By Philip J. Rosenthal
Philip Rosenthal, MD, and a panel of major malaria specialists drawn from academia, the army, and overseas health and wellbeing businesses survey the newest medical realizing of antimalarial chemotherapy, emphasizing the molecular mechanisms of resistance and the outline of significant new ambitions. Their survey covers the present prestige of malarial and antimalarial chemotherapy, the appropriate biology and biochemistry of malaria parasites, the antimalarial medicines at present to be had, new chemical techniques to chemotherapy, and attainable new goals for chemotherapy. accomplished and state of the art, Antimalarial Chemotherapy: Mechanisms of motion, Resistance, and New instructions in Drug Discovery essentially delineates the entire easy and medical learn now addressing one of many world's significant unresolved ailment difficulties, paintings that's now powerfully using the quick velocity of antimalarial drug discovery this day.
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Extra info for Antimalarial Chemotherapy: Mechanisms of Action, Resistance, and New Directions in Drug Discovery (Infectious Disease)
Source: Ref. 5. Artemisinin enters the TVM (competes with dihydroartemisinin; see Table 2) and affects membrane properties there. The endoperoxide bridge is believed to be essential for artemisinin’s antimalarial activity as it allows interaction with heme and hemozoin (Chapter 11), but it has been suggested that these interactions themselves may not lead to parasite killing (65,66). Instead, membrane damage caused by free radicals may be critical. Low, pharmacologically effective concentrations of artemisinin induce aberrant membrane budding in the PVM–TVM (Fig.
Hence, antimalarials need to enter an unusual intracellular niche. Entry and survival of the parasite in this specialized niche is intimately linked to secretory trafficking of its proteins and lipids. Ongoing studies have shown that P. falciparum induces unique structural changes, protein and waste export, and nutrient import in infected red cells. There is evidence both for a nonspecific ion pore and an anion-selective channel that mediate solute transport in the PVM and the infected red cell membrane, respectively (2,3).
32). Daily prophylaxis with atebrine was required for all Allied troops, even though it turned the skin yellow and was reputed to cause impotence. This drug helped protect the health of the Allied troops fighting in some of the most malarious areas of the world and, as Bruce-Chwatt has said, “there is no exaggeration in saying that this probably changed the course of modern history” (33). Interestingly, Japanese troops fighting in this area also used atebrine, but at an inadequate dose. This may have contributed to the development of atebrine resistance in New Guinea (32).