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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 452546, 8 pages
Research Article

Oxidative Stress and Free-Radical Oxidation in BCG Granulomatosis Development

1Research Center of Clinical and Experimental Medicine, USA
2University of Michigan School of Medicine, USA
3Novosibirsk State Medical University, Russia

Received 9 February 2013; Revised 30 March 2013; Accepted 1 April 2013

Academic Editor: Manikandan Panchatcharam

Copyright © 2013 Elena Menshchikova et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Little is known about the role of free-radical and oxidative stress signaling in granuloma maturation and resolution. We aimed to study the activity of free-radical oxidation processes in the dynamics of BCG-induced generalized granulomatosis in mice. Methods. Chronic granulomatous inflammation was induced in male BALB/c mice by intravenously injecting the BCG vaccine, and the production of oxidative stress (activity of free-radical oxidation processes) and histological changes in the lungs, liver, and peritoneal exudate were measured 3, 30, 60, and 90 days after infection. Results. The tuberculous granuloma numerical density and diameter continuously increased from day 30 to day 90, and the macrophage content within the granulomas progressively diminished with a concomitant elevation in the number of epithelioid cells. The activity of the free-radical oxidation processes in the liver (i.e., the intensity of the homogenate chemiluminescence) reached a maximum at postinfection day 60 and subsequently began to decrease. The peak generation of reactive oxygen species by phagocytes in the peritoneal exudate (measured using flow cytometry) was also shifted in time and fell on day 30. Conclusions. The rise in the steady-state concentration of H2O2 in the liver of mice with BCG-induced granulomatosis is not related to local H2O2 production by phagocytes, and a decrease in the severity of generalized inflammation precedes the resolution of local inflammation.