| 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]. |
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 860- | Lae, | Amygdalin as a Promising Anticancer Agent: Molecular Mechanisms and Future Perspectives for the Development of New Nanoformulations for Its Delivery |
| - | Review, | NA, | NA |
| 862- | Lae, | Molecular mechanism of amygdalin action in vitro: review of the latest research |
| - | Review, | NA, | NA |
| 866- | Lae, | Amygdalin from Apricot Kernels Induces Apoptosis and Causes Cell Cycle Arrest in Cancer Cells: An Updated Review |
| - | 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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