02294nas a2200397   4500000000100000008004100001260001700042653001200059653001800071653001200089653002500101653001100126653001800137653001800155653002300173653001100196653002000207653001200227653000900239653000900248653002100257653002900278653002500307653003100332653002600363653001600389100001300405700001700418700001400435245019600449856004100645300000900686490000700695520118000702022001401882       1975                            d  c1975 Jan-Mar10aAnimals10aAscorbic Acid10aDapsone10aDepression, Chemical10aFemale10aGlucaric Acid10aGlucuronidase10aHistocytochemistry10aHumans10aHyaluronic Acid10aleprosy10aMale10aMice10aMice, Inbred C3H10aMycobacterium Infections10aMycobacterium leprae10aMycobacterium lepraemurium10aStimulation, Chemical10aSugar Acids1 aMatsuo E1 aSkinsnes O K1 aChang P H00aAcid mucopolysaccharide metabolism in leprosy. 3. Hyaluronic acid mycobacterial growth enhancement, and growth suppression by saccharic acid and vitamin C as inhibitors of beta-glucuronidase.  uhttp://ila.ilsl.br/pdfs/v43n1a01.pdf  a1-130 v433 a<p>A series of pilot studies are presented utilizing mouse and human infections with M. leprae and mouse infections with M. lepraemurium relating to the previously reported finding that hyaluronic acid seems to be a major nutrient substrate for these bacilli. The "feeding" of hyaluronic acid to the bacilli enhanced the growth of M. leprae in mouse abdominal walls and increased the Morphologic Index of M. lepraemurium infection. Saccharic acid, an inhibitor of beta-glucuronidase previously reported as present in these leprosy bacilli, caused marked regression of advanced M. lepraemurium infection, inhii. Ascorbic acid (vitamin C), also an inhibitor of beta-glucuronidase, given at a level of 1.5 gm/day for 4.5 months to one lepromatous patient without other treatment and for up to 24 months to four other lepromatous patients receiving DDS, was accompanied by lesion regression and changes in bacillary morphology similar to those seen in the inhibitor treated mice. If these observations are confirmed the possible use of beta-glucuronidase inhibitors as a useful adjunct to other leprosy therapy is raised as is also the likelihood of developing new therapies.</p>  a0148-916X