A comparison of dietary fish oil and corn oil in experimental colorectal carcinogenesis

Rats fed either fish oil (n = 16) or corn oil (n = 16) in calorically and nutritionally balanced diets were injected with 1,2-dimethylhydrazine, which is a colorectal specific carcinogen; differential colorectal tumor induction was then measured. In addition, plasma peroxide concentrations were measured in rats in each dietary group as well as in a group receiving a low-fat diet, either with or without prior carcinogen treatment (n = 3 for each of the 6 groups). Tumor incidence did not differ between groups fed corn oil and fish oil. Tumor yield in the left colon was significantly lower in rats fed fish oil (p = 0.0499). Total colorectal tumors induced were also fewer in the rats fed fish oil (p = 0.065). Plasma peroxide concentrations were difficult to interpret because of the wide variation within groups. The data on tumor yield in the left colon support the hypothesis that a diet rich in n-3 fatty acids, which are found in fish oil, may be less supportive of colorectal tumor development than a diet rich in n-6 fatty acids, which is found in corn oil. However, the mechanism by which fish oil decreases tumor induction is still unknown.     

The effects of dietary nitrogen level on the collagen of rat skin

1. Male rats of approximately 120 g body-weight were maintained on a commercial stock diet containing 204 g crude protein (nitrogen x 6.25)/kg, a hydroxyproline-free high-protein (HP) diet containing 200 g casein/kg as the only protein source, or a low-protein (LP) diet containing 40 g casein/kg. After 6 weeks on these diets half of each group was transferred to a non-protein (NP) diet and the experiment was continued for a further 6 weeks. Animals from each group were killed at 4 d, 3 weeks and 6 weeks after the transfer to the NP diet. 2. Throughout the experiment the urinary excretion of N, hydroxyproline and creatinine, and the content and solubility of the skin collagen were determined. 3. When compared with a control group killed at the beginning of the experiment the rats maintained on the LP diet showed an increase of 25% in total N content of the skin but collagen content increased by 100%. Rats transferred from the HP to the NP diet lost both N and collagen from the skin, but those transferred from the LP to the NP diet lost N but increased the collagen content by 42%. 4. Protein deprivation brought about marked changes in the solubility of the skin collagen, suggesting an increase in the rate of maturation of skin collagen.     

The effect of various dietary fats on skin tumor initiation

The type of dietary fat has been shown to modulate the initiation stage of mammary tumorigenesis, with saturated fat fed before and/or during carcinogen treatment resulting in increased tumor incidence. This study was designed to determine whether different types of dietary fat alter the initiation stage of skin carcinogenesis by use of the initiation‐promotion mouse skin carcinogenesis model. Sencar mice were divided into three groups and maintained on one of the experimental diets. The AIN‐76‐based diets consisted of 10% total fat with various types of fat: 8.5% menhaden oil plus 1.5% corn oil, 8.5% coconut oil plus 1.5% corn oil, and 10% corn oil. After three weeks mice were initiated with 10 nmol dimethyl‐benz[a]anthracene (DMBA). Two weeks later, all mice were switched to a diet containing 5% corn oil. Promotion began four weeks after initiation with twice‐weekly application of 1 μg 12‐O‐tetradecanoylphorbol‐13‐acetate and continued for 12 weeks. No statistically significant differences in kilocalories of food consumed or body weights were observed between diet groups during the study. The final papilloma incidence, yield, and size were not significantly different among the diet groups. In a parallel study, [³H]DMBA binding to epidermal DNA showed no dietary differences. Unlike the mammary carcinogenesis model, these data suggest that the type of fat fed during DMBA initiation had minimal effects on this stage of skin carcinogenesis.     

Null effect of dietary restriction on prostate carcinogenesis in the Wistar-Unilever rat

Chronic dietary restriction inhibits carcinogenesis in several sites in laboratory animals. To determine the effects of dietary restriction on prostate carcinogenesis, prostate cancers were induced in male Wistar-Unilever rats by a sequential regimen of cyproterone acetate (50 mg/day; 21 days); testosterone propionate (100 mg/kg/day; 3 days); N-methyl-N-nitrosourea [MNU; 30 mg/kg; single dose]; and testosterone (subcutaneous implants of 2 pellets containing 40 mg each). Dietary restriction (0% [ad libitum control], 15%, or 30%) was initiated 2 wk post-MNU, and continued until study termination at 12 mo. Dietary restriction induced a rapid suppression of body weight gain but conferred no protection against prostate carcinogenesis. 74% of carcinogen-treated ad libitum controls developed accessory sex gland cancers, versus cancer incidences of 64% and 72% in groups restricted by 15% and 30%, respectively. Similarly, 44% of dietary controls developed cancers limited to the dorsolateral/prostate, versus incidences of 45% and 53% in groups restricted by 15% and 30%. The results of the present study do not support the hypothesis that prostate carcinogenesis can be prevented by reducing caloric intake. Reducing mean body weight by up to 25% through chronic dietary restriction has no effect on the induction of prostate cancers in the Wistar-Unilever rat model.     

The effect of various dietary fats on skin tumor initiation.

The type of dietary fat has been shown to modulate the initiation stage of mammary tumorigenesis, with saturated fat fed before and/or during carcinogen treatment resulting in increased tumor incidence. This study was designed to determine whether different types of dietary fat alter the initiation stage of skin carcinogenesis by use of the initiation-promotion mouse skin carcinogenesis model. Sencar mice were divided into three groups and maintained on one of the experimental diets. The AIN-76-based diets consisted of 10% total fat with various types of fat: 8.5% menhaden oil plus 1.5% corn oil, 8.5% coconut oil plus 1.5% corn oil, and 10% corn oil. After three weeks mice were initiated with 10 nmol dimethylbenz[a]anthracene (DMBA). Two weeks later, all mice were switched to a diet containing 5% corn oil. Promotion began four weeks after initiation with twice-weekly application of 1 microgram 12-O-tetradecanoylphorbol-13-acetate and continued for 12 weeks. No statistically significant differences in kilocalories of food consumed or body weights were observed between diet groups during the study. The final papilloma incidence, yield, and size were not significantly different among the diet groups. In a parallel study, [3H]DMBA binding to epidermal DNA showed no dietary differences. Unlike the mammary carcinogenesis model, these data suggest that the type of fat fed during DMBA initiation had minimal effects on this stage of skin carcinogenesis.     

Promotion of epidermal carcinogenesis by repeated damage to mouse skin

Chemically induced epidermal carcinogenesis is usually divided into two stages: initiation, which involves the conversion of some epidermal cells into latent neoplastic cells; and promotion, which results in tumors. The hallmark of chemical promoters is epidermal hyperplasia. The hyperplasia caused by a strong promoter, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), differs morphologically from that caused by weak promoters, such as acetic acid and mezerin. The epidermal regeneration that follows abrasion results in a hyperplastic epidermis that resembles the effects of strong promoters. Repeated mechanical injuries are capable of enhancing papillomas and carcinomas in mouse skin initiated with 7,12-dimethylbenzanthracene (DMBA). Thus, a regenerative epidermal hyperplasia appears to be a precondition for tumor promotion. It is highly probable that many epidermal cells are initiated during the lifetime of man. In the work place, repeated mechanical injury could predispose to epidermal neoplasms.     

Comparative effects of dietary corn oil,safflower oil,fish oil and palm oil on metabolism of ethanol and carnitine in the rat

OBJECTIVE: This study was launched to determine comparative effects of corn oil (CO), safflower oil (SO), fish oil (FO) and palm oil (PO) on carnitine status and ethanol metabolism in rats. METHODS: Twenty-four male Sprague-Dawley rats (300 g bw) were randomly divided into four groups (n = 6) and fed a semisynthetic diets containing fat as oils listed above. Blood and 24 hour urine samples were collected before and after dietary treatment and acute ethanol administration. Samples were analyzed for blood-ethanol concentration (BEC) and carnitine species. RESULTS: The diets containing FO and PO retarded ethanol metabolism compared to the diets containing CO and SO. The effect of these dietary fats on carnitine species in plasma and urine was varied before and after dietary treatment and following a single oral ethanol dose. The liver carnitine content was higher in the PO group after dietary and ethanol treatment. CONCLUSION: It is concluded that attenuation of ethanol clearance was related to unique fatty acid makeup of the oils that in part may be attributed to the composite ratio of saturated to unsaturated fatty acids in the oils.     

Jute batching oil: a tumor promoter on mouse skin

A mineral oil essentially used in the jute industry for the "batching" of jute fibers, and earlier reported to be nontumorigenic on mouse skin, has been found to be a tumor promoter following a two-stage mouse-skin bioassay protocol. The types of tumors developed after initiation with a single dose of urethane or 3-methylcholanthrene (subcutaneously), followed by repeated skin painting with jute batching oil (JBO) included benign papillomas, keratoacanthomas, and fibrosarcomas. Chemical analysis of this oil indicated the total aromatic content was 11.71% and the amount of fluoranthene, pyrene, chrysene, and triphenylene was in the range of 192.54 to 227.79 mg/kg in the test sample. The underlying biochemical mechanisms for the tumor-promoting effect of JBO seemed to operate through a different pathway rather than involving the induction of cytochrome-dependent monoxygenase and N-demethylase activities in the tissue.     

Effect of dietary olive oil, corn oil and medium-chain triglycerides on the lipid composition of rat red blood cell membranes

The effects of dietary olive oil, corn oil and medium-chain triglycerides (MCT) on factors that characterized erythrocyte membrane lipid fluidity were studied. Weanling rats were fed for 3 or 5 wk high fat diets (10%) containing olive oil, corn oil or a mixture of MCT with olive oil or corn oil. Total phospholipids and phosphatidylcholine of erythrocyte ghosts obtained from olive oil-fed animals, as compared to those fed corn oil, showed an increase in long-chain polyunsaturated fatty acids (PUFA) of the (n-6) and (n-3) series and a decrease in saturated fatty acids. The addition of MCT to the olive oil diet induced an increase in palmitic, palmitoleic and delta-5,8,11-eicosatrienoic acids and a decrease in long-chain PUFA of the (n-6) series in erythrocyte membrane phospholipids. Conversely, rats fed a mixture of MCT and corn oil, as compared to those fed exclusively corn oil, showed increase in long-chain PUFA of the (n-6) and (n-3) series, with no changes in saturated fatty acid levels. The cholesterol/phosphorus molar ratio showed only a slight increase with MCT supplementation. Olive oil feeding induced important changes in fatty acid composition of erythrocyte membrane phospholipids as compared to corn oil feeding without modifying the cholesterol/phosphorus ratio and MCT feeding slightly affected red blood cell membrane lipid composition.     

The impact of dietary fat and fiber on intestinal carcinogenesis

The effect of dietary fiber on intestinal carcinogenesis in animals is controversial. Some find that the addition of wheat bran or cellulose inhibits intestinal cancer in rats, while others report no effect. Such mixed results often are due to differences in the design of experiments. One important aspect in this regard is the amount of fat in the diet. Some fiber supplements inhibit cancer formation when the fat content is normal but not when it is high. However, a recent epidemiological study in Scandinavia showed a lower cancer incidence in a rural population compared with an urban area, in spite of the fact that the dietary fat content was high in both regions. There was a modest difference in the amount of fiber, and this may not have accounted completely for the variation in cancer incidence. Other dietary factors might have added inhibitory response to help overcome the promotional effect of an excessive amount of fat. The interaction among dietary components must be considered when designing animal experiments to assess the effect of fiber on cancer development.     

Ras signaling pathway in the chemopreventive action of different ratios of fish oil and corn oil in experimentally induced colon carcinogenesis

Dietary factors play a significant role in colon cancer. The essential polyunsaturated fatty acids (PUFAs), n-3 PUFAs, and n-6 PUFAs exert inverse effect on cancer. This study was designed to understand the mechanism of chemopreventive action of different ratios of fish oil (FO) and corn oil (CO) in colon carcinoma. Wistar rats were divided into 3 groups: Group 1 received purified diet whereas Groups 2 and 3 received modified diet with FO:CO (1:1) and FO:CO (2.5:1), respectively. The groups were further subdivided into controls receiving ethylenediamine-tetra acetic-acid and treated groups received dimethylhydrazine-dihydrochloride (DMH)/wk for 4 wk. Animals sacrificed 48 h after last injection constituted initiation phase and that sacrificed after 16 wk constituted post-initiation phase. Differential effect of different ratios of FO and CO was analyzed in isolated colonocytes. In both phases, DMH treatment showed an increase in pan Ras, Raf, MEK1/2, extracellular signal regulated kinase (Erk)1/2, and c-fos levels. Akt levels were increased in post-initiation phase only. Treatment with FO + CO (1:1) + DMH decreased pan Ras, MEK1/2 and Erk1/2 levels in post-initiation phase whereas Raf and c-fos were decreased in both phases. Treatment with FO + CO (2.5:1) + DMH decreased Ras, Raf, MEK1/2, Erk1/2, and c-fos levels in both phases. Akt was decreased in post-initiation phase only. The chemo-preventive action of FO and CO may be mediated by time- and dose-dependent effect.     

Effects of an essential fatty acid deficiency, pair-feeding and level of dietary corn oil on the hypothalamic-pituitary-gonadal axis and other physiological parameters in the male chicken

Two studies were conducted to observe the effects of an essential fatty acid (EFA) deficiency, added dietary corn oil and pair-feeding on growth, reproduction and other physiological parameters in the mature cockerel. A purified, linoleic acid (LA)-deficient diet (0.01% LA), or additions of 5% (3.01% LA) or 15% (9.04% LA) corn oil, were fed ad libitum from hatching through 24 weeks of age. Reductions in growth, feed consumption, and comb, and testes size, incomplete spermatogenesis, increased tissue eicosatrienoic acid (20: 3 omega 9) and changes in weights of selected internal organs were observed in deficient cockerels. Total pituitary gonadotropic activity was measured by two bioassay procedures and blood luteinizing hormone was measured by radioimmunoassay. By maturity both of these parameters were significantly reduced in deficient chickens. When these chickens were fed diets with 5% or 15% corn oil under pair-feeding or ad libitum conditions from 20 to 24 weeks, the reduced growth, comb and testes size and gonadotropin metabolism appeared to be caused by depressions in appetite and energy intake rather than EFA per se. The degenerate testicular histology of the 20-week old deficient cockerels, while responding fully to the ad libitum intake of the diets containing corn oil, showed only partial rehabilitation of spermatogenesis when diets with either 5% or 15% corn oil were pair-fed. In general, increasing the level of dietary fat from 5% to 15% did not cause many physiological changes.