Please forward this error screen to host. This article relies too much on references to primary sources. Some fruit juices and fruits can inhibit enzymes that absorb and metabolize medications. Some fruit sildenafil interactions and fruits can interact with numerous drugs, in many cases causing adverse effects.
Fruit consumed three days before the medicine can still have an effect. If the active drug is metabolized by the inhibited enzyme, then the fruit will stop the drug being metabolized, leaving elevated concentrations of the medication in the body, which can cause adverse effects. Low drug concentrations can also be caused when the fruit suppresses drug absorption from the intestine. The effect of grapefruit juice with regard to drug absorption was originally discovered in 1989. The first published report on grapefruit drug interactions was in 1991 in the Lancet entitled “Interactions of Citrus Juices with Felodipine and Nifedipine,” and was the first reported food-drug interaction clinically. Grapefruit, Seville oranges, bergamot, and possibly other citrus also contain large amounts of naringin. Furanocoumarins seem to have a stronger effect than naringin under some circumstances. This section may require cleanup to meet Wikipedia’s quality standards. Organic compounds that are derivatives of furanocoumarin interfere with liver and intestinal enzyme CYP3A4 and are believed to be primarily responsible for the effects of grapefruit on the enzyme. When drugs are taken orally, they enter the gut lumen to be absorbed in the small intestine and sometimes, in the stomach. In order for drugs to be absorbed, they must pass through the epithelial cells that line the lumen wall before they can enter the hepatic portal circulation to be distributed systemically in blood circulation.
Drugs are metabolized by drug-specific metabolizing enzymes in the epithelial cells. As a result, many drugs are impacted by consumption of citrus juice. This interaction is particularly dangerous when the drug in question has a low therapeutic index, so that a small increase in blood concentration can be the difference between therapeutic effect and toxicity. Citrus juice inhibits the enzyme only within the intestines if consumed in small amounts. When larger amounts are consumed they may also inhibit the enzyme in the liver. The degree of the effect varies widely between individuals and between samples of juice, and therefore cannot be accounted for a priori. The interaction is greatest when the juice is ingested with the drug or up to 4 hours before the drug. The location of the inhibition occurs in the lining of the intestines, not within the liver. 4-hour interval between grapefruit consumption and the medication should suffice. The first approach involves risk to trial volunteers. The first and second approaches have another problem: the same fruit cultivar could be tested twice with different results.
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Depending on growing and processing conditions, concentrations of the interacting polyphenol compounds can vary dramatically. Citrus fruits clustered by genetic similarity. Most commercial varieties of citrus are hybrids of the three species at the corners of the ternary diagram, and genetically distinct hybrids often bear the same common name. A descendant of citrus cultivars that cannot produce the problematic polyphenol compounds would presumably also lack the genes to produce them. Many citrus cultivars are hybrids of a small number of ancestral species, which have now been fully genetically sequenced. Many traditional citrus groups, such as true sweet oranges and lemons, seem to be bud sports, mutant descendants of a single hybrid ancestor.
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