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Decrease of hepatic delta-aminolevulinate dehydratase activity in an animal model of fatigue
Tsuyoshi Tahara1, Masaaki Tanaka, Satoshi Nozaki
1Department of Physiology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585, Japan.
Biochemical and Biophysical Research Communications
|January 6, 2007
Summary
Researchers identified delta-aminolevulinic acid (ALA) as a potential biomarker for fatigue. Increased ALA levels in plasma and urine of fatigued rats suggest its utility in fatigue diagnostics.
Area of Science:
- Biochemistry
- Physiology
- Biomarker Discovery
Background:
- Fatigue is a physiological inability to maintain power output, lacking standardized biomarkers.
- The heme biosynthetic pathway involves key enzymes and intermediates, including delta-aminolevulinic acid (ALA).
Purpose of the Study:
- To investigate delta-aminolevulinic acid (ALA) levels as potential biomarkers for fatigue.
- To examine the activity and gene expression of heme biosynthesis enzymes during fatigue and recovery.
Main Methods:
- Induced fatigue in rats by housing them in shallow water for 5 days.
- Measured plasma and urinary ALA levels.
- Assessed liver ALA dehydratase (ALAD) activity and gene expression.
- Measured liver ALA synthase (ALAS) activity.
Main Results:
- Fatigued rats showed increased plasma and urinary ALA levels compared to controls.
- ALAD activity and gene expression in the liver were decreased in fatigued rats.
- ALAS activity in the liver was increased in fatigued rats.
- ALA levels and ALAD activity/expression returned to normal after 1 day of rest.
Conclusions:
- Elevated plasma and urinary ALA levels can serve as biomarkers for fatigue.
- Changes in heme biosynthesis enzymes (ALAD, ALAS) are associated with fatigue.
- ALA levels and enzyme activity/expression are reversible upon recovery from fatigue.
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