Degradation of starch and its hydrolytic products by oral bacteria.

Abstract:

:Selected strains of oral bacteria were analyzed for their ability to degrade wheat starch, maltose, maltotriose, and maltoheptaose. S. sanguis IUOM-11M and JC804, S. mutans 6715, S. salivarius IUOM-8, A. viscosus IUOM-62, and A. naeslundii ATCC 12104 degraded all four substrates. S. mutans NCTC 10449 degraded starch, maltose, and maltotriose, while A. viscosus ATCC 15987 degraded starch and maltose, and S. sanguis SS34 degraded only maltose. L. casei IUOM-14 did not degrade any of the substrates. Analysis of starch degradation products from S. sanguis IUOM-11M and A. viscosus IUOM-62 demonstrated oligosaccharides, maltose, and trace amounts of glucose for the former and oligosaccharides, maltotriose, and maltose for the latter. S. sanguis IUOM-11M alpha-glucosidase (EC 3.2.1.20) demonstrated a pH optimum of 6.5 and greatly enhanced activity from maltose-cultured cells as compared with cells cultured in glucose or fructose. The presence of fructose in the growth medium prevented this enhancement of activity by maltose. Maltose inhibited sucrose-dependent synthesis of S. sanguis IUOM-11M insoluble polysaccharide and both primer-dependent and primer-independent synthesis of soluble polysaccharide. Maltoheptaose inhibited primer-dependent but not primer-independent soluble polysaccharide synthesis. Several oral bacteria have the ability to hydrolyze starch and to degrade further the products to acidogenic substrates. These products may also inhibit sucrose-dependent synthesis of polysaccharides, which enhances the production of the acidogenic substrate fructose. The results add further support to the growing body of evidence suggesting that caries-promoting properties of starch may be expressed only when starch is present in diets containing sucrose.

journal_name

J Dent Res

authors

Glor EB,Miller CH,Spandau DF

doi

10.1177/00220345880670011501

keywords:

subject

Has Abstract

pub_date

1988-01-01 00:00:00

pages

75-81

issue

1

eissn

0022-0345

issn

1544-0591

journal_volume

67

pub_type

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