| Features: Sourced from apricot kernels |
| Banned in some states. May cause cyanide poisoning. Laetrile B17 (Amygdalin ) Summary: -Activation of the caspase-3 protease and downregulating Bcl-2, upregulates BAX -Bax-to-Bcl-2 ratio and caspase-3 activity were increased -Inhibits NF-kβ and NLRP3 signaling pathways -Release of cyanide through the decomposition of amygdalin by the gut microfloral B-glucosidase enzyme. (bad) -IV might be better to avoid the digestive tract which could convert to hydrogen cyanide.???? Selective Toxicity (some challenges to this statement) The amygdalin itself is not toxic, but the HCN released from it causes the amygdalin toxic effect [35]. Cancer cells are dominant in anaerobic glycolysis and β -glucosidase is at its highest activity in lactate-induced acidic conditions [36]. Therefore, cancer cells have a high level of the unlocking enzyme β -glucosidase activity that breaks down amygdalin, leading to the release of HCN On the other hand, normal cells are normo-oxygenated and contain low levels of the β -glucosidase enzyme as well as high levels of rhodanese enzyme which transforms hydrogen cyanide into harmless thiocyanate [46, 47]. Thiocyanate has positive effects on organisms such as lowering blood pressure and is also considered a precursor for vitamin B12. It is poisonous when combined with plant-rich beta-glucosidase. Upon ingestion, amygdalin is hydrolyzed to cyanide by beta-glucuronidase in the small intestine [2]. Oral intake of 500 mg of amygdalin may contain as much as 30 mg of cyanide [3]. Oral amygdalin is estimated to be 40 times more potent than intravenous form due to its enzymatic conversion to hydrogen cyanide in the gastrointestinal tract [4]. |
| Source: HalifaxProj(inhibit) |
| Type: |
| Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals. -Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. -COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors. COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers. The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression: Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways. Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer. Drugs specifically targeting COX-2, such as celecoxib, have been developed. COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS. |
| 864- | Lae, | Can Amygdalin Provide any Benefit in Integrative Anticancer Treatment? |
| - | Review, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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