Deep-frying Fat Research Articles

Biological effects of short-term feeding to rats of repeatedly used deep-frying fats in relation to fat mutagen content

The effects of short-term feeding of mutagen containing, heated deep-frying oils on urinary and faecal mutagenicity, plasma clinical biochemical parameters, peroxidative effects and cell proliferative indices in the gastro-intestinal tract were determined in rats. Repeatedly used frying oils [a saturated fatty acid-rich coconut oil (CO) and a polyunsaturated fatty acid (PUFA)-rich (> 60% PUFA) vegetable frying oil (PO)] were administered to groups of seven rats at a level of 10% (by weight) in the diet for 4 wk; control groups were fed equal amounts of the unheated oils. Both heated oils showed direct-acting mutagenicity to Salmonella tester strain TA97; heated PO was also mutagenic to strain TA100. Both heated CO and heated PO contained detectable amounts of thiobarbituric acid-reactive substances (TBA-RS). In heated PO, hydroperoxides of linoleic acid were also present. In groups fed heated oils the mutagenicity of urine and faeces to strain TA97 was not found to be increased in comparison with the control groups. Faecal mutagenicity to strain TA100 was also unaffected by consumption of heated oils. Urinary excretion of TA100 mutagens was significantly increased in rats fed heated PO. Plasma alkaline phosphatase activity was clearly raised in rats fed heated PO, in comparison with rats fed unheated oils or heated CO. In addition, other clinical biochemical plasma parameters showed a tendency to be increased in rats fed heated PO, indicating hepatic and renal cellular toxicity. Urinary and faecal excretion of thiobarbituric acid-reactive substances (TBA-RS) were also slightly, but not significantly, increased in rats fed heated PO. Feeding heated CO to rats did not result in increased plasma enzyme activities and excretion of TBA-RS, nor in increased cell proliferation in gastro-intestinal tissues. Cell proliferation of the oesophageal tissues were slightly, but significantly, increased in rats fed heated PO, in comparison with the group fed unheated PO. Tissues of the glandular stomach and colon/rectum did not show significantly enhanced cell proliferation in the group fed heated PO. The results obtained in this study indicated that consumption of heated oils containing TA100 mutagens and oxidation products of linoleic acid produced indications of cellular damage to liver and kidneys, and increased urine mutagenicity, as well as enhanced cell proliferation in the oesophagus.

Mutagenicity of deep-frying fat, and evaluation of urine mutagenicity after consumption of fried potatoes

Mutagen formation during deep-frying was evaluated using standard frying conditions. Portions of pre-fried, sliced potatoes were fried in a commercial brand of hydrogenated vegetable frying fat, which was used repeatedly and for a prolonged period of time. Concentrations of polar oxidation and degradation products, and of dimeric and polymeric triglycerides, were found to increase in the frying fat as well as in fried potatoes with prolonged use of the fat. Thiobarbituric acid-reactive substances were detectable neither in the frying fat nor in the fried potatoes. Polar fractions of repeatedly used frying fat significantly increased the number of revertants in Salmonella typhimurium strain TA97 without S-9 mix. In the presence of S-9 mix mutagenic activity was reduced. As a consequence of ongoing formation of polar degradation and oxidation products, the mutagenicity of the fat increased after repeated use. Polar fractions of lipids extracted from commercially obtained pre-fried potatoes, as well as from fried potatoes, marginally increased the number of revertants in strain TA97 without S-9 mix. The mutagenicity of the lipid fractions of fried potatoes was not related to the heating time of the fat. Methanol extracts of fat-free residues of fried potatoes significantly increased numbers of revertants in strain TA97 after metabolic activation, which indicated that a different class of mutagens had been isolated. The mutagenicity of methanol extracts was not increased after either prolonged or repeated use of the fat. Urine samples of six healthy, non-smoking volunteers, collected during the 24 hr following consumption of portions of potatoes fried in repeatedly used fat, showed no increase in mutagenicity compared with control samples. Since the exact identity of mutagens formed during deep-frying, as well as their metabolic fate in man, is unclear at present, evaluation of possible adverse biological effects associated with consumption of fried foods will require strictly controlled metabolic studies.

Linoleic acid hydroperoxide concentration in relation to mutagenicity of repeatedly used deep-frying fats.

A high-performance liquid chromatography procedure was developed to measure linoleic acid hydroperoxides (LAHPO) in 19 used, deep-frying fat samples that were screened for mutagenicity. The detection limit of the method was found to be 10 nmol of LAHPO/g of fat. In eight samples, LAHPO were not detected; levels in the other samples ranged from 17 to 267 nmol/g of fat. LAHPO were not detectable in unused hydrogenated frying fat samples. Concentrations of LAHPO correlated positively with mutagenicity to Salmonella tester strains TA97 and TA100, in presence of S9 mix only; coefficients of correlation were, respectively, r=0.48 (p less than 0.05) and r=0.24 (n.s.). Without metabolic activation no significant associations or secondary autoxidation products of linoleic acid generated in presence of liver S9 mix may contribute to mutagenicity of some of the used deep-frying fat samples.

Assessment of mutagenic activity of repeatedly used deep-frying fats

Mutagenic activity of repeatedly used deep-frying fats was evaluated in relation to chemical characteristics. Deep-frying fat samples were collected from local restaurants and snack bars after sensory indication of abuse. A total of 20 deep-frying fat samples and 2 unused control fat samples was tested. Fat samples were fractionated into non-polar and polar compounds by column chromatography. Amounts of polar compounds obtained ranged from 2% (by weight) for unused fat to 44% for used deep-frying fat. Levels of di- and poly-meric triglycerides (DPTG) were determined using gel-permeation chromatography. DPTG concentrations of 13 used deep-frying fat samples exceeded the treshold level of 10% above which fats are rejected for use. In addition thiobarbituric acid-reactive substances (TBA-RS) were measured. Amounts of TBA-RS were just above detection levels for most fat samples. Five used fat samples, however, contained relatively high concentrations of TBA-RS, ranging from 82 to 177 moles malondialdehyde/g. Non-polar and polar fractions were screened for mutagenic activity using the Ames mutagenicity assay. Mutagenic activity was found predominantly in polar fractions at doses higher than 1 mg/plate in strains TA97, TA100 and TA104, variously with and without metabolic activation. The highest number of mutagenic samples was detected by strain TA97, which appeared to be most sensitive. Some samples exhibited toxic effects. Chromatography blanks, consisting of solvents processed according to the same procedures as used for fat samples, were not mutagenic. Mutagenic activity was also detected in polar material obtained from unused frying fat. Non-polar fractions of unused frying fats showed no mutagenicity. A frying experiment carried out under laboratory conditions indicated that during repeated and prolonged use of deep-frying fat mutagenic polar substances were formed. Fat samples taken after 20 and 40 h of frying contained increasing amounts of polar compounds. Mutagenic activity was highest after 20 h of frying but was slightly decreased after 40 h of frying. At this stage, however, mutagens also appeared in the non-polar fraction. Mutagenic activity of polar fractions of used deep-frying fats in strain TA97 was positively correlated with levels of TBA-RS, which may indicate the involvement of lipid oxidation products in mutagenicity of used deep-frying fats. No significant correlations were found with other chemical characteristics. In the process of deep-fat frying numerous degradation products are formed, which may include mutagenic heterocyclic amines and other pyrolysates. At present the specific nature of mutagens formed during deep fat frying is unclear.

Finished product formulation

AbstractRules of formulation are discussed. Some characteristic properties of raw materials and finished products can be instrumentally determined, others more empirically. Such approach applies to raw material interchangeability as well. Formulation problems will differ according to the type of finished product: margarines, shortenings, salad dressings, deep frying fats, specialty fats. They will also vary depending on the user: household, catering, manufacturer or food industry. Modern methods for formulation are then described.

Fractionation of Interesterified Fats for the Preparation of Plastic Fats

AbstractSome specific directed interesterified fat products which had high slip points and had little potentiality for use as edible fats, were crystallized from acetone at different low temperatures. The appropriate fractions obtained from interesterified products of Ricebran containing Mowrah, Palm, Sal and of Sal and Cottonseed mixture (1:1, w/w), appeared to be suitable for utilization as vanaspati and margarine like fat products with high essential fatty acid content and without trans unsaturated fatty acids and also as highly stable deep frying fats and bakery fats.

Microbiological studies investigation mutagenicity of deep frying fat fractions and some of their components.

In this study, the Salmonella/microsome mutagenicity test according to Ames et al. (Mutation Res. 31:347, 1975) was performed in order to detect possible mutagenicity of oxidized deep frying fat fractions. Furthermore, the mono-, di-, tri- and tetrahydroxyoctadecanoic acids and the hydroperoxide of linoleic acid were investigated as model test substances. The Ames assay was carried out with and without metabolic activation including preincubation and liquid culture procedures as described by Mitchell (Mutation Res. 54:1, 1978). The results show no mutagenic effects for the oxidized fractions of deep frying fats nor for the model test substances. At higher concentrations, however, limited test reliability resulted from direct toxic effects on bacterial growth.

Uptake and fate of Di-2-ethylhexyl phthalate in aquatic organisms and in a model ecosystem.

Di-2-ethylhexyl phthalate (DEHP), often referred to as dioctyl phthalate or DOP, is the most widely used plasticizer for vinyl plastics, and approximately 350 million pounds were produced in the United States during 1970. Altogether the production of phthalate ester plasticizers was 855 million pounds (1). The cumulative production of DEHP and related phthalate plasticizers in the United States since 1943 is in excess of 8000 million pounds (2). DEPH is an external plasticizer which softens resins without reacting with them chemically, and it may be present in concentrations up to 40% of the weight of the plastic as in the familiar laboratory tubing. As a result of the large production and wide distribution and destruction of plastics, DEHP has become uniquitous and has been found in milk (3), deep frying fat (4), and human blood plasma (5). DEHP has also begun to appear as a micropollutant in the tissues of a variety of organisms. Taborsky (6) isolated it from bovine pineal glands, and Nazir et al. (7) found it in mitochondria from the hearts of cattle, dogs, rabbit, and rat. DEHP has been