The team found that the drug's lethal effect is caused by damage to two power stations within the parasite's cell.
The findings, published in the journal Nature, improve the understanding of how these drugs work and may ultimately lead to the development of new treatments for tropical diseases.
African sleeping sickness is a disease caused by a parasite transmitted to humans through the bite of the tsetse fly. It is characterized by fever, weakness, neurological disorders and ultimately coma. The disease is found in sub-Saharan Africa and affects millions of people.
The standard treatment for African sleeping sickness is the drug pentamidine, which has severe side effects, such as dangerously low blood pressure and kidney failure, but pentamidine is the only treatment available for more severe stages of the disease when the parasite is in the brain and spinal cord.
Pentamidine is one of a class of drugs called aromatic diamidines, which are commonly used to treat tropical parasitic diseases. However, little is known about how aromatic diamidines kill parasites.
To address this, researchers at the University of Glasgow used advanced microscopic techniques and molecular biology to investigate how pentamidine kills T. brucei. They discovered that pentamidine causes damage to two power stations within the parasite's cell, the mitochondria and the kinetoplast.
The mitochondria is the cell's powerhouse, where most energy is produced. The kinetoplast is a unique DNA structure found in trypanosomes and other kinetoplastid protozoa, playing crucial roles in energy production, and is essential for survival.
The study is the first to identify the specific molecular targets of aromatic diamidines in parasites. These findings could lead to the development of new treatments for tropical diseases that are safer and more effective than current treatments.
