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Increase in complement component C3 is an early response to experimental magnesium deficiency in rats
F I Bussière1, A Tridon, W Zimowska
1Centre de Recherches en Nutrition Humaine d'Auvergne, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 St-Genès-Champanelle, France.
Life Sciences
|May 22, 2003
Summary
Magnesium deficiency triggers an early inflammatory response, increasing complement C3 levels in plasma and liver. However, complement activation is not involved in the acute phase of this deficiency.
Area of Science:
- Biochemistry
- Immunology
- Nutritional Science
Background:
- The inflammatory process is key in experimental magnesium deficiency.
- The exact sequence of events leading to inflammation in magnesium deficiency is unclear.
Purpose of the Study:
- To investigate the effect of magnesium deficiency on the complement system.
- To analyze complement C3 concentration, mRNA levels, and activation.
Main Methods:
- Rats were fed magnesium-deficient or control diets for 2 or 8 days.
- Measurements included total C3 concentration, liver C3 mRNA abundance (RT-PCR), haemolytic activity, and C3 activation (Western Blot).
Main Results:
- Magnesium deficiency induced inflammation (hyperaemia, leukocytosis, enlarged spleen) by day 8.
- Total plasma C3 and liver C3 mRNA levels increased in deficient rats.
- Elevated C3 suggests inflammation is an early event, but C3 cleavage was not detected.
Conclusions:
- Increased complement C3 indicates inflammation is an early response to magnesium deficiency.
- Complement activation does not appear to be involved in the acute phase of magnesium deficiency.