Related Experiment Videos
Anthocyanin administration elevates plasma homocysteine in rats.
Kiyotaka Nakagawa1, Yumiko Maruyama, Teruo Miyazawa
1Food & Biodynamic Chemistry Laboratory, Graduate School of Life Science and Agriculture, Tohoku University, Sendai 981-8555, Japan.
Journal of Nutritional Science and Vitaminology
|May 31, 2003
Summary
Dietary anthocyanins, found in food colorants, significantly increased plasma homocysteine levels in rats. This suggests anthocyanins may impact sulfur amino acid metabolism and potentially cardiovascular disease risk.
Area of Science:
- Biochemistry
- Nutritional Science
- Cardiovascular Research
Background:
- Elevated plasma homocysteine is linked to increased cardiovascular disease risk.
- Dietary factors influencing homocysteine levels, beyond folate and B-vitamins, are largely unknown.
- Anthocyanins, dietary phenolics, possess a chemical structure suggesting potential effects on methionine metabolism.
Purpose of the Study:
- To investigate the effect of dietary anthocyanin administration on plasma homocysteine concentrations in rats.
- To explore the impact of anthocyanins on sulfur amino acid metabolism in the liver and kidney.
Main Methods:
- Female Sprague-Dawley rats were administered a single oral dose of an anthocyanin mixture.
- Plasma homocysteine levels were measured at intervals post-administration.
- Sulfur amino acid levels (SAM, SAH) and the SAH/SAM ratio were analyzed in liver and kidney tissues.
Main Results:
- Anthocyanin intake resulted in a 1.4 to 1.8-fold increase in plasma homocysteine levels.
- Significant alterations in S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) levels were observed in the liver and kidney.
- The SAH/SAM ratio increased significantly in both liver and kidney tissues.
Conclusions:
- Dietary anthocyanins stimulate homocysteine synthesis from SAH in rat liver and kidney.
- Increased homocysteine produced in these organs transfers to the bloodstream.
- Anthocyanin consumption may influence sulfur amino acid metabolic regulation and potentially increase vascular disease risk in humans.