Onion Extract Inhibits Bone Resorption

Researchers studying osteoporosis used a rat model to show that a compound isolated from white onions decreased bone loss by inhibiting osteoclast bone absorption activity.

Osteoclasts are multinucleated cells that degrade and reabsorb old bone. They lie in small cavities called Howship's lacunae, formed from the digestion of the underlying bone. The sealing zone is the attachment of the osteoclast's plasmalemma to the underlying bone. The osteoclasts release hydrogen ions into the cavity, acidifying and dissolving the mineralized bone matrix.

In addition, several hydrolytic enzymes are released by lysosomes to digest the organic components of the matrix, such as collagenase and cathepsin K. Products of digestion, such as calcium and phosphate ions, are absorbed into small vesicles that move across the cell and are eventually released into the extracellular fluid. Several hormones, including parathyroid hormone (PTH) and interleukin 6 (IL-6) regulate osteoclast activity.

Investigators at the University of Bern (Switzerland; www.unibe.ch) extracted onion powder and fractionated the extract by column chromatography and medium-pressure liquid chromatography. A single active peak was obtained by semi-preparative high-performance liquid chromatography. This material was tested on isolated rat osteoclasts growing in tissue culture and was found to reduce bone resorption.


The investigators reported in the March 30, 2005, online edition of the Journal of Agricultural and Food Chemistry that analysis of the onion fraction by high-performance liquid chromatography-electrospray ionization-mass spectrometry, time-of-flight electrospray ionization mass spectrometry, and nuclear magnetic resonance spectroscopy showed the active single peak to be gamma-L-glutamyl-trans-S-1-propenyl-L-cysteine sulfoxide (GPCS). It is a peptide with a molecular mass of 306 Daltons that demonstrated dose-dependent inhibition of osteoclast resorption activity with the minimal effective dose being about 2 mM.




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