The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function in the rat

Sheri Zidenberg-Cherr, Carl L Keen, Lucille S. Hurley

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8 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)31-48
Number of pages18
JournalBiological Trace Element Research
Volume7
Issue number1
DOIs
StatePublished - Feb 1985

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Manganese
Rats
Liver
Trace Elements
Animals
Oxygen

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

Cite this

The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function in the rat. / Zidenberg-Cherr, Sheri; Keen, Carl L; Hurley, Lucille S.

In: Biological Trace Element Research, Vol. 7, No. 1, 02.1985, p. 31-48.

Research output: Contribution to journalArticle

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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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AB - 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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