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Mentions: The EPR signals of MNIC–DETC recorded in the lungs, spleen, liver and kidney tissues of mice 2 weeks after their infection with the drug-resistant or drug-sensitive strain of Mtb are shown in Fig. 1. Regarding their shape and spectroscopic characteristics (g = 2.035, presence of a triplet hyperfine structure determined by interaction of the unpaired electron with the nitrogen nucleus of NO, etc.), these signals are identical with those reported previously for MNIC–DETC [29, 30, 33–41]. The concentrations of NO incorporated into MNIC–DETC in lung, spleen, liver and kidney tissues during 30 min estimated from the corresponding EPR signals are listed in Table 1. For comparison sake, Table 1 provides the NO content in respective organs of control (noninfected) animals. From Table 1 and Fig. 1, it follows that infection of mice with the drug-resistant Mtb strain caused a dramatic increase in the NO level in all internal organs as early as 2 weeks after infection. The pathological changes were especially well-pronounced in the spleen and the lungs, most probably due to specific localization of Mtb in these organs.Fig. 1
Direct EPR Detection of Nitric Oxide in Mice Infected with the Pathogenic Mycobacterium Mycobacterium tuberculosis
Bottom Line: A reverse correlation, i.e., low level of NO in the lungs and other internal organs and extensive injury of lung tissue, was established for H37Rv-infected mice.Four weeks after infection, NO production in the lungs increased dramatically for both M. tuberculosis strains resulting in 80-84% damage of lung tissue.The lesion is suggested to be due to the development of defense mechanisms in M. tuberculosis counteracting NO effects.
Abstract: It has been shown that treatment of mice preinfected with Mycobacterium tuberculosis with spin NO traps (iron complexes with diethyldithiocarbamate) enables detection of large amounts of NO in internal organs 2 and 4 weeks after infection (up to 55-57 mumol/kg of wet lung tissue accumulated with spin NO traps during 30 min). The animals were infected with the drug-sensitive laboratory strain H37Rv and a clinical isolate nonrespondent to antituberculous drugs (the multidrug-resistant strain of M. tuberculosis) obtained from a patient with an active form of tuberculosis. Two weeks after infection with the multidrug-resistant strain, the NO level in the lungs, spleen, liver and kidney increased sharply concurrently with slight lesions of lung tissue. A reverse correlation, i.e., low level of NO in the lungs and other internal organs and extensive injury of lung tissue, was established for H37Rv-infected mice. Four weeks after infection, NO production in the lungs increased dramatically for both M. tuberculosis strains resulting in 80-84% damage of lung tissue. The lesion is suggested to be due to the development of defense mechanisms in M. tuberculosis counteracting NO effects.
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