Structure/antileishmanial activity relationship study of naphthoquinones and dependency of the mode of action on the substitution patterns

Planta Med. 2011 Dec;77(18):2003-12. doi: 10.1055/s-0031-1280092. Epub 2011 Jul 28.

Abstract

A series of naphthoquinones was tested for activity against both extracellular promastigote and intracellular amastigote Leishmania major GFP in vitro. In parallel, the compounds were evaluated for cytotoxic effects against bone marrow-derived macrophages (BMM Φ) as a mammalian host cell control. Most of the compounds noticeably inhibited the growth of extracellular parasites (IC (50) 0.5 to 6 µM) and the intracellular survival of L. major GFP amastigotes (IC (50) 1 to 7 µM) when compared with the antileishmanial drug amphotericin B (IC (50) of 2.5 and 0.2 µM, respectively). In general, antiprotozoal activity and host cell cytotoxicity seemed to increase in parallel. Conspicuously, the cytotoxic effect was less pronounced on infected host cells when compared with that on noninfected cells. Concerning structure/activity relationships for the tested naphthoquinones, some interesting structural features emerged from this study. Introduction of a methyl or methoxyl group at C-2 of the parent 1,4-naphthoquinone slightly increased the antileishmanial activity against clinically relevant amastigotes, while the presence of a hydroxyl function in this position dramatically reduced the effectiveness. In contrast, hydroxylation at C-5 and dihydroxy substitution at C-5 and C-8 significantly enhanced the antiprotozoal activity. Similarly, the presence of a side chain hydroxyl group PERI to a carbonyl function as represented in the series of shikonin/alkannin derivatives increased the activity when compared with substituted analogs. Within the series of naphthoquinones tested, the dimeric mixture of vaforhizin and isovaforhizin showed the highest activity IN VITRO against the clinically relevant intracellular amastigote with an IC (50) of 1.1 µM. With IC (50) values mostly in the range of 1-3 µM, the shikonin/alkannin derivatives proved to be similarly considerably leishmanicidal. None of the compounds tested was capable to induce NO production known to play a crucial role in the host resistance against intracellular pathogens, excluding activation of microbicidal mechanisms in macrophages. The mode of action apparently depended on the substitution pattern, associated with the electrophilicity of the naphthoquinone or the efficiency of redox cycling. Conspicuously, members oxygenated in the quinone ring proved to be leishmanicidal when coincubated with glutathione, while the majority of the remaining compounds lost activity.

MeSH terms

  • Amphotericin B / pharmacology
  • Animals
  • Antiprotozoal Agents / pharmacology*
  • Bignoniaceae / chemistry
  • Boraginaceae / chemistry
  • Culture Media / chemistry
  • Drosera / chemistry
  • Flow Cytometry
  • Glutathione / pharmacology
  • Green Fluorescent Proteins / chemistry
  • Hydroxylation
  • Inhibitory Concentration 50
  • Leishmania / chemistry
  • Leishmania / drug effects*
  • Leishmania / genetics
  • Leishmania / pathogenicity
  • Macrophages / drug effects
  • Macrophages / parasitology*
  • Mammals
  • Naphthoquinones / chemistry
  • Naphthoquinones / pharmacology*
  • Organisms, Genetically Modified / genetics
  • Parasitic Sensitivity Tests
  • Structure-Activity Relationship

Substances

  • Antiprotozoal Agents
  • Culture Media
  • Naphthoquinones
  • alkannin
  • Green Fluorescent Proteins
  • shikonin
  • Amphotericin B
  • Glutathione