- Dietary fatty acids reduces prostate tumors Full source:Nutrition and Cancer 1997, Vol 29, Iss 2, pp 114-119
This study examined the effects of unsaturated fatty acids (FAs) on human prostate cancer cell growth in mice. In one group, mice were fed 23% fat diets containing 18% corn oil, 5% linseed oil, and 18% menhaden oil. Seven days later they were injected with prostate cancer cells. The diets were continued for six weeks. There was a 30% reduction in tumor growth in the 18% menhaden oil group. The tumor phospholipid fatty acid patterns suggested It is believed that the tumor inhibitory effect of the high menhaden oil diet was due, in part, to a reduction of arachidonic acid available for prostaglandin biosynthesis. In another group, mice were injected with prostate cancer cells directly into the prostate gland and fed a high-fat linoleic acid rich, or a low-fat diet for 10 weeks. All but 7 of the 50 mice had developed large macroscopic tumors. However, the mean tumor weight in the high-fat group was twice that in the low-fat group. This shows that a stimulatory effect of dietary fatty acids on prostate cancer cell growth may work on an initial tumor cell mass.
- Dietary energy and nutrients in relation to preclinical prostate cancer Full source: Nutrition and Cancer 1997, Vol 29, Iss 2, pp 120-126
Previous studies of diet and prostate cancer have focused on advanced disease and have suggested a positive association with saturated fat intake. This study focused on 215 men with preclinical prostate cancer and 593 controls with no evidence of cancer. The study population comprised two groups: 1) men treated surgically for benign prostatic hypertrophy 2) participants in a prostate cancer screening program. The participants were interviewed on their usual diet using a diet history questionnaire. A positive association was observed between total energy intake and preclinical prostate cancer. The odds ratios for prostate cancer increased with each quartile of energy intake. The study provides some evidence that total energy intake is related to preclinical prostate cancer and suggests that diet could be involved earlier than thought in the occurrence of prostate cancer.
- Polyphenols inhibit pancreatic cancer
The effects of green tea polyphenols (GTP), beta-carotene, and palm carotene on the progression stage of pancreatic cancer were studied in Syrian hamsters. Inhibitory effects were noted for beta-carotene at 25 ppm, and palm carotene at 40 ppm. GTP at doses of 500 and 5000 ppm also significantly decreased the numbers of hyperplasia and total duct lesions. Combined administration of 40 ppm palm carotene, and 50 ppm GTP similarly inhibited the lesion development. The results suggest that chemopreventive effects are exerted by beta-carotene and GTP above critical doses and that combined administration of palm carotene and green tea polyphenols might be a chemoprevention strategy for pancreatic cancer in humans.
- Green tea induces cancer cell death Full source: Journal of the National Cancer Institute 1997, Vol 89, Iss 24, pp 1881-1886
The polyphenolic compounds present in green tea show cancer chemopreventive effects in many animal tumor models. This study investigated the effect of green tea polyphenols and the major constituent, epigallocatechin-3-gallate, on the induction of apoptosis (programmed cell death) and regulation of cell cycle in human and mouse carcinoma cells. Treatment of cancer cells with green tea polyphenols and its components resulted in the formation of internucleosomal DNA fragments, characteristic of apoptosis. Hence, green tea may protect against cancer by causing cell cycle arrest and inducing apoptosis. It needs to be evaluated in human trials.
- Prevention of photoimmunosuppression and photocarcinogenesis by topical nicotinamide Full source: Nutrition and Cancer 1997, Vol 29, Iss 2, pp 157-162
Ultraviolet (UV) B irradiation is a potent suppressor of the immune systems's capacity to reject tumors. If this immunosuppression is critical for the development of most skin tumors, then prevention of immunosuppression should result in prevention of photocarcinogenesis. Treatment of UV-irradiated mice with nicotinamide twice weekly starting two weeks before UV irradiation and throughout the experiment prevented this immunosuppression. UVB irradiation consisted of five weekly 30-minute exposures to banks of six fluorescent sunlamps. Application of nicotinamide to UV-irradiated mice reduced skin tumor incidence from 75% to 42.5%.
- Antioxidative effect of melatonin in the brain Full source: Journal of Physiology and Biochemistry 1997, Vol 53, Iss 3, pp 301-305
A single high dose (25 mg/kg)of adriamycin (AD) (an antibiotic which causes oxidative stress) was administered to the rat brain. Melatonin was injected daily three days before and after oxidative stress induction. Melatonin prevented significant lipoperoxide increase in plasma, hypothalamus and brain cortex. CAT (computerized axial tomography) activity which was decreased in hypothalamus by AD, increased by simultaneous melatonin administration. These results, especially those concerning lipoperoxide content changes, showed a powerful antioxidative effect of melatonin at both neural and extraneural levels in rats. CAT changes in the presence of melatonin suggest that there is a relationship between a scavenger role of melatonin and a high oxidative activity in the brain hypothalamy area. These results also show that melatonin, besides producing the extraneural effect, can act as a powerful antioxidative agent in organs such as the brain, very rich in lipids, susceptible to oxidation in the neuronal as well as the extraneuronal tissues.
- Aminoguanidine prevents age-related arterial stiffening and cardiac hypertrophy Full source: Proc Natl Acad Sci USA (UNITED STATES) Feb 3 1998
Aging is associated with cardiac hypertrophy (enlargement)and arterial stiffening possibly associated with accumulation of advanced glycation end products (AGEs) (glycation is the product of reaction between a sugar and the free amino group of proteins -cross-linking). We evaluated the effect of aminoguanidine, an inhibitor of AGE production, on end-stage alterations of renal and cardiovascular systems. Aminoguanidine prevented the age-related cardiac hypertrophy. The increase in membrane surface in aging rats was reduced by 30% by aminoguanidine. Collagen content of the arterial wall increased between 24 and 30 mo. The age-related increase in aortic impedance in control 24 and 30 mo. old rats and the decrease in carotid stretchability were prevented by aminoguanidine. The prevention of arterial stiffening and cardiac hypertrophy suggests that the effect of aminoguanidine is related to a decrease in the AGE-induced cross-linking of the extracellular matrix.
- Deprenyl restores noradrenergic nerve fibers in the spleen Full Source:Journal of Neuroimmunology, 1998, Vol 81, Iss 1-2, pp 144-157
It is well-established that noradrenergic (NA) nerve fibers in spleen and lymph nodes influence cell-mediated immune responses. Such responses are diminished in young animals following chemical sympathectomy (interruption of the sympathetic nervous pathway). and in older animals accompanying an age-related decline in NA nerve fibers in spleen and lymph nodes. This study determined that Deprenyl, an irreversible monoamine oxidase-B (MAO-B) inhibitor, would hasten the process of splenic NA nerve fiber restoration following chemical sympathectomy in young rats and would reverse the age-related loss of sympathetic NA fibers in the spleen of old rats. In this study, there was a severe loss of NA distribution or supply of nerves in the spleens of young sympathectomized rats, compared with unlesioned control animals. Treatment of sympathectomized rats with 1.0 mg, 2.5 mg, and 5.0 mg/kg deprenyl for 30 days increased the density of NA compared with vehicle-treated controls. The spleens of untreated and saline-treated old rats showed a reduction in the density of NA innervation in the white pulp compared with young animals. The results provide strong evidence for a neurorestorative property of deprenyl on sympathetic NA innervation of the spleen which may lead to an improvement in cell-mediated immune responses.
- Vitamin C improves vasodilation in diabetes mellitus Full Source:Journal of the American College of Cardiology 1998, Vol 31, Iss 3, pp 552-557
Endothelium dependent vasodilation is impaired in patients with diabetes mellitus. Oxidatively mediated degradation of endothelium-derived nitric oxide contributes to abnormal endothelium-dependent vasodilation in animal models of diabetes mellitus. In this study, vitamin C selectively restored the impaired endothelium-dependent vasodilation in the forearm resistance vessels of patients with insulin-dependent diabetes mellitus. The findings indicate that nitric oxide degradation by oxygen free radicals contributes to abnormal vascular reactivity in humans with insulin-dependent diabetes mellitus.
- Genistein, an anticancer phytoestrogen from soy Full Source: Journal of the National Cancer Institute 1998, Vol 90, Iss 5, pp 381-388
Soy products contain high levels of genistein, a phytoestrogen that is a potent inhibitor of cell proliferation and angiogenesis. Genistein has been found to inhibit the growth of carcinogen-induced cancers in rats and human leukemia cells transplanted into mice, In this study, cell cultures were treated with azetidine, a proline analog, which elicits a stress response that includes the induction of stress proteins (glucose-related proteins and heat shock proteins) has been shown to protect tumor cells against programmed cell death; This stress response was inhibited by genistein, The anticancer effects of genistein may be related to its ability to reduce the expression of stress response-related genes.
- Risk for breast cancer: Diet, nutrition, and physical exercise Full Source: Journal of the National Cancer Institute 1998, Vol 90, Iss 5, pp 389-394
The percentages of breast cancer cases in a given population attributable to specific risk factors can be calculated. Determination of such risks associated with potentially modifiable risks factors, such as diet (e,g,, levels of consumption of fruits, vegetables, vitamins, etc.), alcohol consumption, exercise, and body weight, are necessary to focus prevention strategies. With the use of data from a case-control study conducted in Italy from June 1991 through April 1994 on 2569 breast cancer case subjects and 2588 control subjects, calculations were made for odds ratios and population-attributable risks for breast cancer in relation to 1) dietary beta-carotene and vitamin E intake, 2) alcohol consumption, 3) physical activity, and, for postmenopausal women, 4) body mass index. The following attributable risks for the indicated risk factors were observed: 10.7% for high alcohol intake, 15.0% for low beta-carotene intake, 8.6% for low vitamin E intake, and 11.6% for low levels of physical activity, The risks associated with alcohol and beta-carotene intake were larger among premenopausal women, and the risk associated with physical activity was larger among post menopausal women, Being overweight accounted for 10.2% of breast cancer cases in postmenopausal women. Beta-Carotene plus alcohol accounted for 28.1% of the cases. Beta-Carotene and physical activity accounted for 32%, and these three factors together accounted for 33% of the breast cancer cases in the overall dataset. Exposure to a few selected and potentially modifiable risk indicators explained about one third of the cases of breast cancer in this Italian population, indicating the theoretical scope for prevention of the disease.
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