Male Wistar rats were fed ad libitum a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control) or used frying oil recovered from Japanese food manufacturing companies (recovered oil) for 12 weeks and subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to recovered oil were observed. There was a tendency toward higher consumption of the diet in the experimental group as compared to the control group. In the serum of the experimental group, no difference was detected in the levels of glucose, triacylglycerol, and phospholipids. But many dark-red patches, necrosis, and bleeding were found in the livers of 75% of the experimental rats; these rats had extremely high aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values. Average AST and ALT values of the experimental group were significantly higher than those of the controls. The renal cells were also obviously damaged. These results raise the concern that frying oil contained in ready-made foods, snacks, etc., if deteriorated to an extent equal to or greater than that of the recovered oil, may be able to change human serum AST/ALT levels and damage the liver and kidneys.
Heated frying oils with different chemical properties in terms of AV (acid value), POV (peroxide value), COV (carbonyl value), and contents of polar compounds (PC) and triacylglycerol (TG), as well as color and odor, were obtained. Male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control) or one of the frying oils described above. The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oils were observed. However, the rats fed a diet containing the heated oil developed apparent liver damage to different degrees regardless of the chemical properties of the ingested oils. Thus, it was suggested that the chemical properties evaluated here had little to do with the cytotoxicity of heated oil, although the properties express quality of oil. Volatile compounds seem to be major candidates for the toxic agents in heated oil because oils with rancid and deteriorated odor show strong toxicity.
Frying oil in use of cooking may contain acrylamide formed from frying foodstuffs. We have reported that administration of a diet containing 7% practically used frying oil for 12 weeks damaged liver and kidneys severely in Wistar rats. Then, male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control group) or frying oil heated with Asn + glucose for 20 h at 180 under a nitrogen flow in order to form acrylamide under the least thermal deterioration (experimental group). The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oil were observed. But the experimental rats had significantly low insulin and triacylglycerol levels. The liver and kidneys from the experimental rats had damages, but the degree of the histological changes looked lighter than that of the rats fed practically used frying oil described above. The serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were also not much increased. Thus, it was suggested that continuous intake of trace acrylamide induced characteristically low serum insulin level and that the effects of the used frying oil on the liver and kidneys were hardly attributable to acrylamide possibly contained therein.
Male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control), and frying oils heated for 20 h at 180 degrees C with amino acids, gluten, sugar, and wheat starch, respectively. The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oils were observed. The serum of all the experimental groups showed a tendency toward lower levels of triacylglycerol and free fatty acids and higher levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) than that of the control group. Among experimental groups, the rats fed a diet containing oil heated with gluten were least influenced by thermally deteriorated oil in terms of serum levels of glucose, triacylglycerol, phospholipids, cholesterol, and insulin; histological evaluations; and number of dark-red patches found on the surface of the liver.
Used frying oil recovered from food manufacturing companies in Japan and recycled often shows lower carbonyl (COV) and peroxide values (POV) than oil simply heated at 180 degrees C for 20 h does. In this study the reasons for the low COV of oil used for deep-frying were investigated by employing model experiments and actual commercial frying. The results suggested that in actual frying, the factor most influencing the low COV was vaporization of carbonyl compounds, together with steam generated from water contained in frying foodstuffs. It was also suggested that the low levels of COV were attributable partly to inhibition by protein, amino acids exuded from frying foodstuffs, and starch, and slightly to the effects of natural antioxidants in fresh oil and frying foodstuffs, oil absorption by frying foodstuffs, and dilution of oil in use by fresh oil added between uses. On the other hand, the chemical properties of oil in a fryer and in batter coatings of deep-fried foods made with the former oil were checked. Content of polar compounds (PC) and color score were obviously worse in the oil extracted from batter coatings than in that in the fryer, but there were no differences in COV or content of triacylglycerol (TG) of the two oils.
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