Source

Bitter amygdalin is mainly found in the kernels and leaves of bitter apricot, bitter lentil, peach, nectarine (nectarines), loquat, plum, apple and black cherry, etc. Bitter almond skin does not contain bitter amygdalin.

Bitter amygdalin is a β-type glycoside composed of gentian disaccharide and bitter almond eye, molecular formula: C20H27NO11, molecular weight: 457.43.

Its trihydrate is rhomboidal columnar crystal, melting point 200℃, anhydrous substance melting point about 20℃, [α]: 20D-42℃. 1g can be soluble in 12ml H2O, 900ml ethanol and 11ml ethanol, easily soluble in boiling water.

The content of bitter amygdalin in bitter almond is about 3%, which is 20~30 times higher than that of sweet almond, of which, the content of skin tip is slightly higher, and the skin does not contain bitter amygdalin. Raw almonds contain 0.179% HCN, decoction loss of 98% of hydrocyanic acid (HCN, H-C≡N), fried loss of 3-7% HCN.

Bitter almonds in the protein including the decomposition of bitter amygdalin enzyme, need to make it inactive in the preparation process, commonly used blanching method, the method is boiling water (90-100 ℃), the bitter almonds (with skin) into the decoction, it is appropriate to master the length of time to be appropriate (generally about 5 minutes, too long is lost about 34.1% of the original amount, too short is not enough to make the bitter amygdalin enzyme inactive.) After the decoction, the skin is removed, dried and decocted again.

Bitter almond contains 50% fatty acids, which are advanced lubricants and edible, mainly linoleic acid (27%), oleic acid (67%) and palmitic acid (5.2%), which are anthelmintic, antiseptic, laxative and soften the skin cuticle, but need to be removed when preparing bitter almond glycosides, and the oil yield is 44%.

 

In vivo metabolism

Consistent with the open two-compartment model.

Half-life of intravenous distribution 6.2 min; half-life of mean elimination phase 120.3 min; mean clearance 99.3 ml/min.

Excreted in the urine in its original form.

Bitter amygdalinase and cherry leaf enzyme are both β-glucosidases, and gastric acid also hydrolyzes bitter amygdalin.

Benzaldehyde produced in the stomach has the effect of inhibiting the function of pepsin and can be used in anti-ulcer therapy; its oxidation product benzoic acid is rapidly absorbed from the digestive tract and combines with glycine in the liver to form marsupialic acid, which is rapidly excreted from the urine within 12 hours, reaching 97% of the dosage within the first 4 hours.

Hydrocyanic acid can cause respiratory depression in tissues and is the culprit of poisoning, and its toxicity can be reduced by simultaneous administration of sugar.

Hydrocyanic acid is believed to have anticancer effects.

 

Action

Bitter amygdalin specifically inhibits alloxan-induced blood glucose elevation, and the intensity of action is related to the concentration of bitter amygdalin in the blood. Bitter amygdalin also has an anticoagulant effect. The analgesic effect of bitter amygdalin was confirmed by hot plate method and acetic acid torsion method in mice, and it was not tolerated. Bitter amygdalin was administered to mice at 15mg/each and 35mg/each, and it significantly promoted the proliferation of mitogenic T lymphocytes in the spleen of mice. The right frontotemporal lobe of rat brain was stained by incubation with cytochrome oxidase. The staining system was observed by microscopic television image measurement system and the data were processed by microcomputer. The results showed that bitter amygdalin could increase the activity of type I collagenase secreted by human kidney fibroblasts (KFB), inhibit the value-added and type I collagen expression of human kidney KFB, and promote the apoptosis of human kidney KFB in the optimal concentration range and time of action. The combined effect of bitter amygdalin and Cordyceps sinensis on the synthesis and secretion of albumin in rat fibroblast hepatocytes cultured in vitro in primary monolayers was monitored by ELISA. The effect of bitter amygdalin on the phagocytosis or rDNA activation of mouse hepatocytes was observed by Ag-NOR method using 99Mtc-sodium phytate injection into mice or liver tissue blots.