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The effects of manganese deficiency during prenatal and postnatal development on mitochondrial structure and function
S Zidenberg-Cherr1, C L Keen, L S Hurley
1Department of Nutrition, University of California, 95616, Davis, California.
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.
Insights
Manganese deficiency in rats led to lower liver manganese and manganese-superoxide dismutase (MnSOD) activity early in development. Despite later normalization of MnSOD, mitochondrial damage occurred, suggesting a lasting impact.
Area of Science:
- Biochemistry
- Toxicology
- Developmental Biology
Background:
- Manganese is an essential trace element vital for various physiological processes.
- Manganese-superoxide dismutase (MnSOD) is a critical antioxidant enzyme.
- Manganese deficiency can impact cellular function and development.
Purpose of the Study:
- To investigate the effects of manganese deficiency on liver trace element levels.
- To assess manganese-superoxide dismutase (MnSOD) activity during postnatal development.
- To examine mitochondrial structure and function in manganese-deficient rats.
Main Methods:
- Rats were divided into normal and manganese-deficient groups.
- Liver manganese concentration was measured at various ages.
- MnSOD activity and mitochondrial function (oxygen uptake, P/O ratios) were assessed.
- Liver mitochondrial structure was examined.
Main Results:
- Manganese-deficient rats exhibited lower liver manganese concentrations throughout development.
- MnSOD activity paralleled manganese levels, being lower in deficient rats early on.
- Despite normalization of MnSOD by 9 months, mitochondrial abnormalities were observed in deficient rats.
- Oxygen uptake and P/O ratios remained normal despite mitochondrial damage.
Conclusions:
- Early manganese deficiency leads to lasting mitochondrial damage in rat livers.
- Reduced MnSOD activity during critical developmental periods may contribute to mitochondrial abnormalities.
- The functional consequences of these mitochondrial changes require further investigation.
