Scientists at The University of Nottingham say adverse side-effects caused by the anti-parasitic drug quinine in the treatment of malaria could be controlled by what we eat.
The research, carried out by Nottingham scientists on the University's campuses in the UK and Malaysia, indicates that natural variation in our levels of the amino acid, tryptophan, has a marked bearing on how we respond to quinine treatment. It appears that the lower our levels of tryptophan the more likely it is that we would suffer side-effects. And because tryptophan is an essential amino acid the body cannot produce it we get it from the food we eat.
Discovered back in the 1600s, quinine is still used for anti-malaria treatment. However, it is associated with a long list of side effects ranging from sickness and headaches to blindness, deafness and in rare cases death. This latest study, published in the Journal of Antimicrobial Chemotherapy, could offer a cheap and simple way of combating our adverse reaction to quinine treatment and improving the performance of this important drug.
The study, funded by The University of Nottingham's doctoral award scheme, was led by Dr Simon Avery and Dr Kang-Nee Ting from the Schools of Biology in the UK and Biomedical Sciences in Malaysia, in collaboration with Professor Richard Pleass now at the University of Liverpool.
Reinforcing previous research
These findings reinforce a discovery they made three years ago.
Using a yeast model, which is a relatively close evolutionary neighbour of the human, they showed that quinine can block take-up of tryptophan, causing quinine toxicity in cells. This research, published in 2009, gave the scientific community a new insight into the way quinine behaves and led Dr Avery and his team to believe that a quinine/tryptophan combination therapy might allow the use of higher quinine dosages to improve the effectiveness of the drug and reduce the
|Contact: Lindsay Brooke|
University of Nottingham