Leishmania is a digenetic protozoan parasite causing leishmaniasis in humans. 
The different clinical forms of leishmaniasis are caused by more than twenty 
species of Leishmania that are transmitted by nearly thirty species of 
phlebotomine sand flies. Pentavalent antimonials (such as Pentostam or 
Glucantime) are the first line drugs for treating leishmaniasis. Recent studies 
suggest that pentavalent antimony (Sb(V)) acts as a pro-drug, which is converted 
to the more active trivalent form (Sb(III)). However, sensitivity to trivalent 
antimony varies among different Leishmania species. In general, Leishmania 
species causing cutaneous leishmaniasis (CL) are more sensitive to Sb(III) than 
the species responsible for visceral leishmaniasis (VL). Leishmania 
aquaglyceroporin (AQP1) facilitates the adventitious passage of antimonite down 
a concentration gradient. In this study, we show that Leishmania species causing 
CL accumulate more antimonite, and therefore exhibit higher sensitivity to 
antimonials, than the species responsible for VL. This species-specific 
differential sensitivity to antimonite is directly proportional to the 
expression levels of AQP1 mRNA. We show that the stability of AQP1 mRNA in 
different Leishmania species is regulated by their respective 3'-untranslated 
regions. The differential regulation of AQP1 mRNA explains the distinct 
antimonial sensitivity of each species.