GARLIC (ALLIUM SATIVUM)The putative

GARLIC (ALLIUM SATIVUM)

The putative antihypercholesterolemic effect of garlic supplements makes them one of the most widely used botanical supplements in the U.S. Their efficacy, however, remains equivocal due to conflicting results from numerous published clinical trials.69 This is probably a function of the type of product used, its quality, and poor characterization of the phytochemical agent(s) responsible for garlic’s serum lipid lowering effect.
Three general categories of garlic supplements are available commercially (gar- lic oil, dehydrated garlic powder, and aged garlic extract), each with their own unique composition of purported bioactive components.70,71 Within these products, a plethora of organosulfur compounds, steroid saponins, and other phytochemicals have been identified.70–72 Of these, the oil-soluble organosulfur compounds, includ- ing allyl thiosulfinates (allicin), alkyl sulfides (diallyl sulfide), vinyldithiins, and ajoene, have received the most attention. Allicin has long been touted as the agent responsible for garlic’s hypocholesterolemic effects, yet the compound is unstable in the gastrointestinal tract, is not bioavailable, and is rarely found in commercial products.70,71 Its degradation products, diallyl sulfide, diallyl disulfide, diallyl trisul- fide, dithiin, and ajoene, may contribute to the lowering of serum cholesterol levels; however, many products, particularly those containing garlic oil, have relatively poor efficacy.73,74 In addition, many in vivo studies indicate that garlic oil and individual alkyl sulfides, most notably diallyl sulfide, inhibit murine and human CYP2E1.7,28,75–78 This is likely a result of the CYP2E1-catalyzed biotransformation of diallyl sulfide to diallyl sulfoxide and diallyl sulfone, in which the latter is a mechanism-based inhibitor of the enzyme.77 Despite inhibition of human CYP2E1, few interactions involving garlic products and CYP2E1 substrates have been reported, a consequence that probably reflects the paucity of drugs metabolized by this enzyme. Conversely, prolonged administration of diallyl sulfide and diallyl disulfide induced other hepatic and intestinal murine CYP subfamilies (CYP2B, CYP1A, CYP3A), in addition to various transferases (glutathione transferase, uri- dine 5-diphosphate (UDP)-glucuronyl transferase).7,75,76

Hasil (Bahasa Indonesia) 1:

BAWANG PUTIH (ALLIUM SATIVUM)Diduga efek antihypercholesterolemic suplemen bawang membuat mereka salah satu yang paling banyak digunakan suplemen botani di Amerika Serikat Efektivitas mereka, bagaimanapun, tetap equivocal karena hasil yang bertentangan dari berbagai trials.69 klinis yang diterbitkan, ini mungkin adalah fungsi dari jenis produk yang digunakan, kualitas, dan miskin karakterisasi agent(s) fitokimia yang bertanggung jawab untuk bawang putih di serum lipid menurunkan efek.Three general categories of garlic supplements are available commercially (gar- lic oil, dehydrated garlic powder, and aged garlic extract), each with their own unique composition of purported bioactive components.70,71 Within these products, a plethora of organosulfur compounds, steroid saponins, and other phytochemicals have been identified.70–72 Of these, the oil-soluble organosulfur compounds, includ- ing allyl thiosulfinates (allicin), alkyl sulfides (diallyl sulfide), vinyldithiins, and ajoene, have received the most attention. Allicin has long been touted as the agent responsible for garlic’s hypocholesterolemic effects, yet the compound is unstable in the gastrointestinal tract, is not bioavailable, and is rarely found in commercial products.70,71 Its degradation products, diallyl sulfide, diallyl disulfide, diallyl trisul- fide, dithiin, and ajoene, may contribute to the lowering of serum cholesterol levels; however, many products, particularly those containing garlic oil, have relatively poor efficacy.73,74 In addition, many in vivo studies indicate that garlic oil and individual alkyl sulfides, most notably diallyl sulfide, inhibit murine and human CYP2E1.7,28,75–78 This is likely a result of the CYP2E1-catalyzed biotransformation of diallyl sulfide to diallyl sulfoxide and diallyl sulfone, in which the latter is a mechanism-based inhibitor of the enzyme.77 Despite inhibition of human CYP2E1, few interactions involving garlic products and CYP2E1 substrates have been reported, a consequence that probably reflects the paucity of drugs metabolized by this enzyme. Conversely, prolonged administration of diallyl sulfide and diallyl disulfide induced other hepatic and intestinal murine CYP subfamilies (CYP2B, CYP1A, CYP3A), in addition to various transferases (glutathione transferase, uri- dine 5-diphosphate (UDP)-glucuronyl transferase).7,75,76