| Summary: | 博士 === 國立中興大學 === 食品科學系 === 90 === The aim of this study is to investigate the safety of oil fume produced from peanut oil heated to its smoke point. The mutagenicity, genotoxicity and possible mechanisms of the oil fume were evaluated, and mutagens present in oil fumes were identified. The peanut oil was then refined and treated with addition of antioxidants in order to reduce the mutagenicity of the oil fumes from heated oil.
The first part of this study focuses on investigation of the Seven commercial edible oils including soybean oil, corn germ oil, sunflower oil, peanut oil, blend peanut oil, calola oil and lard were investigated for their physical and chemical properties as well as for the mutagenicity of oil fumes by applying the Ames test. The smoke points of those oils were 118, 119, 95, 98, 107, 138 and 137 oC, respectively. Lard had the best oxidative stability among those seven oils as determined by the Rancimat method. Peanut oil produced the largest amount of fume. The oil fumes of these edible oils showed various degrees of mutagenicity toward Salmonella
typhimurium TA98 and TA100 (p<0.05).
According to the undesirable fumes formation of peanut oil at relatively low temperature, which is the major edible oilproduced in Taiwan. The mutagenicity of fumes obtained from heating peanut oil was studied and the mutagenic compounds was identified. The result revealed that the peanut prepared from roasted peanut kernel (ROPO) showed a lower smoke point, less unsaturated fatty acids, more fume formation and stronger mutagenicity than that from unroasted kernel (UROPO). Further investigation of mutagenic compounds was performed by the Ames test and GC/MS analysis. Amoung the twelve compounds identified from the neutral fraction of methanol extract four compounds at a dose of 10 g per plate were mutagenic to Salmonella TA98 and TA100 cells in the order trans-trans-2,4-decadienal (t-t-2,4-DDE) >trans-trans-
2,4-nonadienal (t-t-2,4-NDE) >trans-2-decenal (t-2-DCA) >trans-2-undecenal (t-2-UDA). Results report the enal compounds formed as the mutagens in the fumes of peanut oil and indicate that inhaling cooking fumes might cause
carcinogenic risk.
The cytotoxicity of peanut oil fumes (POF) and their genotoxicity using single-cell electrophoresis (comet assay), and their induction of reactive oxygen species (ROS) in human A-549 cells were investigated. POF was found to show cytotoxicity to A-549 cells and DNA damage. The glutathione (GSH) content in cell and the activity of GSH antioxidative enzymes were reduced. t-t-2,4-DDE at 37 oC could produce superoxide anion, hydrogen peroxide, and hydroxyl radicals in phosphate buffer (pH 7.4), and form intracellular reactive oxygen species (ROS) in A-549 cells which was determined by dichlorofluorescein assay. Moreover, t-t-2,4-DDE caused a significant (p<0.05) oxidative damage of 8-hydroxy-2’
deoxyguanosine (8-OHdG)to 2’-deoxyguanosine in A-549 cells. While increasing damage of t-t-2,4-DDE and reaction time, the results demonstrated that the DNA damage in A-549 cells induced by t-t-2,4-DDE was related
to the formation of ROS.
The influence of degumming treatment of peanut oil on the contents of mutagenic compounds in fumes from heated peanut oil was investigated. The results indicated that the peanut oil prepared from roasted peanut kernels underwent degumming treatment had lower free fatty acid (FFA) content and higher smoke point, was more clear in color, and produced less fumes when heated at smoke point. Moreover, when compared to untreated peanut oil, the mutagenicity of oil fumes of degummed peanut oil toward Salmonella typhimurium TA98 and TA100 was reduced to 81 and 73% (p<0.05), respectively. The degummed peanut oil which was obtained by adding 3% water and heating at 60℃ for 20 min produced the least amount of mutagenic fume. The contents of four mutagenic compounds, t-t-2,4-DDE, t-t-2,4-NDE, t-2-DCA,and t-2-UDA in oil fumes of
degummed peanut oils were drastically decreased (p<0.05), especially the t-t-2,4-DDE. The results also indicated that FFA content had a high linear correlation with mutagenicity (r2 = 0.9978) and content of t-t-2,4-DDE (r2 = 0.7685). Moreover, there was a correlation (r2 = 0.7816) between the content and the mutagenicity of t-t-2,4-DDE. The decrease of FFA by degumming might explain the reduction of mutagenic alkenal compounds and mutagenicity of fumes from heated peanut oil.
The preventive effects of various antioxidants on the mutagenicity and the formation of enal mutagenic compounds in degummed peanut oil (DPO) fumes were investigated. The mutagenicity of the DPO fumes was significantly reduced (p< 0.05) by various antioxidants added before heating. The addition of antioxidants increase the smoke point and oxidative stability of DPO, and decreased the yield of oil fumes and the amount of mutagens. Synthetic antioxidants including butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT), and
tertiary butylhydroquinone (TBHQ) were more
effective in reducing the mutagenicity and the amount of four enal compounds in fumes from DPO than natural antioxidants such as -tocopherol, catechin, and rosemary extracts. Adding appropriate antioxidants not only reduced the mutagens but also improved the physical and chemical properties of DPO. The results obtained in this study might be useful for developing edible cooking oils with high smoke point, lesser fume, and lower mutagenicity
with the addition of antioxidants.
In this study, the oil fumes from heated oil were found to be mutagenic and genotoxicity. After fractionation, 4 mutagens including t-t-2,4-DDE, t-t-2,4-NDE, t-2-DCA and t-2-UDA were identified. The ROS present in oil fumes could lead to the cleavage of DNA as well as the mutations of base pairs in the DNA. It was found that both the degumming process and the addition of antioxidants could generally improve the physico-chemical properties of peanut oil, reduce the content of all four mutagens present in the oil fumes, and therefore decrease the potential health hazards to household women exposed to the oil fumes.
|
|---|
