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Table of Contents | |
MANGANESE AND MAGNESIUM
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J Nutr 2000 Aug;130(8):2032-5 |
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High dietary manganese lowers heart magnesium in pigs fed
a low-magnesium diet.
Miller KB, Caton JS, Schafer DM, Smith DJ, Finley JW
Department of Animal and Range Science, North Dakota State University (NDSU),
Fargo 58105, USA.
Young pigs were fed a diet moderately high or low in manganese (Mn) (0.95
+/- 0.10 mmol Mn/kg, n = 8 or 0.040 +/- 0.003 mmol Mn/kg, n = 6) and
deficient in magnesium (Mg) (4.1 mmol Mg/kg) for 5 wk. All eight pigs
consuming the high Mn diet died following convulsive seizures, whereas only
two of six died in the group fed low Mn. In an attempt to determine the
cause of death, a subsequent study examined the interactive effect of
deficient dietary Mg and Mn on the tissue distribution of Mg and Mn. Pigs
were individually fed, for 5 wk, diets that contained: 4.1 mmol Mg/kg and
36.0 micromol Mn/kg, 4.1 mmol Mg/kg and 0.91 mmol Mn/kg, 4.1 mmol Mg/kg and
0.91 mmol Mn/kg with added ultratrace minerals, or 41.1 mmol Mg/kg and 0. 91
mmol Mn/kg, and ultratrace minerals. Liver and skeletal muscle Mn
concentrations were significantly elevated by increased dietary Mn.
Increased dietary Mn did not affect heart Mn, but heart Mg concentrations
were significantly depressed by high, as compared to low, dietary Mn (38.7
+/- 3.3 vs. 32.7 +/- 2.6 mmol Mg/kg). These data suggest high dietary Mn may
exacerbate Mg deficiency in heart muscle and thus may be a complicating
factor in the deaths observed in Mg-deficient pigs.
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J Am Coll Nutr 1999 Oct;18(5):475-80 |
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Magnesium-manganese interactions caused by magnesium
deficiency in rats.
Sanchez-Morito N, Planells E, Aranda P, Llopis J
Department of Physiology, School of Pharmacy and Institute of Nutrition and
Food Technology, University of Granada, Spain.
OBJECTIVE: We investigated the effect of dietary magnesium (Mg) deficiency
on the nutritive utilization and tissue distribution of manganese (Mn).
METHODS: Wistar rats were fed a Mg-deficient diet (56 mg/kg) for 70 day.
Absorbed Mn, Mn balance and Mn content in plasma, whole blood, skeletal
muscle, heart, kidney, liver, femoral bone and sternum were determined after
21, 35 and 70 days. RESULTS: The Mg-deficient diet significantly increased
Mn apparent absorption and Mn balance from week five until the end of the
experimental period. This effect was accompanied by a significant increase
in the concentration of Mn in heart at all three time points. Whole blood,
skeletal muscle and kidney Mn were significantly increased from day 35, and
femur Mn content was increased only at the end of the study (day 70).
However, Mn concentration in the sternum decreased significantly from day
35. No changes were found in liver Mn content. CONCLUSION: Mg deficiency
increased Mn absorbed, and this favored the deposition of Mn in all
tissues studied except the liver and trabecular bone. The lack of response
by the liver to increased Mn absorption may have led to the redistribution
of this ion to other tissues.
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Neurotoxicology 1995 Fall;16(3):511-7 |
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Effects of calcium-deficient diets on manganese
deposition in the central nervous system and bones of rats.
Yasui M, Ota K, Garruto RM
Division of Neurological Diseases, Wakayama Medical College, Japan.
The presence of both aluminum (Al) and manganese (Mn) in central nervous
system tissues (CNS) has been reported in Parkinson's disease and in
parkinsonism-dementia (PD) on Guam. Epidemiological surveys on Guam have
suggested that low calcium (Ca), magnesium (Mg) and high Al and Mn in river,
soil and drinking water may be implicated in the pathogenesis of PD.
Experimentally, low Ca-Mg diets with or without added Al have been found to
accelerate Al deposition in the CNS of rats and monkeys. Although excessive
deposition of Mn produces similar neurotoxic action to Al in CNS tissues,
the mechanism of Mn deposition coupled with Al loading in the presence of
low Ca-Mg intake is not yet known. In this study, the deposition and
mental-metal interaction of both Al and Mn in the CNS, visceral organs and
bones of rats fed unbalanced mineral diets were analyzed. Male Wistar rats,
weighing 200 g, were maintained for 90 days on the following diets: (A)
standard diet, (B) low Ca diet, (C) low Ca-Mg diet, (D) low Ca-Mg diet with
high Al. Al and Mn content were determined in the frontal cortex, spinal
cord, kidney, muscle, abdominal aorta, femur and lumbar spine using neutron
activation analysis (NAA). Our results demonstrate that serum Ca levels were
decreased in the following dietary order: C<D<B<A. Serum Mg levels
were significantly lower in rats from Groups C and D, compared with those in
Groups A and B, reflecting the content of Mg and other interacting minerals
in the diet. There was no significant difference in serum Al, zinc and
phosphorus levels. Ca and Mg contents in lumbar vertebrae and the femur were
significantly lower and Al levels significantly higher in rats maintained on
the low Ca-Mg diet with or without added Al. Al content in CNS tissues and
visceral organs were highest in rats fed diets deficient in Ca alone or low
in Ca-Mg with or without added Al. Bone Mn levels significantly increased in
rats fed the low Ca-Mg diet with added Al. Mn content in the frontal cortex
significantly increased in rats fed diets low in Ca-Mg with or without added
Al. But the Mn content of other tissues including the spinal cord, kidney,
muscle and abdominal aorta was unchanged in rats given Ca deficient diets.
Intake of low Ca and Mg with added Al in rats led to the high concentrations
of Mn and Al in bones and in the frontal cortex. We conclude that unbalanced
mineral diets and metal-metal interactions may lead to the unequal
distribution of Al and Mn in bones and ultimately in the CNS inducing CNS
degeneration.
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