: cancer

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DHA:

2008-01-21 _MP_ (javascript: – _DHA_ (javascript: may help kill

cancer cells

Aires V, Hichami A, Filomenko R, et al. Docosahexaenoic acid induces

increases in [Ca2+]i via inositol 1,4,5-triphosphate production and activates

protein (title truncated). Mol Pharmacol. 2007;72(6):1545-56.

We investigated, in monocytic leukemia U937 cells, the effects of

docosahexaenoic acid (_DHA_ (javascript: ; 22:6 n-3) on calcium signaling and

determined the implication of phospholipase C (PLC) and protein kinase C (PKC)

in this pathway. DHA induced dose-dependent increases in [Ca2+]i, which

were contributed by intracellular pool, via the production of

inositol-1,4,5-triphosphate (IP3) and store-operated Ca2+ (SOC) influx, via

opening of

Ca2+ release-activated Ca2+ (CRAC) channels. Chemical inhibition of PLC,

PKCgamma, and PKCdelta, but not of PKCbeta I/II, PKCalpha, _or_ (javascript:

PKCbetaI, significantly diminished DHA-induced increases in [Ca2+]i. In

vitro PKC assays revealed that DHA induced a approximately 2-fold increase in

PKCgamma and -delta activities, which were temporally correlated with the

DHA-induced increases in [Ca2+]i. In cell-free assays, DHA, but not other

structural analogs of fatty acids, activated these PKC isoforms. Competition

experiments revealed that DHA-induced activation of both the PKCs was

dose-dependently inhibited by phosphatidylserine (_PS_ (javascript: ).

Furthermore, DHA induced apoptosis via reactive oxygen species (ROS)

production,

followed by caspase-3 activation. Chemical inhibition of PKCgamma/delta and

of SOC/CRAC channels significantly attenuated both DHA-stimulated ROS

production and caspase-3 activity. Our study suggests that DHA-induced

activation of PLC/IP3 pathway and activation of PKCgamma/delta, via its action

on PS

binding site, may be involved in apoptosis in U937 cells.

2007-11-27 ZWCWKZZ - omega-3PUFAs inhibit the growth of gastric cancer

cells through promoting apoptosis

Yin Y, Zhan W, Peng J, et al. [Apoptosis of human gastric cancer cells

induced by _omega-3_ (javascript: polyunsaturated fatty acids.] Zhonghua

Wei Chang Wai Ke Za Zhi. 2007;10(6):570-573.

OBJECTIVE: To investigate the effect of _omega-3_ (javascript:

polyunsaturated fatty acids(omega-3PUFAs) on the apoptosis of human gastric

cancer

cell line SGC-7901 and to explore the potential mechanisms. METHODS: Cells

were treated with eicosapentaenoic acid (20:5omega-3,_EPA_ (javascript: )

_or_ (javascript: docosahexaenoic acid (22:6omega-3, _DHA_ (javascript:

) at concentrations of 10, 20 and 40 mug/ml. Cell growth and apoptosis

were analyzed with MTT assay, cell morphology, DNA electrophoresis and flow

cytometry. Mitochondrial membrane potential ( triangle right psi mt) was

measured by fluorescent probe rhodamine 123. The distribution of cytochrome C

in mitochondria and cytosol was determined by enzyme-linked immunoadsorbent

assay. The composition of mitochondrial membrane phosphlipid(MMP)was

examined by gas chromatography. RESULTS: Both EPA and DHA markedly inhibited

the

SGC-7901 cell growth and induced apoptosis in a time- and dose-dependent

manner. After incubation of the cells with 40 mug/ml EPA or DHA for 24

hours, the level of triangle rightpsimt siginificantly decreased (P<0.001), and

cytochrome C largely released into cytosol from mitochondria. The

proportions of EPA and DHA in MMP rapidly elevated while that of arachidonic

acid

sharply decreased. CONCLUSIONS: omega-3PUFAs inhibit the growth of gastric

cancer cells through promoting apoptosis. Compositional and functional

alterations in mitochondrial membrane may be an important initiator of

apoptosis

induced by omega-3PUFAs.

_Back to Immune Health_

(http://www.omega-research.com/research.php?catid=4) 2004-12-01 _JNut_

(javascript: - Omega-3s in oncology - looking

at outcomes, alternatives.

Hardman, WE. (n-3) Fatty Acids and Cancer Therapy. J. Nutr,

2004;134:3427S-3430S.

Supplementing the diet of tumor-bearing mice _or_ (javascript: rats

with oils containing (n-3) (_omega-3_ (javascript: ) or with purified (n-3)

fatty acids has slowed the growth of various types of cancers, including

lung, colon, mammary, and prostate.

The efficacy of cancer chemotherapy drugs such as doxorubicin, epirubicin,

CPT-11, 5-fluorouracil, and tamoxifen, and of radiation therapy has been

improved when the diet included (n-3) fatty acids.

Some potential mechanisms for the activity of (n-3) fatty acids against

cancer include modulation of eicosanoid production and inflammation,

angiogenesis, proliferation, susceptibility for apoptosis, and estrogen

signaling.

In humans, (n-3) fatty acids have also been used to suppress

cancer-associated cachexia and to improve the quality of life.

In one study, the response to chemotherapy therapy was better in breast

cancer patients with higher levels of (n-3) fatty acids in adipose tissue

[indicating past consumption of (n-3) fatty acids] than in patients with lower

levels of (n-3) fatty acids.

Thus, in combination with standard treatments, supplementing the diet with

(n-3) fatty acids may be a nontoxic means to improve cancer treatment

outcomes and may slow or prevent recurrence of cancer.

Used alone, an (n-3) supplement may be a useful alternative therapy for

patients who are not candidates for standard toxic cancer therapies.

____________________________________

From: Szukidavis@...

Date: Thu, 18 Mar 2010 23:10:42 -0400

Subject: Protocell

cures for cancer

CC: jb31784@...; badillo9@...

Does anyone know where the best source for Protocell is and is there

anything not recommended to take with it?

____________________________________

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