Abstract
The influence of manganese deficiency on liver trace element concentration, MnSOD activity, and mitochondrial structure and function during postnatal development was determined in rats. In both normal and manganese-deficient animals, liver manganese concentration increased with time, but in deficient rats liver manganese was lower than in controls at all ages measured. At 9 mo of age, liver manganese concentration in the deficient rats was only 20% that of controls. The developmental pattern observed for MnSOD paralleled that of liver manganese concentration in normal and deficient rats; it was lower than in controls on days 20 and 60. However, at 9 mo of age, MnSOD levels were similar in the two groups. Although there were no differences at 9 mo of age in MnSOD activity between the groups, manganese-deficient rats showed mitochondrial abnormalities in liver. Despite mitochondrial abnormalities, however, oxygen uptake and P/O ratios were normal. We suggest that the mitochondrial damage apparent at 9 mo of age is, at least in part, the result of lower than normal MnSOD activity occurring earlier. The functional significance of the abnormalities remains to be established.
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Zidenberg-Cherr, S., Keen, C.L. & Hurley, L.S. The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function in the rat. Biol Trace Elem Res 7, 31–48 (1985). https://doi.org/10.1007/BF02916545
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DOI: https://doi.org/10.1007/BF02916545