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Why are many anti-malaria drugs gap junction antagonists?
My professor recently just mentioned that many of the anti-malaria drugs block gap junctions. i am wondering if this blocking is important for stopping malaria, and how blocking gap junctions is anti-malarial. How does this effect connect to the mechanism of malaria?
I wasn't sure when I first read this, but this is actually a very interesting question.
Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.
One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and interfere with the formation of hemazoin (a parasite-friendly form of red blood cell proteins) in the vacuoles of the plasmodium (the parasite that causes malaria). Some folks have recently gotten some pretty reasonable crystals of chloroquine interacting directly with hemazoin. This all provides strong evidence for the view that, as regards killing plasmodium, the most significant interaction for an antimalarial is the one between it and hemazoin.
In (probably) unrelated news it was discovered that many of these antimalarials are also potent channel blockers of various kinds. I haven't dug into this too deeply yet, but most antimalarial people seem to view the channel blocking activity as a side effect. There are a number of other studies underway right now evaluating the psychological effect of the channel blocking activity of the antimalarials. There's one out of Iran that says that the blocking activity of Mefloquine can be used to ease the symptoms of morphine withdrawal.
Another thing to keep in mind is that Mefloquine fell out of favor not due to a decrease in efficacy, but was instead mostly taken out of circulation due to it's (justified) reputation for causing psychotic episodes in patients. So maybe this gap junction blocking stuff could be used to explain Mefloquine psychological side-effects. That would be neat!
