Fatty Acid Study

Cancer Research

RECNAC , Fatty Acid , Lipoic-Acid , Natural Extracts , Bindweed , LF Bacterium

Fatty Acid Study - The RECNAC goal is to find a non-toxic way to treat cancer. One of our works is finding anticancer agents that have little to no toxic affect on the human body. In the RECNAC release last year, we reported a plant extract that had tumor inhibition on three different animal models:

The inhibition rate for B16 melanoma model was 53%, Lewis lung carcinoma model was 62% and S-180 sarcoma model was 77%. The inhibition rate for B16 melanoma model was 53%, Lewis lung carcinoma model was 62% and S-180 sarcoma model was 77%.

Another extract from a bacterium showed very good tumor inhibition and low toxicity in animal tests.

First, we made our extracts through a series of physical and chemical steps. Then we send our agents to Beijing, China for the animal testing. First, we made our extracts through a series of physical and chemical steps. Then we send our agents to Beijing, China for the animal testing.

In a tumor institute in Beijing, tumor cells were injected into the mice. For this S-180 sarcoma model, the tumor can grow 8% of the mouse body weight in two weeks if there is no any treatment. In a tumor institute in Beijing, tumor cells were injected into the mice. For this S-180 sarcoma model, the tumor can grow 8% of the mouse body weight in two weeks if there is no any treatment.

The mice were divided into 11 treating groups and one control group. The treating groups were given our extracts and the control group was given normal saline every day. The mice were divided into 11 treating groups and one control group. The treating groups were given our extracts and the control group was given normal saline every day.

After two weeks of treatment, the tumors were measured by size and weight. The upper left slide is the tumor in control group---more than half inch in diameter. The lower right slide is the tumor in treating group---a quarter inch in diameter. After two weeks of treatment, the tumors were measured by size and weight. The upper left slide is the tumor in control group---more than half inch in diameter. The lower right slide is the tumor in treating group---a quarter inch in diameter.

The tumor in the control group---2.3 g. The tumor in control group is 5 times than that in treating group in weight. The tumor in the control group---2.3 g. The tumor in control group is 5 times than that in treating group in weight.

This tumor is from tne treating group---0.46 g. The tumor inhibition of treating group to control group is 80%. This tumor is from tne treating group---0.46 g. The tumor inhibition of treating group to control group is 80%.

To see the toxicity of this bacterium extract, LD50 was executed. LD50, 50% lethal dosage, is the observation of the toxic symptoms and death rate of the testing animal after giving a relative high dose of the testing agent.

In general, the high toxicity is between 1 and 50 mg per kg body weight and the actual non-toxicity is above 15000 mg per kg body weight. Our bacterium extract is about 4300 mg/kg. It is close to the micro-toxicity. The lethal dosage is about 250 g in human beings. In general, the high toxicity is between 1 and 50 mg per kg body weight and the actual non-toxicity is above 15000 mg per kg body weight. Our bacterium extract is about 4300 mg/kg. It is close to the micro-toxicity. The lethal dosage is about 250 g in human beings.

Here is the comparison of the clinical chemotherapy drug, cyclophosphamide and our extract for their LD50. Cyclophosphamide is 160 mg/kg. That means that giving this much of dosage will cause 50% animal dead. Our bacterium extract is about 4300 mg/kg. That means that to cause the same rate of animal death, the dosage of our bacterium extract is 26 times more than that of cyclophosphamide. The daily dosage of cyclophosphamide for the clinical cancer treatment is 0.2 g, 2% of its lethal dosage. The daily dosage of our bacterium extract based on 80% tumor inhibition in animal test is about 1 g, 0.4% of the lethal dosage in human beings. So, our bacterium extract is a very low-toxic anticancer agent.

These extracts are crude extract. After the animal test, we are trying to analyze and separate the active components further with our liquid chromatography systems. These extracts are crude extract. After the animal test, we are trying to analyze and separate the active components further with our liquid chromatography systems. Thanks for all the support to the RECNAC, we are going to add a more powerful instrument to our group, the capillary electrophoresis system. With that system, we can analyze the carbohydrates, peptides, amino acids and nuclear acids in our extracts and make the purification work more efficient.

Fatty Acid Metabolism in Tumor and Normal cells:
Like other nutrients, the metabolism disorder of fatty acid may be the cause or the result of a disease. Four normal cell lines and seven cancer cell lines were tested for their fatty acids. There were many differences in fatty acids between normal and cancer cells, but today I just report some of them briefly.

This slide shows the difference of arachidonic acid in normal and cancer cells. The left two are colon cell lines. The green one is normal cell line. The yellow one is cancer cell line. The right two are lung cell lines. The colon cancer cells had lower arachidonic acid than colon normal cells. So did lung cancer cells and normal cells. This slide shows the difference of arachidonic acid in normal and cancer cells. The left two are colon cell lines. The green one is normal cell line. The yellow one is cancer cell line. The right two are lung cell lines. The colon cancer cells had lower arachidonic acid than colon normal cells. So did lung cancer cells and normal cells.

This slide shows the difference of eicosapentaenoic acid in normal and cancer cells. The colon cancer cells had higher eicosapentaenoic acid than colon normal cells. So did lung cancer cells and normal cells. This slide shows the difference of eicosapentaenoic acid in normal and cancer cells. The colon cancer cells had higher eicosapentaenoic acid than colon normal cells. So did lung cancer cells and normal cells.

Arachidonic acid and eicosapentaenoic acid are the precursors of prostaglandins in the human body. The changes of these fatty acids may reflect the metabolic change of the prostaglandins in the cancer cells. A cancer might be controlled by adjusting the balance of the fatty acids.

The right area is for tumor cell lines. The dot line indicates the value 0.7.

In this slide, the left area of the arrow is for normal cell lines. The right area is for tumor cell lines. The dot line indicates the value 0.7. Among the 7 tested tumor cell lines, this ratio was below 0.7. The value for normal cell lines was above 0.7. They were significantly different in statistics (p<0.01). Other people reported previously that the SA/OA ratio could be an index to malignant tumors. Benign tumors showed a higher ratio and malignant tumors showed a lower ratio. Our results in cultured cells confirmed the same thing.
The stearic to oleic ratio is also changed along with the aging of normal cells. When the cells cultured in vitro are confluent in the flask, they need to be divided into another flask. This is called a generation or a passage of the cells. For the normal cells, the passage number is limited to 30~50. Closing to this number, the cells are dying and the growth is very slow. We found that the SA/OA ratio was positively correlated to the age of normal cells. At lower passage number, SA/OA ratio was lower. At hither passage number, SA/OA ratio was higher. The old cells had less oleic acid. Their metabolic rate was slower. Oleic acid is one of the monounsaturated fatty acids. The total monounsaturated fatty acid was decrease also along with the passage number. Does it happen in the human body? Can monounsaturated fatty acid slower down the aging? These questions need to be answered by further study.