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Dihydroergotamine has also been shown to be an inhibitor of cytochrome P450 3A catalyzed reactions and rare reports of ergotism have been obtained from patients treated with dihydroergotamine and macrolide antibiotics (e.g., troleandomycin, clarithromycin, erythromycin), and in patients treated with dihydroergotamine and protease inhibitors (e.g., ritonavir), presumably due to inhibition of cytochrome P450 3A metabolism of ergotamine (see CONTRAINDICATIONS)
It acts as a crucial electron donor, sacrificing its own electrons to stabilize free radicals before they can attack the mitochondrial lipid membranes
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The insulin-induced increased rate of cancer cell replication also works to the advantage of the patient, since most chemotherapeutic agents destroy preferentially those cells that are undergoing subdivision/replication
