Affiliations: Department of Animal and Range Science, North Dakota
State University, Fargo, ND, USA | Grand Forks Human Nutrition Research Center, Grand
Forks, ND, USA
Note: [] Address for correspondence: Joel S. Caton, Department of Animal
and Range Science, NDSU, Fargo, ND 58105, USA. Tel.: +1 701 231 7653; Fax: +1
701 231 7590; E-mail: joel.caton@ndsu.edu
Abstract: It has previously been reported that moderately high dietary
manganese (Mn) in combination with marginal magnesium (Mg) resulted in
ultrastructural damage to heart mitochondria. Manganese may replace Mg in
biological functions, including the role of enzyme cofactor. Manganese may
accumulate and substitute for Mg during the condition of Mg-deficiency. The
objective of the current study was to determine whether high Mn alters heart
muscle respiration and Mg-enzyme activity as well as whole body Mn retention
under marginal Mg. An additional objective was to determine whether high Mn
results in increased oxidative stress. In experiment 1: forty-eight rats were
fed a 2 × 3 factorial arrangement of Mn (10, 100, or 1000 mg/kg) and Mg
(200 or 500 mg/kg). In experiment 2: thirty-two rats were fed one of four diets
in a 2 × 2 factorial arrangement of Mn (10 or 250 mg/kg) and Mg (200 or
500 mg/kg). In experiment 3: thirty-two rats were fed one of four diets in a 2
× 2 factorial arrangement of Mn (10 or 650 mg/kg) and Mg (200 or 500
mg/kg). In experiment 2, high Mn and marginal Mg reduced (P<0.05) oxygen
consumption of left ventricle muscle. Marginal Mg, but not Mn, reduced
(P<0.05) activity of sarcoplasmic reticulum calcium-ATPase enzyme. Dietary
Mg had no affect on ^{54}Mn kinetics, but high dietary Mn
decreased (P<0.01) absorption, retention, and rate of excretion of
^{54}Mn. Neither cellular stress, measured by Comet assay,
nor antioxidant activities were increased by high Mn. A strong interaction
(P<0.001) between increasing Mn and adequate Mg on hematology was observed.
These results confirm previous research in swine that high Mn alters myocardial
integrity as well as function, but not as a result of altered calcium transport
or oxidative stress.
Keywords: Manganese, magnesium, rat, heart, mitochondria
Journal: BioFactors, vol. 28, no. 1, pp. 33-46, 2006
