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More fish oil, less vegetable oil, better for your health

easing the amount of fish oil did not change the way it binds to COX-2, so a significant portion of vegetable oil was still converted to prostanoids.

This was completely unexpected, Smith says. This new result shows that COX-2 does not prefer fish oil to vegetable oil. Regardless of the amount of extra fish oil that we added, COX-2 still helped convert all the vegetable oil available.

This finding reveals for the first time a limit to how the body naturally regulates levels of prostanoids produced by fish and vegetable oil. If both oil types are present in the body, levels of prostanoids from fish oil will, in general, be higher than those coming from vegetable oil, but mechanisms such as the one involving COX-2 can counter this trend.

The researchers are now investigating why COX-1 and COX-2 act differently. One possibility is that since COX-2 has two binding sites, it can bind to both fish and vegetable oils. When fish oil binds to one of the two sites, it may prepare the other site to bind more easily to vegetable oil, a process called allostery.

Smith and his colleagues hope that by further investigating how prostanoids are regulated in the body, they can design potential drugs that bind to COX-2 and decrease levels of the vegetable oil prostanoids.

The drugs that are currently used to inhibit COX-1 and COX-2 provide relief from the symptoms of inflammation and pain, but they still have many side effects, Smith says. By better understanding how prostanoids work at the cellular level, we hope to find new ways to regulate inflammation and create better anti-inflammatory drugs.


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Contact: Pat Pages
ppages@asbmb.org
301-634-7366
American Society for Biochemistry and Molecular Biology
26-Jul-2007


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