decrease: additionally, these changes were more prominent in the rats fed the low Ca-Mg diet than those fed only a low Ca diet [10], Experimental animals exhibited mild Ca and A1 deposition and degenerative changes in motor neurons of the spinal cord, brainstem, substantia nigra and cerebrum [11], These morphological changes were accelerated by the added oral administra tion of A1 to a low Ca-Mg diet, and the same phenomenon was observed in mineral metabolism of rats [12], At the site of motor neuron death and degeneration of spinal cord tracts of ALS cases. Ca-hydroxyapatite forma tion, suspected to be responsible for the ALS pathogene sis, was observed [2,13].…”

mentioning

confidence: 99%

Magnesium and Calcium Contents in CNS Tissues of Amyotrophic Lateral Sclerosis Patients from the Kii Peninsula, Japan

Yasui¹,

Yase²,

Kihira³

et al. 1992

Eur Neurol

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To further elucidate the involvement of metals as a factor in the pathogenesis of amyotrophic lateral sclerosis (ALS) on the Kii peninsula of Japan, a well-known high incidence area of ALS with low calcium and magnesium contents in soil and drinking water, we determined concentrations of these metals in samples of central nervous system tissue taken from postmortem ALS cases. Calcium content was determined by neutron activation analysis and magnesium by inductively coupled argon plasma emission spectrometry. From 5 ALS cases and 5 neurologically normal controls, we examined tissues from the precentral gyrus, including the motor cortex, internal capsule, cms cerebri and spinal cord, and from 22 other areas. The average calcium content in precentral gyrus, internal capsule, crus cerebri and spinal cord in ALS cases was higher than that in the controls, and the mean value of all 26 areas in the ALS cases was also higher than that of the controls. The average magnesium content of each region as well as the mean value of the 26 regions in the ALS cases was significantly lower than that in the controls. The Ca/Mg ratio of the 26 ALS regions was significantly higher than that of controls. This study strengthens our hypothesis that an abnormal metal metabolism plays a responsible role in the Ca-hydroxyapatite formation observed in central nervous system tissue of ALS cases, leading to motor neuron death and degeneration of the pyramidal tracts.

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Amyotrophic Lateral Sclerosis Toxic and Animal Models

Kidman¹,

Gow²,

Johanson³

et al. 1983

Molecular Pathology of Nerve and Muscle

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Experimental Calcium-Magnesium Deficiency in Rats: Chemical and Histochemical Study

Cited by 11 publications

References 11 publications

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans

Magnesium and Calcium Contents in CNS Tissues of Amyotrophic Lateral Sclerosis Patients from the Kii Peninsula, Japan

Amyotrophic Lateral Sclerosis Toxic and Animal Models

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