The Cytotoxic Effect of Zno Nps Against the Intracellular Amastigotes of Leishmania Donovani in Vitro

Abstract

Leishmania parasite preferentially infect host phagocytic cells, primarily dendritic cells and macrophages. One of the main problems with Leishmania infections is the capability of these parasites to evade and subvert immune responses of the host. Leishmaniasis is treated with a small arsenal of drugs; all of them have disadvantages in terms of efficacy, high price, toxicity or treatment regimen. In this study, the effect of Zinc oxide nanoparticles (ZnO NPs) was evaluated against intracellular amastigotes Leishmania donovani in vitro conditions. The effect of different concentrations from ZnO NPs (0.18, 0.37, 0.75 and 1.5 μg / ml) was used to study on the viability of amastigotes and macrophages "following infection" using the colorimetric (MTT) assay. The results have been shown that the ZnO NPs have a cytotoxic effect on the proliferation of the amastigotes forms and have no effect. The IC50 of ZnO NPs on amastigotes was (0.610 µg/ ml).This study concluded that the used concentrations of ZnO NPs have the ability to stimulate macrophages activity and promote the suppressive effects on L. donovani intracellular amastigotes in vitro following infection. These results may contribute to the production of an effective, non-toxic and cheap drug against Leishmania parasites Keywords: Zinc oxide nanoparticles, Visceral leishmaniasis, Macrophages. ‫متنا‬ ‫الزنك‬ ‫أوكسید‬ ‫لدقائق‬ ‫السمي‬ ‫التأثیر‬ ISSN: 0067-2904 Salih and ZghairIraqi Journal of Science, 2017, Vol. 58, No.4C, pp: 2285-2290 IntroductionLeishmaniasis is caused by an obligate intramacrophage protozoan of the genus Leishmania. In tropical regions protozoan parasitic diseases pose a main public health problem. After malaria, leishmaniasis stands second in having a high morbidity and mortality burden leading to economic loss. It widely manifests as cutaneous leishmaniasis (CL), mucocutaneous and visceral leishmaniasis (VL), or kala-azar. Leishmania donovani is the causative agent of VL in the Indian subcontinent and Africa; L. infantum causes VL in the Mediterranean basin [1]. VL is the most dangerous leishmaniasis form, it is characterized by fever, cachexia, hyper-gamaglobulinemia and hepatosplenomegaly, when untreated can be fatal [2]. The innate immune responses against Leishmania include phagocytes, Natural killer (NK) cells and cytokines [3]. Phagocytosis and anti-leishmanial activity of macrophages are the major factors in the elimination of Leishmania parasites .One route to estimate the infectivity of Leishmania and the anti-parasite immune response is to assess the germicidal activity of macrophages via the generation of reactive oxygen and nitrogen intermediates, particularly nitric oxide (NO) [4,5]. The treatment for leishmaniasis is primarily dependent upon antimonial compounds as first-line drugs (e.g., meglumine antimoniate and sodium stibogluconate). Amphotericin B is a second-line drug exhibiting teratogenic effects and nephrotoxicity. Miltefosine is the only oral treatment available to cure leishmaniasis. Treatment failure rates...