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Journal of Dental Research, Vol 69, 1131-1137, Copyright © 1990 by International & American Associations for Dental Research Online Journals
ARTICLES |
C. H. Sissons, H. E. Perinpanayagam, E. M. Hancock and T. W. Cutress
Dental Research Unit, Medical Research Council of New Zealand, Wellington.
Potential mechanisms for regulation of urease levels in Streptococcus salivarius were examined, including: induction by urea, nitrogen or carbon source repression, and effects of pH and CO2 (because CO2 enrichment enhanced urease detection on urea agar plates). Regulation by either pH or CO2 was confirmed by comparison of the urease accumulation pattern during anaerobic growth under CO2 with that under N2. Under CO2, there was an initial buffering plateau at pH 6.2 and a rate of Streptococcus salivarius urease accumulation three-fold that under N2, with a pH 7.6 plateau. With both gas phases there was also an increase in the rate of urease appearance coincident with the decrease in medium pH following the pH plateau. The effects of pH, CO2, and HCO3- on urease levels and on growth were separately assessed by culture in media containing 0, 25, 100 mmol/L KHCO3 buffered at different pH levels. There was an inverse relationship between the logarithm of the urease level after 24-hour growth and the pH during growth-the urease specific activity was 100-fold higher at pH 5.5, compared with pH 7.0 and above. HCO3-/CO2 (100 mmol/L) had little effect on urease levels, but was essential for growth at pH 5.5. There was no significant urease induction by urea, or repression by ammonia or glucose. There was also evidence of pH regulation of urease levels in some staphylococci, Klebsiella pneumonia, and Corynebacterium renale, but not in Actinomyces naeslundii and several other species. We conclude that the external pH is a major factor regulating urease levels in S. salivarius and possibly some other species-a mechanism equivalent to urease repression by OH-.
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