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  • Title: [Mechanisms of development of antiproteolytic deficiency in tuberculosis and in nonspecific lung diseases].
    Author: Kaminskaia GO, Blonskaia GIu, Puriaeva NL, Lovacheva OV.
    Journal: Probl Tuberk; 1991; (6):55-8. PubMed ID: 1780313.
    Abstract:
    In the course of 3 series of experiments on CBA mice intravenously infected with tuberculosis and the use of bronchoalveolar washings (BAW) as a test material, it was revealed that the period of developed tuberculosis is accompanied by a simultaneous rise in antitryptic activity (ATA) and that of neutrophilic elastase (NE). The treatment of the affected animals with alpha-tocopherol, a liposoluble antioxidant, failed to prevent the loss of antielastase activity in pulmonary antiproteinases. In vitro incubation of BAW with 0.01M of ascorbic acid water-soluble antioxidant completely recovered the antielastase activity in pulmonary antiproteinases and provided a three-fold increase of their ATA. As a result of clinical experience gained in the management of 30 patients with different types of chronic pulmonary pathology, ATA, NE and NE complexes with alpha 1-proteinase inhibitor were defined both in blood serum and in BAW. Concentration of these complexes and the NE indices in BAW were seen to be directly related to the content of neutrophils. In blood serum, a direct correlation of the above complexes with NE and a reverse one with ATA were traced. It is concluded that in the development of antiproteolytic deficiency in patients with tuberculosis and other types of chronic pulmonary pathology, an oxidizing inactivation of antiproteinases and their consumption during conjugation with the surplus of proteolytic enzymes have an important role to play.
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