Disease relevance of EINECS 206-865-2

• D-Saccharic acid-1,4-lactone inhibited the increase in mutagenicity produced by the faecal extracts and extracts of beta-glucuronidase-positive bacteria except for Peptostreptococcus strains 204 and 952 [1].

High impact information on EINECS 206-865-2

• The apparent Km and Vmax values for the formation of DAG in the absence and presence of 4 mM D-saccharic acid-1,4-lactone (saccharolactone) were the following: Km = 0.05 +/- 0.02 vs 0.08 +/- 0.02 mM and Vmax = 0.20 +/- 0.06 vs 0.43 +/- 0.07 nmol/min/mg protein (0 and 4 mM saccharolactone, respectively) [2].
• The reaction products extracted into ethyl acetate were characterized by their mobilities in thin-layer chromatography and identified as glucuronides by their sensitivity to hydrolysis with beta-glucuronidase and inhibition of hydrolysis by the specific beta-glucuronidase inhibitor D-saccharic acid-1,4-lactone [3].

Biological context of EINECS 206-865-2

• The identity of the glucuronides is shown by their response to hydrolysis by beta-glucuronidase in the presence and absence of D-saccharic acid-1,4-lactone and, in some instances, by chromatographic and spectral analyses of the released aglycones [4].

Analytical, diagnostic and therapeutic context of EINECS 206-865-2

• The bile acid glucuronides were characterized by their mobilities in thin-layer chromatography and identified by their sensitivity to hydrolysis with beta-glucuronidase and inhibition of hydrolysis by the specific beta-glucuronidase inhibitor D-saccharic acid-1,4-lactone [5].

References