02086nas a2200373   4500000000100000008004100001260001300042653002500055653001200080653001100092653002000103653001200123653002600135653002900161653002800190653002000218653000900238653001500247653002800262653003000290100001600320700001600336700001100352700001400363700001500377700001400392245007700406856005900483300001000542490000700552050003200559520110700591022001401698       1995                            d  c1995 Sep10aAlkaline Phosphatase10aAnimals10aKidney10aKidney Diseases10aleprosy10aLeucyl Aminopeptidase10aLuminescent Measurements10aMacrophages, Peritoneal10aMalondialdehyde10aMice10aMicrovilli10aReactive Oxygen Species10aGamma-Glutamyltransferase1 aAgnihotri N1 aGanguly N K1 aKaur S1 aKhullar M1 aSharma S C1 aChugh K S00aRole of reactive oxygen species in renal damage in experimental leprosy.  uhttp://leprev.ilsl.br/pdfs/1995/v66n3/pdf/v66n3a02.pdf  a201-90 v66  aInfolep Library - available3 a<p>Renal involvement is known to occur in leprosy. In the present study the possible role of reactive oxygen species (ROS) in causation of renal damage in mice infected with Mycobacterium leprae has been investigated. At least six animals from each group (control and infected) were killed at 0 day, 3, 6 and 9 months postinfection. The results showed a significant increase in the chemiluminescence (CL) response of peritoneal macrophages which was maximum between 3 and 6 months. No significant increase was observed in CL response of blood neutrophils. A significant increase in lipid peroxidation was observed at 3 and 6 months as evident by an increase in malondialdehyde levels. The increased ROS production might be the cause of lipid peroxidation. The renal damage is alos evident by decrease in the activity of renal brush border membrane enzymes, namely, alkaline phosphatase, leucine aminopeptidase and r-glutamyl transpeptidase. Thus ROS might play a role during early stages of M. leprae infection but in the later stages other immunological mechanisms may overpower the effect of ROS.</p>  a0305-7518