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Abstract
Malaria parasites have been shown to be more susceptible to oxidative stress than their host erythro- cytes. In the present work, a chloroquine resistant malaria parasite, Plasmodium falciparum (FCR-3) was found to be susceptible in vitro to a pyridoxal based iron chelator — (l-[N-ethoxycarbonylmethyl- pyridoxlidenium]-2-[2′-pyridyl] hydrazine bromide — (code named L2–9). 2h exposure to 20μM L2–9 was sufficient to irreversibly inhibit parasite growth. Desferrioxamine blocked the drug effect, indicating the requirement for iron. Oxygen however, was not essential. Spectrophotometric analysis showed that under anoxic conditions, L2–9-Fe(II) chelate undergoes an intramolecular redox reaction which presumably involves a one electron transfer and is expected to result in the formation of free radical. Spin trapping coupled to electron spin resonance (ESR) studies of L2–9-iron chelate showed that L2–9-Fe(II) produced free radicals both in the presence and absence of cells, while L2–9-Fe(III) produced free radicals only in the presence of actively metabolising cells.