Oligochitosans obtained through degradation of macromolecules of chitosan with a high degree of deacetylation turned out to be biologically active, contributing to an increase of nitric oxide levels in Ehrlich ascites tumor (EAT) cells through inducing expression of the isoform of inducible nitric oxide synthase (iNOS) gene. An increase of NO levels in EAT cells in the presence of the investigated oligochitosans might contribute to nitrosylation of L-cysteine – an allosteric effector of the M2 isoenzyme of pyruvate kinase (PK), which switches the PK kinase activity, responsible for ATP synthesis, to the histone kinase activity that may participate in histone H1 phosphorylation. Lack of the histone activity of the PK M2 isoenzyme may contribute to decreased histone H1 phosphorylation and thus inhibit EAT cells proliferation.
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