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Wednesday, June 1, 2016

Phytochemicals In Foods: The effects of Beta Sitosterol

Kyle J. Norton(Scholar and Master of Nutrients, all right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bio science, ISSN 0975-6299.

                 Beta Sitosterol

Beta Sitosterol is a phytochemincal in the class of Phytosterols, belonging to the group of Lipids, found abundantly in avocados, rice bran, wheat germ, corn oils, fennel, peanuts, soybeans, hawthorn, basil, buckwheat. etc.

Health Benefits
1. Benign prostatic hyperplasia (BPH)
In the investigation of the effects of stinging nettle (Urtica dioica L.) (UD) on benign prostatic hyperplasia (BPH) induced by testosterone. Two biochemical markers viz., β-sitosterol and scopoletin, were isolated and characterised in the extracts utilising High-performance thin layer chromatographic shown that UD can be used as an effective drug for the management of BPH, according to "Ameliorative effects of stinging nettle (Urtica dioica) on testosterone-induced prostatic hyperplasia in rats" by Nahata A, Dixit VK.(1)

2. Prostate cancer
In the investigation of the effect of two dietary sterols on prostate cancer cells in vitro. beta-Sitosterol (SIT), the most common plant sterol, and cholesterol, an animal sterol, were compared for effect on LNCaP cell growth, differentiation, apoptosis, and sphingomyelin cycle intermediates, found that the decrease in cell number and increase in apoptosis associated with SIT treatment are mediated by activating the sphingomyelin cycle, according to "beta-Sitosterol activates the sphingomyelin cycle and induces apoptosis in LNCaP human prostatecancer cells" by von Holtz RL, Fink CS, Awad AB.(2)

3. Breast cancer
in the evaluation of examine the effect of the two most common dietary PS, beta-sitosterol (SIT) and campesterol, as compared to cholesterol, the main sterol in the Western diet, on growth, apoptosis and cytotoxicity of MDA-MB-231 human breast cancer cells in culture, found that SIT supplementation for 3 days at 16 microM resulted in a 6-fold increase in apoptosis in cells when compared to cholesterol treated cells. SIT treatment was found to have no effect on the level and content of tumor cell PP2A. It is concluded that SIT, by a still unknown mechanism, may offer protection from breast cancer by inhibiting growth and stimulating apoptosis, according to "Inhibition of growth and stimulation of apoptosis by beta-sitosterol treatment of MDA-MB-231 human breast cancer cells in culture" by Awad AB, Downie AC, Fink CS.(3)

4. Stomach cancer
In the examination of the proliferation, cytotoxicity, and apoptosis of beta-sitosterol in SGC-7901 human stomach cancer cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, clone formation, lactate dehydrogenase (LDH) leakage assay, acridine orange (AO)/ethidium bromide (EB) double staining, 4',6-diamidine-2'-phenylindole dihydrochloride (DAPI) staining, comet assay, and Western blotting, showed that beta-sitosterol suppresses the proliferation and induces the cell cytotoxicity of SGC-7901 stomach cancer cells in a time- and dose-dependent manner. Cells treated with different concentrations of beta-sitosterol also showed changes typical of apoptosis: morphological changes, according to "Beta-sitosterol inhibits cell growth and induces apoptosis in SGC-7901 human stomach cancer cells" by Zhao Y, Chang SK, Qu G, Li T, Cui H.(4)

5. Leukemia
In the investigation of the mechanism of apoptosis induced by beta-sitosterol in human leukemic U937 cells. beta-Sitosterol induced cytotoxicity and apoptosis in U937 cells in a concentration dependent manner, found that caspase-3 activation is partially essential for beta-sitosterol-induced apoptosis. Bcl-2 overexpression also significantly blocked caspase-3 activation and the decrease in PARP cleavage by beta-sitosterol, and effectively attenuated the apoptotic response tobeta-sitosterol. These results show that beta-sitosterol potently induces apoptosis in U937 cells and that beta-sitosterol-induced apoptosis is related to the selective activation of caspase-3 and induction of Bax/Bcl-2 ratio, according to "Beta-sitosterol induces anti-proliferation and apoptosis in human leukemic U937 cells through activation of caspase-3 and induction of Bax/Bcl-2 ratio" by Park C, Moon DO, Rhu CH, Choi BT, Lee WH, Kim GY, Choi YH.(5)

6. Anti cancers
Phytochemical analysis of Fijian populations of the green alga Tydemania expeditionis led to the isolation of two unsaturated fatty acids, 3(zeta)-hydroxy-octadeca-4(E),6(Z),15(Z)-trienoic acid (1) and 3(zeta)-hydroxy-hexadeca-4(E),6(Z)-dienoic acid (2), along with the known 3(zeta)-hydroxy-octadeca-4(E),6(Z)-dienoic acid (4). Investigations of the red alga Hydrolithon reinboldii led to identification of a glycolipid, lithonoside (3), and five known compounds, 15-tricosenoic acid, hexacosa-5,9-dienoic methyl ester, beta-sitosterol, 10(S)-hydroxypheophytin A, and 10(R)-hydroxypheophytin A. Compounds 1, 2, and 4, containing conjugated double bonds, demonstrated moderate inhibitory activity against a panel of tumor cell lines (including breast, colon, lung, prostate and ovarian cells) with IC(50) values ranging from 1.3 to 14.4 microM. The similar cell selectivity patterns of these three compounds suggest that they might act by a common, but unknown, mechanism of action, according to "Antineoplastic unsaturated fatty acids from Fijian macroalgae" by Jiang RW, Hay ME, Fairchild CR, Prudhomme J, Roch KL, Aalbersberg W, Kubanek J.(6)

7. Etc.

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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/21806658
(2) http://www.ncbi.nlm.nih.gov/pubmed/9824850
(3) http://www.ncbi.nlm.nih.gov/pubmed/10762659
(4) http://www.ncbi.nlm.nih.gov/pubmed/19456133
(5) http://www.ncbi.nlm.nih.gov/pubmed/17603173
(6) http://www.ncbi.nlm.nih.gov/pubmed/18757069

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