Biological observations from feeding heated corn oil and heated peanut oil to rats

Abstract

Five groups of male weanling rats were provided purified diets containing 15% by weight of either fresh or laboratory-heated corn oil (FCO, HCO) or fresh, laboratory-heated, or commercial pressure deep-fry peanut oil (FPO, HPO, PPO). Total weight gain, feed consumption, and feed efficiency were consistently greater for the FCO, FPO, and PPO groups. Although relative heart weights were unaffected, the HCO and HPO produced elevated liver and kidney weights. The dietary fats had no effect on the hematological status of the animals or the proportions of cells comprising the total leukocytes of the blood. Physical, chemical, and microscopic evaluation of the urine detected no pathologic conditions. Rats fed diets containing HCO or HPO demonstrated toxicity of thermally oxidized fats by the appearance of diarrhea, dermatitis, seborrhea, and hair loss. Histological examinations revealed injury of the thymus by all fat samples except the FCO; the liver was damaged by the HCO, HPO, and PPO, and the testes and epididymides by HPO and PPO. In the latter case there was complete cessation of spermatogenesis.

Effects of Deteriorated Frying Oil in SHR/NDmc-cp Rats

“…It was reported that body weight gains of animals were retarded remarkably by the administration of oxidized oil (4,5,7). In the present work, the experimental group developed neither diarrhea nor seborrhea and showed a higher tendency toward body weight gain than the control group did, as in the study by Izaki et al (6).…”

“…But it seems obvious that the difference did not play a big role in the evaluation of the recovered oil because Naito et al (10) observed no changes in body weight, food and water intake, and kidney weight when they fed spontaneously hypertensive rats a commercial defatted diet added 10 wt% soybean oil or canola oil respectively, and gave drinking water containing 1% NaCl for 26 weeks. One of the reasons for the lack of development of gross symptoms in the previous studies (6, 7) seems to be that the experimental oils employed by Gabriel et al (4) and Alexander et al (5) were oxidized to a level that does not occur in oils normally consumed in human diets. In general, deterioration of oil is easily perceived by its smell and viscosity, and therefore it is hard to imagine that present-day people would ingest such highly deteriorated edible oil.…”

“…The weights of liver and kidney were 24.7 4.4 g and 2.7 0.1 g for the experimental group, and 24. 5 1.8 g and 2.6 0.1 g for the control group, showing no difference between the two. The weight of adipose tissue was higher in the control group (31.5 5.9 g) than in the experimental group (28.…”

Forestomach tumor induction by 2,4-hexadienal in F344N rats and B6C3F1 mice

“…Feeding lipid oxidation products and oxidized fats to laboratory animals has been reported to cause adverse biological effects, including growth retardation; teratogenicity; cellular damage to the liver, kidneys, testes, and epididymides; increased cellular proliferation in the gastrointestinal tract; increased peroxidation of membrane and tissue lipids; induction of cytochrome P450 activities in the liver and colon; and other nonspecific tissue injuries and irritations (Alexander et al 1987;Crawford and Wheeler 1983;Izaki et al 1984;Kanazawa et al 1985Kanazawa et al , 1986Poulsen et al 1998). The role of consumed oxidized oils in gastrointestinal carcinogenesis, including the effects of oral intake of different doses of various biologically active compounds present in heated oils, oxidative stress induced by chronic consumption of repeatedly heated oils, and interactions with other modulating dietary factors encompassing both macro-and micronutrients has not been investigated (Hageman et al 1991).…”

Lipid hydroperoxides from processed dietary oils enhance growth of hepatocarcinoma cells

“…In our cell model, the long incubation times of 24 h combined with high LOOH concentrations of 100 lM exhibited toxic effects. Similarly, toxic effects were observed in animal models after feeding with oxidized oils [37,38]. Again, in our cell model shorter incubation times and lower doses of LOOH did not decrease cell number but influenced cell proliferation and gene expression.…”