OBJECTIVES

Leprosy is a chronic granulomatous infection caused by Mycobacterium leprae involving cutaneous tissue and peripheral nerves producing skin lesions, nerve degeneration, anaesthesia and deformities. In leprosy, the activated phagocytes produce reactive oxygen species (ROS) as a part of their microbicidal function. Such ROS are capable of damaging the host tissue by lipid peroxidation. Increased lipid peroxidation has been reported in leprosy. The glutathione antioxidant system with glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione (GSH) as components protect the cells from ROS toxicity and lipid peroxidation. The objective of the present study was to assess blood glutathione content and erythrocyte antioxidant enzyme activities of glutathione peroxidase and glutathione reductase in leprosy.

DESIGN

The parameters were studied in 100 leprosy patients and 50 normal healthy controls. The data was analysed by grouping the patients into Ridley-Jopling (RJ) types [tuberculoid leprosy (TT), borderline tuberculoid leprosy (BT), borderline leprosy (BB), borderline lepromatous leprosy (BL), lepromatous leprosy (LL)] and into different levels of Bacteriological Index (BI) [bacteriologically negative (BI=0), BI=0.1-1, BI=1.1-2, BI=2.1-3, BI=3.1-4, BI=4.1-6].

METHODS

Venous blood sample was used for the study. The GSH level was estimated in the blood by DTNB [5,5'-dithiobis(2-nitrobenzoic acid)] reduction method. The enzyme activities were measured in the red blood cell haemolysate by kinetic methods using NADPH.

RESULTS

GSH, GSH-Px and GR were significantly low in leprosy (total patients) as compared to the control group (p<0.001). A progressive decrease in GSH level and enzyme activities was noted along the leprosy spectrum from TT to LL. A significant decline of GSH in BB (p<0.05), BL (p<0.005) and LL (p<0.001); and of GSH-Px and GR in BT (p<0.05, p<0.02), BB (p<0.02), BL (p<0.005) and LL (p<0.001) was noted as compared to controls. A significant lowering of GSH-Px in LL (p<0.005); the GR in BB (p<0.02), BL (p<0.05) and LL (p<0.05); and the GSH in BL (p<0.01) and LL (p<0.001) was noted in comparison to the TT group. The GSH and GSH-Px were significantly low in LL (p<0.05) as compared to BT. A progressive decreasing trend in GSH level and enzyme activities was also noticed along the leprosy groups with advancing level of BI. The GSH, GSH-Px and GR were significantly low in BI levels 1.1-2 (p<0.005, p<0.05, p<0.02), 2.1-3 (p<0.005, p<0.001, p<0.005), 3.1-4 (p<0.005) and 4.1-6 (p<0.01, p<0.005, p<0.05) as compared to controls. A significant decline in GSH was noted in BI levels 1.1-2 (p<0.005), 2.1-3 (p<0.005), 3.1-4 (p<0.005) and 4.1-6 (p<0.01) as compared to the bacteriologically negative group. The GSH-Px (p<0.05) and GR (p<0.05) were significantly low in BI levels 2.1-3, 3.1-4 and 4.1-6 as compared to the bacteriologically negative group.

CONCLUSION

The findings suggest oxidative stress associated with diminished antioxidant defence potential in leprosy. The study identifies association of diminished antioxidant potential with bacterial load and type of leprosy.