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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #147862
Title: DIETARY BORON SUPPLEMENTATION EFFECTIVELY MITIGATES COLLAGEN-INDUCED ARTHRITIS IN MICE

Author
item DURICK, KELLY - UNIV OF NORTH DAKOTA
item LAMOUREUX, JENNIFER - UNIV OF NORTH DAKOTA
item O'BRYANT, DEANNA - UNIV OF NORTH DAKOTA
item GRIFFITHS, MARIE - UNIV OF UTAH
item HUNT, CURTISS
item BRADLEY, DAVIS - UNIV OF NORTH DAKOTA

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 4/10/2003
Publication Date: 4/24/2003
Citation: Durick, K., Lamoureux, J., O'Bryant, D., Griffiths, M.M., Hunt, C.D., Bradley, D.S. 2003. Dietary boron supplementation effectively mitigates collagen-induced arthritis in mice [abstract]. Presented at Frank Low Research Day, University of North Dakota, School of Medicine & Health Sciences, April 24, 2003.

Interpretive Summary:

Technical Abstract: Boron is a light, non-metallic element that occurs naturally in plants and is a component of all human diets. Boric acid was patented as an anti-inflammatory agent over 30 years ago in Germany, and boron has been used as a treatment for arthritis for over 25 years in India. However, there is still very little scientific study of the mechanism or efficacy of boron in regulating inflammation. There is evidence that boric acid or substituted boric acid compounds competitively inhibit the NAD+-, NADP- and FAD-requiring oxidoreductase enzymes and serine proteases, enzymes that have many important regulatory functions in the molecular aspects of inflammation. It has been postulated that boron may be acting as an unobtrusive metabolic regulator by quenching the activity of some enzymes and/or stabilizing reactive compounds to limit a hyperactive response of the normal inflammatory process. We have previously shown that physiological amounts of boron prevent collagen-induced arthritis (CIA), a murine model of polyarthritis sharing many characteristics with human rheumatoid arthritis (RA). We present evidence here of an anti-inflammatory influence of boron on ongoing CIA. CIA-susceptible B10.T(6R) mice were weaned onto commercial rodent chow (~12.0 mg/kg boron), immunized at 6-8 weeks of age with type II collagen, and observed for the onset of clinical arthritis. At the onset of clinical signs of arthritis, mice were separated and fed one of three diets: commercial rodent chow, or a ground corn-high protein casein-corn oil-based chow (~0.04 mg/kg boron; inadequate) supplemented with 0 or 2 (adequate) mg B/kg diet. The corn-based chow was replete in all other nutrients considered essential for the mouse. The arthritic condition in mice fed either the commercial rodent chow or the boron-deficient chow worsened with time. However, progression of the clinical arthritis stopped in all mice fed the boron-adequate chow and several of these mice showed signs of recovery, as indicated by clearance of inflammation. Thus, we provide evidence that dietary boron may provide a successful alternative therapy for RA and perhaps other inflammatory diseases such as multiple sclerosis. We demonstrated previously that commercial rodent chow does not protect against the onset of collagen-induced arthritis and led us to the hypothesis that the boron in commercial chow is unavailable or that its protective effects are masked by other undefined proinflammatory dietary constituents. Therefore, the bioavailability of boron in commercial rat chow needs to be examined further.