Clinical evidence of herb-drug interactions: a systematic review by the natural standard research collaboration.

UNLABELLED: To evaluate the pharmacokinetics and adverse effects of medicinal herbs, as well as clinical evidence of herb-drug interactions. METHODS: Electronic searches were conducted in multiple databases, including MEDLINE, EMBASE, the Cochrane Library, CINAHL, NAPRALERT, International Pharmaceutical Abstracts, CANCERLIT, CISCOM, and HerbMed. Search terms used included common names, scientific names, and synonyms for the herbs and their primary active constituents. Bibliographies of relevant articles were also searched by hand to obtain additional references. No restrictions were placed on language or quality of publications. All literature collected pertained to adverse effects, pharmacokinetics, and suspected or confirmed cases of herb-drug interactions. RESULTS: Over 80 herbs or botanicals (including plants, fungi, algae, and common constituents) were identified that had clinically significant interactions with prescription and over-the-counter drugs. Interestingly, herbs beginning with the letter "g" (garlic, ginger, ginkgo, and grapefruit) were among the herbs most commonly involved in herb-drug interactions. Drugs with anticoagulant/antiplatelet activity (e.g. warfarin, aspirin) were frequently implicated in herb-drug interactions, with documented interactions with over 30 herbs and herbal products. Because many herbs have demonstrated adverse effects on the liver, the potential for interaction with hepatotoxic agents (such as acetaminophen) is also significant. Clinical outcomes of reported herb-drug interactions ranged from mild to severe. Of note, fatalities (though rare) have occurred with concomitant ephedra and caffeine use. CONCLUSION: As herbal products (and dietary supplements in general) continue to grow in popularity, patients and health care providers should be vigilant of potential herb-drug interactions.

Kinetics of cyclosporine A-induced inhibition of succinate-coenzyme Q dehydrogenase in rat renal cortical mitochondria.

The kinetic mechanism of succinate-coenzyme Q dehydrogenase (Complex II) inhibition by cyclosporine A (CS) on rat renal cortical mitochondria was investigated. CS showed two modes of inhibition of Complex II of the mitochondrial electron transport system: (a) a mixed linear noncompetitive inhibition of resting succinate-limited and ADP-stimulated respirations suggesting that CS binds to Complex II at a different site than the substrate, affecting the dissociation constant for the enzyme-substrate complex and (b) a competitive inhibition of the DNP-stimulated electron transport system suggesting competition with the oxidized form of a component of Complex II. CS action to renal mitochondrial Complex II limits its function, an effect which may be related to CS nephrotoxicity.