415
human metastatic PC-3, LNCaP and TSU prostate cell lines, the rat metastatic MatLy- Lu cell line and rat non-metastatic epithelial cell lines EPYP1, EPYP2 and
EPYP3. Cell lines were treated with linoleic acid (LA), an omega-6 FA (n-6), as
well as linolenic (LLA) and eicosapentaenoic (EPA) acids, which are both omega-3
FAs (n-3). All cell lines were treated with 10% and 0.5% serum supplemented
media plus fatty acid for comparison. The results demonstrate that linoleic acid
(n-6) has promotional effects at doses of 1–100 ng/ml in all cell lines with the
exception of EPYPl. Experiments with linolenic acid (n-3) demonstrated consistent
growth promotion in all cell lines except EPYP2. EPA demonstrated promotion at
low concentrations and inhibited prostate cell growth at higher concentrations.
Recently, Palakurthi et al. (2000) demonstrated the anticancer activity of eicosapentaenoic acid (EPA), through in vitro and in vivo models of experimental cancer. The
molecular basis for the anticancer effects is EPA inhibits cell division by inhibiting
translation initiation. This is a consequence of the ability of EPA to release Ca
2+
from intracellular stores while inhibiting their refilling via capacitative Ca
2+
influx
that results in partial emptying of intracellular Ca
2+
stores and thereby activation of
protein kinase R. In a KLN-205 squamous cell carcinoma mouse model, daily oral
administration of EPA resulted in a significant reduction of tumor size and malignant hypertetraploid cells. Recently, Simopoulos (2008) stated that excessive
amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/
omega-3 ratio, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased
levels of omega-3 PUFA (a lower omega-6/omega-3 ratio), exert suppressive effects.
A ratio of omega-6/omega-3 at 2.5/1 reduced rectal cell proliferation in patients
with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3
PUFA had no effect. A lower ratio of omega-6/omega-3 fatty acids is more desirable
in reducing the risk of cancer.
The fat-soluble vitamins (Vitamin A, D, E, and K) present in the plant and animal
sources and cooking oils, has been found to inhibit proliferation of several types of
cancer cells, including those of breast, lung, and endometrium. Amir et al. (1998)
evaluated the mechanistic aspects of vitamin A (lycopene) treatment, which resulted
in a concentration-dependent reduction in HL-60 cell growth as measured by [ 3 H]
thymidine incorporation and cell counting. This effect was accompanied by inhibition of cell cycle progression in the G 0 /G 1 phase as measured by flow cytometry.
Furthermore, the combination of low concentrations of lycopene with 1,25- dihydroxy
vitamin D 3 exhibited a synergistic effect on cell proliferation and differentiation and
an additive effect on cell cycle progression. Likewise, Weinstein et al. (2007)
reported that Alpha-tocopherol supplementation (50 mg daily for 5–8 years) reduced
prostate cancer incidence by 32% in the alpha-Tocopherol, Beta-Carotene Cancer
Prevention Study. They also investigated the effect of serum alpha-tocopherol or
intake of vitamin E (eight tocopherols and tocotrienols) on prostate cancer risk with
up to 19 years of follow-up study. Higher serum alpha-tocopherol was associated
with reduced risk of prostate cancer.
Likewise, Noto et al. (1989) reported the anticancer activity of vitamin K3 in
combination with Vitamin C. VitaminK3 (Menadione) in combination with vitamin
Nutraceutical Properties of Lipids
human metastatic PC-3, LNCaP and TSU prostate cell lines, the rat metastatic MatLy- Lu cell line and rat non-metastatic epithelial cell lines EPYP1, EPYP2 and
EPYP3. Cell lines were treated with linoleic acid (LA), an omega-6 FA (n-6), as
well as linolenic (LLA) and eicosapentaenoic (EPA) acids, which are both omega-3
FAs (n-3). All cell lines were treated with 10% and 0.5% serum supplemented
media plus fatty acid for comparison. The results demonstrate that linoleic acid
(n-6) has promotional effects at doses of 1–100 ng/ml in all cell lines with the
exception of EPYPl. Experiments with linolenic acid (n-3) demonstrated consistent
growth promotion in all cell lines except EPYP2. EPA demonstrated promotion at
low concentrations and inhibited prostate cell growth at higher concentrations.
Recently, Palakurthi et al. (2000) demonstrated the anticancer activity of eicosapentaenoic acid (EPA), through in vitro and in vivo models of experimental cancer. The
molecular basis for the anticancer effects is EPA inhibits cell division by inhibiting
translation initiation. This is a consequence of the ability of EPA to release Ca
2+
from intracellular stores while inhibiting their refilling via capacitative Ca
2+
influx
that results in partial emptying of intracellular Ca
2+
stores and thereby activation of
protein kinase R. In a KLN-205 squamous cell carcinoma mouse model, daily oral
administration of EPA resulted in a significant reduction of tumor size and malignant hypertetraploid cells. Recently, Simopoulos (2008) stated that excessive
amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/
omega-3 ratio, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased
levels of omega-3 PUFA (a lower omega-6/omega-3 ratio), exert suppressive effects.
A ratio of omega-6/omega-3 at 2.5/1 reduced rectal cell proliferation in patients
with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3
PUFA had no effect. A lower ratio of omega-6/omega-3 fatty acids is more desirable
in reducing the risk of cancer.
The fat-soluble vitamins (Vitamin A, D, E, and K) present in the plant and animal
sources and cooking oils, has been found to inhibit proliferation of several types of
cancer cells, including those of breast, lung, and endometrium. Amir et al. (1998)
evaluated the mechanistic aspects of vitamin A (lycopene) treatment, which resulted
in a concentration-dependent reduction in HL-60 cell growth as measured by [ 3 H]
thymidine incorporation and cell counting. This effect was accompanied by inhibition of cell cycle progression in the G 0 /G 1 phase as measured by flow cytometry.
Furthermore, the combination of low concentrations of lycopene with 1,25- dihydroxy
vitamin D 3 exhibited a synergistic effect on cell proliferation and differentiation and
an additive effect on cell cycle progression. Likewise, Weinstein et al. (2007)
reported that Alpha-tocopherol supplementation (50 mg daily for 5–8 years) reduced
prostate cancer incidence by 32% in the alpha-Tocopherol, Beta-Carotene Cancer
Prevention Study. They also investigated the effect of serum alpha-tocopherol or
intake of vitamin E (eight tocopherols and tocotrienols) on prostate cancer risk with
up to 19 years of follow-up study. Higher serum alpha-tocopherol was associated
with reduced risk of prostate cancer.
Likewise, Noto et al. (1989) reported the anticancer activity of vitamin K3 in
combination with Vitamin C. VitaminK3 (Menadione) in combination with vitamin
Nutraceutical Properties of Lipids