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>The poison acts on tumor cells via a phenomenon called ferroptosis, a type of cell death linked to the peroxidation of certain fatty acids. The greater the amo

>The poison acts on tumor cells via a phenomenon called ferroptosis, a type of cell death linked to the peroxidation of certain fatty acids. The greater the amount of unsaturated fatty acids in the cell, the greater the risk of their oxidation. Normally, in the acidic compartment within tumors, cells store these fatty acids in lipid droplets, a kind of bundle in which fatty acids are protected from oxidation. But in the presence of a large amount of DHA, the tumor cell is overwhelmed and cannot store the DHA, which oxidizes and leads to cell death. By using a lipid metabolism inhibitor that prevents the formation of lipid droplets, researchers were able to observe that this phenomenon is further amplified, which confirms the identified mechanism and opens the door to combined treatment possibilities. Neat. Lipid metabolism inhibition to overload tumour cells w/ DHA which oxizides'em till cell death.

trhway 5y ago
Artemisinin being peroxide also acts through ferroptosis. Would be interesting to see it in that combo.
loudtieblahblah 5y ago
this is all above me and i'm not following it exactly. it was my understanding the polyunsaturated fats (3s and 6s alike) were both prone to oxidation far more so than saturated or monosaturated fats and it was this reason alone why there's correlation between high PUFA consumption and prostate cancer It was also my understanding, that this phenomenon is why astaxanthin an antioxidant found in certain algae and things that feed off that algae, such as krill, salmon, and to a small degree - shrimp, crab, and lobster, and noted for being more powerful than the antioxidants found in blueberries, green tea, and even CoQ10, as well as never flipping to a pro-oxidant, the way say.. VitC, E or reservatol can, is extremely useful when consuming Omega3s. Supposedly astaxanthin protects against the oxidation of PUFAs. So if preventing the oxidation of PUFA's is seen as vital to getting their benefits while avoiding the problems of oxidation - how is it, again, that oxidation of Omega3s is a good thing? Is this one of the cases where it's oxidation can result in both tumor cell death in one area but create it in another? Or am i misreading?
- adrian_b 5y ago
  The polyunsaturated fatty acids are much more prone to spontaneous oxidation by the air. In your body the oxidation reactions are not spontaneous, they are catalyzed by enzymes. All the cells have large quantities of enzymes used for the oxidation of the mono-unsaturated fatty acids and of the saturated fatty acids, which are stored together in the fat used as an energy reserve. So MUFA and saturated fatty acids are either oxidized rapidly when you do physical work or they are stored in reserve fat when in excess. The poly-unsaturated fatty acids are not used as an energy reserve, they are used mainly for building various kind of cellular membranes. Most cells do not need to transform PUFA and they do not contain enzymes for this. Excess PUFA are processed mainly in the liver, where they are transformed through a chain of reactions to fatty acids that can be oxidized through the normal path. When there is a deficit of PUFA, but there are precursors with a shorter chain, e.g. ALA for DHA & EPA, the liver will perform elongation reactions, to increase the quantities of PUFA, instead of preparing them for oxidation. However all these reactions with PUFA, either for synthesis or for degradation, are rate-limited by modest quantities of the necessary enzymes, so either too small or too large quantities of PUFA can exceed the processing capability needed to adjust the PUFA concentration in the body.

trhway 5y ago

Artemisinin being peroxide also acts through ferroptosis. Would be interesting to see it in that combo.

loudtieblahblah 5y ago

this is all above me and i'm not following it exactly. it was my understanding the polyunsaturated fats (3s and 6s alike) were both prone to oxidation far more so than saturated or monosaturated fats and it was this reason alone why there's correlation between high PUFA consumption and prostate cancer It was also my understanding, that this phenomenon is why astaxanthin an antioxidant found in certain algae and things that feed off that algae, such as krill, salmon, and to a small degree - shrimp, crab, and lobster, and noted for being more powerful than the antioxidants found in blueberries, green tea, and even CoQ10, as well as never flipping to a pro-oxidant, the way say.. VitC, E or reservatol can, is extremely useful when consuming Omega3s. Supposedly astaxanthin protects against the oxidation of PUFAs. So if preventing the oxidation of PUFA's is seen as vital to getting their benefits while avoiding the problems of oxidation - how is it, again, that oxidation of Omega3s is a good thing? Is this one of the cases where it's oxidation can result in both tumor cell death in one area but create it in another? Or am i misreading?

adrian_b 5y ago
The polyunsaturated fatty acids are much more prone to spontaneous oxidation by the air. In your body the oxidation reactions are not spontaneous, they are catalyzed by enzymes. All the cells have large quantities of enzymes used for the oxidation of the mono-unsaturated fatty acids and of the saturated fatty acids, which are stored together in the fat used as an energy reserve. So MUFA and saturated fatty acids are either oxidized rapidly when you do physical work or they are stored in reserve fat when in excess. The poly-unsaturated fatty acids are not used as an energy reserve, they are used mainly for building various kind of cellular membranes. Most cells do not need to transform PUFA and they do not contain enzymes for this. Excess PUFA are processed mainly in the liver, where they are transformed through a chain of reactions to fatty acids that can be oxidized through the normal path. When there is a deficit of PUFA, but there are precursors with a shorter chain, e.g. ALA for DHA & EPA, the liver will perform elongation reactions, to increase the quantities of PUFA, instead of preparing them for oxidation. However all these reactions with PUFA, either for synthesis or for degradation, are rate-limited by modest quantities of the necessary enzymes, so either too small or too large quantities of PUFA can exceed the processing capability needed to adjust the PUFA concentration in the body.