Studies to Determine the Nature of the Damage to the Nutritive Value of some Vegetable Oils from Heat Treatment II. Investigation of the Nutritiousness of the Products of Thermal Polymerization of Linseed Oil ,

Crampton, E. W.; Common, R. H.; Farmer, Florence A.; Berryhill, F M; Wiseblatt, L.

doi:10.1093/jn/44.1.177

Cited by 59 publications

(5 citation statements)

References 6 publications

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“…These secondary lipid peroxidation products include volatile and nonvolatile short-chain aldehydes, TG-bound aldehydes, other carbonyl compounds such as ketones, dimeric FA and TG, cyclic FA monomers, and polymerization products (1). Toxic effects due to the consumption of thermally oxidized oils, such as weight loss and high mortality in experimental animals, have been reported (2)(3)(4)(5)(6)(7). The acute toxicity of hydroperoxides has been demonstrated with intravenous doses to rats and mice (8,9); however, equivalent or higher oral doses had no lethal effect (8)(9)(10).…”

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Formation of 4‐hydroxynonenal, a toxic aldehyde, in soybean oil at frying temperature

Seppanen

Csallany

2002

J Americ Oil Chem Soc

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The formation of 4-hydroxy-2-trans-nonenal (HNE), a mutagenic and cytotoxic product of the peroxidation of linoleic acid, was monitored in soybean oil that was heated at 185°C for 2, 4, 6, 8, and 10 h. Unheated soybean oil contained no HNE and a relatively low concentration of polar lipophilic secondary oxidation products (aldehydes and related carbonyl compounds), measured as 2,4-dinitrophenylhydrazine derivatives by HPLC. An increase in the concentration of both HNE and total lipophilic polar oxidation products was observed with increased exposure to frying temperature. A considerable concentration of HNE had already formed at 2 h and the concentration continued to increase at 4 and 6 h of heating. After 6 h the concentration of HNE decreased, possibly due to degradation of the aldehyde with further exposure to high temperature. The loss of endogenous tocopherols was also monitored in the heated oil, and the tocopherol concentration decreased as the secondary lipid oxidation products increased.

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confidence: 99%

Formation of 4‐hydroxynonenal, a toxic aldehyde, in soybean oil at frying temperature

Seppanen

Csallany

2002

J Americ Oil Chem Soc

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“…Among the toxic compounds generated from the deep-fat frying process are carbonyl, cyclic monomer, and dimer derivatives (5,6). Other studies have reported that fats obtained from restaurants and those prepared during frying experiments are not significantly damaged by heating during normal use unless they are abused (7)(8)(9)(10).…”

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Cyclic fatty acid monomers from dietary heated fats affect rat liver enzyme activity

Lamboni

Sébédio

Perkins

1998

Lipids

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This study was conducted to investigate the effects of dietary cyclic fatty acid monomers (CFAM), contained in heated fat from a commercial deep-fat frying operation, on rat liver enzyme activity. A partially hydrogenated soybean oil (PHSBO) used 7 d (7-DH) for frying foodstuffs, or 0.15% methylated CFAM diets was fed to male weanling rats in comparison to a control group fed a nonheated PHSBO (NH) diet in a 10-wk experiment. All diets were isocaloric with 15% fat. Animals fed either CFAM or 7-DH diets showed increased hepatic content of cytochrome (cyt.) b5 and P450 and increased activity of (E.C. 1.6.2.4) NADPH-cyt. P450 reductase in comparison to the control rats. In addition, the activities of (E.C. 2.3.1.21) carnitine palmitoyltransferase-I and (E.C. 1.1.1.42) isocitrate dehydrogenase were significantly decreased when compared to that of rats fed the NH diet. A significantly depressed activity of (E.C. 1.1.1.49) glucose 6-phosphate dehydrogenase was also observed for these animals compared to the control rats fed NH diet. Moreover, liver and microsomal proteins were significantly increased when CFAM or 7-DH diets were fed to animals in comparison to controls while liver glycogen was decreased significantly in experimental groups of rats. The results obtained in this study indicate that the CFAM in the diet from either synthetic sources or used fats increase the activity of liver enzyme systems that detoxify them.

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“…The pioneering work of Crampton et al (1953Crampton et al ( , 1956) suggested a relationship between the nonvolatile, non-urea-adduct-forming fraction of thermally degraded lipids and various toxic responses. Recent reports documented that ingestion of oxidation products of thermally degraded lipids result in various symptoms of toxicity including organ enlargement, growth depression, necrosis of liver cells, extensive cellular damage, and even death (Kaunitz et al, 1959;Perkins & Kummerow, 1959;Alexander, 1978Alexander, , 1981.…”

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Comparison of thermally oxidized lipids and acetaminophen with concurrent consumption of ethanol as inducers of liver cirrhosis

Shahidi

1995

Journal of Toxicology and Environmental Health

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The mechanism(s) of liver damage initiated by ingestion of toxic components of thermally oxidized lipids was compared in a rat model with the documented mechanisms of hepatic failure and necrosis initiated by acetaminophen. Acetaminophen (50 mg/kg body weight) or oxidized lipids (0.15 ml oxidized trilinolein or 1.05 ml oxidized butter oil per rat) were intubated at 12-h intervals to rats. Treated rats were allowed free access to food and water containing 3% ethanol. Changes in relative concentration of acute-phase plasma proteins, determined by two-dimensional (2D) immunoelectrophoresis, were taken as a marker of liver damage. In contrast to simple inflammation, acute-phase plasma proteins in this study disproportionately increased or decreased as histological damage of the liver due to intubation oxidized lipids or acetaminophen. Histological examination of liver of rats intoxicated with oxidized lipids revealed severe liver cirrhosis at the end of the trial, where the remaining viable hepatocytes were separated in a matrix of collagen. [3H1]Thymidine incorporation in hepatic DNA of acetaminophen or oxidized lipid intoxication increased in the early stages of intoxication, indicative of regenerative activity of the liver. Further progression of the cirrhosis inhibited continued liver regeneration and [3H1]thymidine incorporation into hepatic DNA. The cirrhotic liver at this stage failed to regenerate to the original mass upon 75% partial hepatectomy. Therefore, it may be concluded that hepatic necrosis produced by oxidized lipids or by acetaminophen may have similar mechanisms.

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Studies to Determine the Nature of the Damage to the Nutritive Value of some Vegetable Oils from Heat Treatment II. Investigation of the Nutritiousness of the Products of Thermal Polymerization of Linseed Oil ,

Cited by 59 publications

References 6 publications

Formation of 4‐hydroxynonenal, a toxic aldehyde, in soybean oil at frying temperature

Formation of 4‐hydroxynonenal, a toxic aldehyde, in soybean oil at frying temperature

Cyclic fatty acid monomers from dietary heated fats affect rat liver enzyme activity

Comparison of thermally oxidized lipids and acetaminophen with concurrent consumption of ethanol as inducers of liver cirrhosis

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