4-Chlorophenylthioacetone-derived thiosemicarbazones as potent antitrypanosomal drug candidates: Investigations on the mode of action

Bioorg Chem. 2021 Aug:113:105018. doi: 10.1016/j.bioorg.2021.105018. Epub 2021 May 25.

Abstract

Chagas disease (ChD), caused by Trypanosoma cruzi, remains a challenge for the medical and scientific fields due to the inefficiency of the therapeutic approaches available for its treatment. Thiosemicarbazones and hydrazones present a wide spectrum of bioactivities and are considered a platform for the design of new anti-T. cruzi drug candidates. Herein, the potential antichagasic activities of [(E)-2-(1-(4-chlorophenylthio)propan-2-ylidene)-hydrazinecarbothioamides] (C1, C3), [(E)-N'-(1-((4-chlorophenyl)thio)propan-2-ylidene)benzohydrazide] (C2), [(E)-2-(1-(4-, and [(E)-2-(1-((4-chlorophenyl)thio)propan-2-ylidene)hydrazinecarboxamide] (C4) were investigated. Macrophages (MOs) from C57BL/6 mice stimulated with C1 and C3, but not with C2 and C4, reduced amastigote replication and trypomastigote release, independent of nitric oxide (NO) and reactive oxygen species production and indoleamine 2,3-dioxygenase activity. C3, but not C1, reduced parasite uptake by MOs and potentiated TNF production. In cardiomyocytes, C3 reduced trypomastigote release independently of NO, TNF, and IL-6 production. C1 and C3 were non-toxic to the host cells. A reduction of parasite release was found during infection of MOs with trypomastigotes pre-incubated with C1 or C3 and MOs pre-stimulated with compounds before infection. Moreover, C1 and C3 acted directly on trypomastigotes, killing them faster than Benznidazole, and inhibited T. cruzi proliferation at various stages of its intracellular cycle. Mechanistically, C1 and C3 inhibit parasite duplication, and this process cannot be reversed by inhibiting the DNA damage response. In vivo, C1 and C3 attenuated parasitemia in T. cruzi-infected mice. Moreover, C3 loaded in a lipid nanocarrier system (nanoemulsion) maintained anti-T. cruzi activity in vivo. Collectively, these data suggest that C1 and C3 are candidates for the treatment of ChD and present activity in both the host and parasite cells.

Keywords: Chagas disease; Hydrazones; Lipid nanoparticles; Thiosemicarbazones; Treatment; Trypanosoma cruzi.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Survival / drug effects
  • Chagas Disease / drug therapy
  • Chagas Disease / parasitology
  • Chagas Disease / pathology
  • Cysteine Endopeptidases / metabolism
  • Cytokines / metabolism
  • Disease Models, Animal
  • Drug Design
  • Female
  • Life Cycle Stages / drug effects
  • Macrophages / cytology
  • Macrophages / metabolism
  • Macrophages / parasitology
  • Mice
  • Mice, Inbred C57BL
  • Molecular Conformation
  • Nitric Oxide / metabolism
  • Protozoan Proteins / antagonists & inhibitors
  • Protozoan Proteins / metabolism
  • Rats
  • Thiosemicarbazones / chemistry*
  • Thiosemicarbazones / pharmacology
  • Thiosemicarbazones / therapeutic use
  • Trypanocidal Agents / chemistry*
  • Trypanocidal Agents / pharmacology
  • Trypanocidal Agents / therapeutic use
  • Trypanosoma cruzi / drug effects
  • Trypanosoma cruzi / physiology

Substances

  • Cytokines
  • Protozoan Proteins
  • Thiosemicarbazones
  • Trypanocidal Agents
  • Nitric Oxide
  • Cysteine Endopeptidases
  • cruzain, Trypanosoma cruzi