Nanoencapsulation of benznidazole in calcium carbonate increases its selectivity to Trypanosoma cruzi

• Published in: Parasitology 2018-08, Vol.145 (9), p.1191-1198
• Main Authors: Tessarolo, Louise Donadello, de Menezes, Ramon Róseo Paula Pessoa Bezerra, Mello, Clarissa Perdigão, Lima, Dânya Bandeira, Magalhães, Emanuel Paula, Bezerra, Eveline Matias, Sales, Francisco Adilson Matos, Barroso Neto, Ito Liberato, Oliveira, Maria de Fátima, dos Santos, Ricardo Pires, Albuquerque, Eudenilson L., Freire, Valder Nogueira, Martins, Alice Maria
• Format: Article
• Language: English
• Subjects: Animals; Calcium Carbonate - chemistry; Cell Death - drug effects; Cell Line; Chagas Disease - drug therapy; Drug Delivery Systems; Epithelial Cells - parasitology; Membrane Potential, Mitochondrial - drug effects; Nanocapsules - chemistry; Nanocapsules - toxicity; Nitroimidazoles - pharmacology; Trypanosoma cruzi - drug effects
• ISSN: 0031-1820; 1469-8161
• DOI: 10.1017/S0031182018000197

Chagas disease is a public health problem, affecting about 7 million people worldwide. Benznidazole (BZN) is the main treatment option, but it has limited effectiveness and can cause severe adverse effects. Drug delivery through nanoparticles has attracted the interest of the scientific community aiming to improve therapeutic options. The aim of this study was to evaluate the cytotoxicity of benznidazole-loaded calcium carbonate nanoparticles (BZN@CaCO3) on Trypanosoma cruzi strain Y. It was observed that BZN@CaCO3 was able to reduce the viability of epimastigote, trypomastigote and amastigote forms of T. cruzi with greater potency when compared with BZN. The amount of BZN necessary to obtain the same effect was up to 25 times smaller when loaded with CaCO3 nanoparticles. Also, it was observed that BZN@CaCO3 enhanced the selectivity index. Furthermore, the cell-death mechanism induced by both BZN and BZN@CaCO3 was evaluated, indicating that both substances caused necrosis and changed mitochondrial membrane potential.