Ryo Nakamura,† Gian Paolo Littarru,† Karl Folkers,† and Edward G. Wilkinson‡
†Institute for Biomedical Research, The University of Texas at Austin, Austin, Texas 78712 ‡Wilford Hall USAF Medical Center, Department of Periodontics, Lackland Air Force Base, San Antonio, Texas
* This is publication No. 171 in a series on coenzyme Q.
Proc Natl Acad Sci U S A. 1974 April; 71(4): 1456–1460.
Abstract The specific activities of both the succinate dehydrogenase-coenzyme Q10 reductase and the DPNH-cytochrome c reductase [NADH:(acceptor) oxidoreductase, EC 1.6.99.3] were determined in mitochondria from 40 diseased gingival biopsies from patients with periodontal disease and from 24 control biopsies from nondiseased areas (clinically evaluated) of gingival tissues from the same mouths of the patients from whom the diseased gingival tissues were taken. The control tissue was taken during normal surgical procedures, such as for gingival recontouring and tuberosity removal.
The diseased gingival biopsies showed a mean specific activity for the succinate dehydrogenase-coenzyme Q10 reductase which was higher (P < 0.02) than that of the control biopsies, and which increased (P < 0.01) when the assays utilized exogenous coenzyme Q3, and corresponded to an average deficiency of coenzyme Q10-enzyme activity of 35%.
About 60% of the 40 diseased gingival tissues showed a deficiency of coenzyme Q10 at its site in this succinate-coenzyme Q10 enzyme. Of the 24 control tissues, 20% showed deficiencies of coenzyme Q10. As a group, the control tissues showed no deficiency of coenzyme Q10. No deficiency of coenzyme Q10 at its site in DPNH-cytochrome c reductase was observed for either the control or diseased gingival tissues, as groups or individually.