By Neal E. Artz, Elizabeth M. Osman
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Additional resources for Biochemistry of Glucuronic Acid
I-butyrate (which does not form a conjugate of glucuronic acid). Both sodium ter£-butylacetate and Z-menthol increased the excretion of glucuronic acid and it therefore appeared that liver glycogen is a precursor of glucuronic acid. Further evidence that glycogen is a precursor of glucuronic acid may lie in the experiments of Schmid (378) on hibernating frogs. The well-fed frog is able to produce conjugated glucuronic acid in response to various toxic substances. Whereas the liver of a well-fed frog contains 60-200 mg.
On the contrary, methyl alcohol apparently did not increase glucuronic acid production. p. 09°) which has been isolated from the urine of rabbits after ingestion of the alcohol (95). Trichloroethyl alcohol appears to be excreted partly unchanged and partly as trichloroethyl glucuronoside (urochloralic acid) (216). Secondary Alcohols. In addition to reporting that primary alcohols cause an increased excretion of glucuronic acid, Neubauer (299) claimed a similar effect after administration of isopropyl, sec-butyl and seooctyl alcohols.
The well-fed frog is able to produce conjugated glucuronic acid in response to various toxic substances. Whereas the liver of a well-fed frog contains 60-200 mg. 25 mg. during the period of hibernation. Schmid kept three groups of frogs in jars containing 50 ml. of water. The first group was well fed, the second starved, and the third was starved but the water in this jar contained glucose or glycogen. Each animal then received 15-20 mg. of menthol orally. In the first and third groups there resulted no sign of intoxication and the surrounding water eventually gave a positive Tollens naphthoresorcinol test for glucuronic acid.
Biochemistry of Glucuronic Acid by Neal E. Artz, Elizabeth M. Osman