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.
Original language | English (US) |
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Pages (from-to) | 31-48 |
Number of pages | 18 |
Journal | Biological Trace Element Research |
Volume | 7 |
Issue number | 1 |
DOIs | |
State | Published - Feb 1985 |
Keywords
- and mitochondrial functions
- development, and trace elements, in rats
- lipid peroxidation, and Mn deficiency
- Manganese, and mitochondrial functions
- mitochondrial function, in Mn deficient rats
- MnSOD
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology
- Biochemistry, Genetics and Molecular Biology(all)
- Biochemistry, medical
- Inorganic Chemistry
- Clinical Biochemistry
- Biochemistry