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Modified enzymes for pharmaceutical purposes. Extension of the goals and objectives for consistent investigation

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Abstract

The intravenous administration of bienzyme superoxide dismutase–chondroitin sulfate–catalase (SOD–CHS–CAT) conjugate in rats with endotoxic shock induced by a lipopolysac-charide bolus in the preventive and therapeutic regimens demonstrated the possible effective use of antioxidant agents not only for preventing the oxidative stress damage (as was considered previously), but also for its therapy. The results confirmed the importance of investigations of pathogenesis of vascular injury and the role of oxidative stress in it. The intravenous administration of the SOD–CHS–CAT conjugate in the therapeutic regimen during endotoxic shock development in rats was found to induce a variety of effects on the pathological process, besides preserving NO from conversion to peroxynitrite via reaction with the superoxide radical. These results, together with literature data, indicate good prospects of the research into NO-independent therapeutic effect of the SOD–CHS–CAT conjugate and the importance of studying the mechanism of its action using cardiovascular injury models associated with vasoactive agents other than NO.

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Authors and Affiliations

  1. Russian Cardiology Research and Production Complex, Ministry of Health of the Russian Federation, 15a Tret´ya Cherepkovskaya ul., 121552, Moscow, Russian Federation

    A. V. Maksimenko

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  1. A. V. Maksimenko
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Correspondence to A. V. Maksimenko.

Additional information

Based on materials of the Second Interdisciplinary Symposium on the Medicinal, Organic, and Biological Chemistry — MedOrg-BioChem-2015 (MOBI-Chem2015, Crimea, Novyi Svet settlement, September 27—30, 2015).

Published in Russian in Izvestiya Akademii Nauk. Seriya Khimicheskaya, No. 1, pp. 0001—0008, January, 2017.

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Maksimenko, A.V. Modified enzymes for pharmaceutical purposes. Extension of the goals and objectives for consistent investigation. Russ Chem Bull 66, 1–8 (2017). https://doi.org/10.1007/s11172-017-1691-1

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