Role of reactive oxygen species in renal damage in experimental leprosy.

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.

Renal brushborder membrane vesicle. Study of marker enzymes and uptake of nutrients in Mycobacterium leprae infected mice.

The renal brush border membrane vesicles (BBMV) were used to elucidate the early biochemical functional status during the course of experimental M. leprae infection in mice. The activities of the characteristic brush-border enzymes viz: alkaline phosphatase, leucine amino peptidase and gamma-glutamyl transpeptidase were found to be significantly decreased (p less than 0.001) at 3 and 6 months after infection. The transport of nutrients viz: D-glucose, L-alanine, L-lysine and L-aspartate across BBMV showed similar pattern. The activity of brush border enzymes and transport of nutrients across the membrane returned to normal at 9 months post-infection suggesting regeneration of the brush border membrane.