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Fatty Acids: Fish Oils/Fish Kill Mitochondria

Fish Fat Found to Kill Cancer Cells

Fatty acids from fish oils and fatty fish can destroy the power station - the mitochondria- in certain types of cancer cells, making the cells commit suicide.

These are the conclusions in a new study by Hilde Heimli, presented to the Institute for Nutrition Research at the University of Oslo, in Norway. The study was supported by the Norwegian Cancer Society.

In her study, Heimli examined how polyunsaturated omega-3 fatty acid is ingested by different leukemia/lymphoma cell lines. The researcher examined how some types of cancer cells commit suicide in this setting, a process called programmed cell death or apoptosis.

If omega-3 fatty acids are to be capable of killing cancer cells, the cells have to contain a certain enzyme that activates these fatty acids. Cancer cells that contain less of this enzyme do not react to fish fat.

"Polyunsaturated fatty acids from fish also can initiate a less regulated cell death called necrosis. The reason for the necrotic cell death is an increased production of reactive oxygen species in the cells. It is possible to oppose this necrosis by the presence of antioxidants such as Vitamin C and E," says Heimli.

This work contributes to an increased understanding of how cancer cells grow and develop. This knowledge may play an important role in the prevention and treatment of certain types of cancer. Heimli's experiments are developed from cancer cell lines - cells that originally came from leukemia patients, but she doesn't see any reason that cancer cells of other origins shouldn't commit suicide when exposed to fish fat.

"The experiments have been done in dishes in a laboratory setting. The polyunsaturated fatty acids that are used are eicosapentaenoic acid (EPA), which are the same type as found in fatty fish or regular fish oil capsules. The fatty acids are added to the food given to the cancer cells in a way that is most like the body's own process," says Heimli.

SOURCE: Institute for Nutrition Research, University of Oslo, Norway (http://www.kreft.no)



Thanks to Artemis (November, 2002), newsletter from Johns Hopkins.

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