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Background  Allicin has shown antileishmanial activity  in vitro  and  in vivo . However the mechanism of action underlying its antiproliferative effect against  Leishmania  has been virtually unexplored. In this paper, we present the results obtained in  L . infantum  and a mechanistic basis is proposed.    Methodology/Principal Finding  Exposure of the parasites to allicin led to high Ca 2+  levels and mitochondrial reactive oxygen species (ROS), collapse of the mitochondrial membrane potential, reduced production of ATP and elevation of cytosolic ROS. The incubation of the promastigotes with SYTOX Green revealed that decrease of ATP was not associated with plasma membrane permeabilization. Annexin V and propidium iodide (PI) staining indicated that allicin did not induce phospholipids exposure on the plasma membrane. Moreover, DNA agarose gel electrophoresis and TUNEL analysis demonstrated that allicin did not provoke DNA fragmentation. Analysis of the cell cycle with PI staining showed that allicin induced cell cycle arrest in the G 2 /M phase.    Conclusions/Significance  We conclude that allicin induces dysregulation of calcium homeostasis and oxidative stress, uncontrolled by the antioxidant defense of the cell, which leads to mitochondrial dysfunction and a bioenergetic catastrophe leading to cell necrosis and cell cycle arrest in the premitotic phase.

Allicin Induces Calcium and Mitochondrial Dysregulation Causing Necrotic Death in Leishmania