Article

Temperature Dependence of HNE Formation in Vegetable Oils and Butter Oil

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Abstract

The temperature dependence of the formation of toxic 4-hydroxy-2-trans-nonenal (HNE) was investigated in high and low linoleic acid (LA) containing oils such as corn, soybean and butter oils. These oils contain about 60, 54 and 3–4% of LA for corn, soybean and butter oils, respectively. The oils were heated for 0, 0.5, 1, 2, and 3h at 190°C and for 0, 5, 15 and 30min at 218°C. HNE concentrations in the oils were analyzed by high performance liquid chromatography (HPLC). The maximum HNE concentrations in heated (190°C) corn, soybean and butter oils were 5.46, 3.73 and 1.85μg HNE/g oil, respectively. The concentration of HNE at 218°C increased continuously for all the three oils, although they were heated for much shorter periods compared to the lower temperature of heating (190°C). HNE concentration at 30min reached the maximum of 15.48, 10.72 and 6.71μg HNE/g oil for corn, soybean and butter oils, respectively. HNE concentration at higher temperature (218°C) was 4.9, 3.7, and 8.7 times higher than at the lower temperature (190°C) and 30min of heating for corn, soybean and butter oils, respectively. It was found that HNE formation was temperature dependant in the tested oils.

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... In recent years, HNE and HHE were linked to several diseases, like cancer, atherogenesis, diabetes, chronic inflammation, and neurodegenerative diseases (Alzheimer's or Parkinson's diseases), among others (Csala et al. 2015;Esterbauer, Schaur, and Zollner 1991;Gu eraud 2017;Pillon et al. 2012;Sousa, Pitt, and Spickett 2017). Due to the high reactivity and biological activity of these compounds, research on their occurrence in foods has increased, especially on edible oils and fats (Guill en and Uriarte 2012; Han and Csallany 2008;Ma and Liu 2017;Papastergiadis et al. 2014a;Seppanen and Csallany 2001, as well as in foods enriched with PUFA (Meynier et al. 2014;Surh and Kwon 2005;Surh, Lee, and Kwon 2007). The findings indicate that there are other food matrices of interest, namely fish and fish products, and milk, infant formulas and dairy products. ...
... The most frequent methodologies reported in the literature for food analysis of 4-hydroxy-2-alkenals (Table 2) are: high-performance liquid chromatography (HPLC) coupled to ultraviolet (UV) (Aladedunye, Matth€ aus, and Przybylski 2011;Aladedunye and Przybylski 2012;Alghazeer and Howell 2008;Csallany et al. 2015;Gasc et al. 2007;Grune et al. 2001;Han and Csallany 2008;Han and Csallany 2009;Lynch et al. 2008;Tadashi Sakai et al. 1997;T. Sakai et al. 2004;T. ...
... With respect to the applied methods, it is very important to take into account that the total heating time and temperature was similar for intermittent (185 ± 5 C; 1 h/day; during 5 days) and continuous (185 ± 5 C; 6 h) heating, however the treatments were different concerning the equipment and the volume of oil used (Seppanen and Csallany 2006). Han and Csallany (2008) investigated the temperature dependence of HNE formation in vegetable oils and butter. Samples of corn and soybean oils (higher contents of linoleic acid) and butter (lower contents of linoleic acid) were heated for different periods at 190 C (recommended frying temperature) and 218 C. It was found that HNE amounts after 30 min of heating at 218 C were 3.7, 4.9 and 8.7 times higher than at 190 C, for soybean, corn and butter oil, respectively (Han and Csallany 2008). ...
Article
Undoubtedly, significant advances were performed concerning 4-hydroxy-2-alkenals research on foods, and their formation by double oxidation of polyunsaturated fatty acids. But further studies are still needed, especially on their occurrence in foods enriched with n-3 and n-6 fatty acids, as well as in foods for infants and processed foods. Major factors concerning the formation of 4-hydroxy-2-alkenals were discussed, namely the influence of fatty acids composition, time/temperature, processing conditions, salt, among others. Regarding mitigation, the most effective strategies are adding phenolic extracts to foods matrices, as well as other antioxidants, such as vitamin E. Exposure assessment studies revealed 4-hydroxy-2-alkenals values that could not be considered a risk for human health. However, these toxic compounds remain unaltered after digestion and can easily reach the systemic circulation. Therefore, it is crucial to develop in vivo research, with the inclusion of the colon phase, as well as, cell membranes of the intestinal epithelium. In conclusion, according to our review it is possible to eliminate or effectively decrease 4-hydroxy-2-alkenals in foods using simple and economic practices.
... Compounds such as HNE are a consequence of fatty acids degradation in the presence of oxygen, and when vegetable oils are exposed to high temperatures [3]. From a health impact point of view, HNE is appointed as a cytotoxic and mutagenic compound, related with several diseases, such as atherosclerosis, low density lipoprotein oxidation, stroke, Parkinson's and Alzheimer's diseases, among others [4]. Acute effects, including the inhibition of catabolic and anabolic functions that lead to cell death were observed at a cellular level even with low HNE concentrations (>100 µM). ...
... Afterwards, Han and Csallany have studied the formation of HNE at a higher frying temperature, 218C for short periods of time, and compared it to a lower frying temperature, 190C for longer periods of time. In this study, authors have included three types of oils: butter, corn and soybean [4]. HNE concentration at the higher frying temperature was 4.9, 3.7, and 8.7 times higher than at the lower temperature. ...
... HNE concentration at the higher frying temperature was 4.9, 3.7, and 8.7 times higher than at the lower temperature. The concentration of HNE at 30 min reached the maximum of 15.5, 10.7 and 6.7 mg/kg of oil for corn, soybean and butter oils, respectively [4]. Recently, Papastergiadis., et al. have determined the HNE content in some foodstuffs commercialized in Belgium including vegetable oils [6]. ...
... Boskou et al. (2006) reportou resultados para óleos (girassol, palma, azeite e gordura vegetal) usados na fritura de batatas, bem como para o produto frito, e verificou que o teor de HNE está sobretudo relacionado com o tipo de óleo usado na fritura, e não tanto com a deterioração térmica a que o óleo é sujeito[38]. Em 2008,Han and Csallany (2008) compararam óleos vegetais e manteiga, submetidos a elevadas temperaturas durante curtos períodos de tempo, com óleos vegetais e manteiga submetidos a temperaturas mais baixas, mas durante períodos de tempo mais longos. ...
... Boskou et al. (2006) reportou resultados para óleos (girassol, palma, azeite e gordura vegetal) usados na fritura de batatas, bem como para o produto frito, e verificou que o teor de HNE está sobretudo relacionado com o tipo de óleo usado na fritura, e não tanto com a deterioração térmica a que o óleo é sujeito[38]. Em 2008,Han and Csallany (2008) compararam óleos vegetais e manteiga, submetidos a elevadas temperaturas durante curtos períodos de tempo, com óleos vegetais e manteiga submetidos a temperaturas mais baixas, mas durante períodos de tempo mais longos. Deste modo, verificaram que mais uma vez era mais importante a composição em ácidos gordos dos óleos vegetais, do que o próprio tempo de exposição ao tratamento térmico, concluindo que para óleos/gorduras que contém elevados teores de ácido linoleico o tratamento térmico deve ser realizado utilizando temperaturas baixas, para prevenir a formação do HNE.Estudos científicos evidenciam que o HNE pode estar presente em outros alimentos para além de óleos e gorduras de origem vegetal, como por exemplo em fiambre, bacon, e salsichas fumadas, com teores a variar entre 3,77 e 95,2 µmol/kg[39].Han and Csallany (2012), determinaram ...
... The high increase of HNE concentration in imitation cheeses was expected since these cheeses are made with vegetable oils which are high in linoleic acid, a precursor of HNE [14]. This laboratory has previously reported higher HNE formation in high linoleic vegetable oils than in butter oil due to heat treatment [18]. Figure 3 shows the HNE concentration in imitation cheeses and natural cheeses treated at higher temperature at 232°C up to 30 min. ...
... Since imitation cheeses are made with vegetable oils which contain much higher levels of linoleic acid, a precursor for HNE, than dairy fat it is not surprising that heat induced lipid peroxidation results in increased HNE formation in imitations cheeses compared to dairy fat containing cheeses, which are low in linoleic acid. The large increase of HNE formation at higher temperature agrees with the result previously reported for high linoleic acid vegetable oil and butter by this laboratory [18]. Results showed significant temperature dependence in the oxidative degradation of fatty acids and therefore the increased formation of HNE. ...
Article
The formation of 4-hydroxy-2-trans-nonenal (HNE), a toxic aldehyde formation, was investigated in heat treated imitation Mozzarella cheeses which are made with vegetable oils and in natural Mozzarella cheeses which contain dairy fats. The cheeses were heat treated at 204 °C for 30 and 60 min, and at 232 °C for 15 and 30 min. The HNE formations were much higher in imitation cheeses than in natural cheeses due to both heat treatments. Average HNE concentrations in imitation cheeses, after 30 min of heat treatment at 204 °C, were 110.3 ng HNE/g cheese and it increased to 877.1 ng HNE/g cheese when the temperature was raised to 232 °C. In natural cheeses, the average HNE concentration was much lower only 13.4 ng HNE/g cheese after 204 °C heat treatment for 30 min and it increased only to 182.8 ng HNE/g cheese using 232 °C. Since imitation cheeses are made with vegetable oils which contain much higher levels of linoleic acid, a precursor for HNE, than dairy fat, it is not surprising that heat-induced lipid peroxidation results in increased HNE formation in imitations cheeses compared to dairy fat containing cheeses, which are low in linoleic acid.
... This 4-HNE concentration corresponds to our 4-HNE concentration in CO after 6 weeks of storage at 40°C, which is surprising, since the formation of hydroxyalkenals has been shown to be temperature-dependent, so higher levels would have been expected at higher temperatures. 45 4-HHE and 4-HNE levels showed significant positive correlation with AV values in CO and CCO and separately (r > 0.97, p < 0.002), reflecting the AV as a measure of secondary oxidation products. CCO showed a lower 4-hydroxyalkenal formation after 4−9 weeks of storage compared to CO with less plant rest materials. ...
... Formation of MDA and HNE is faster at higher temperature . HNE concentration produced by heating corn oil, soybean oil, and butter at high temperature (218 • C) for 30 min is 4.9, 3.7, and 8.7 times that at low temperature (190 • C) for 30 min, respectively (Han & Csallany, 2008). Therefore, in order to reduce the risk of high MDA and HNE in fried food, it is necessary to increase the frequency of frying oil replacement and use lower frying temperature. ...
Article
Full-text available
Reactive carbonyl compounds are a large group of highly reactive electrophilic compounds containing one or more carbonyl groups, which can be created by lipid oxidation both in vivo and in food. Malondialdehyde (MDA) and 4‐hydroxy‐2‐nonenel (HNE) are the two most important reactive carbonyl compounds in food. They can react with proteins and nucleic acids and cause biological damage to cells and lead to carbonyl stress. Therefore, they are regarded as representative products of lipid oxidation, toxic molecules, and biomarkers of oxidative stress. Apart from biological toxicity, they can also react with myoglobin and myofibrillar protein and further affect color, gel properties, hydrophobicity, or other properties of food. However, the effects of MDA and HNE on food qualities have not received as much attentions and it is noteworthy that the existing analytical methods for detecting MDA and HNE have a variety of limitations due to the complexity of food samples. To provide a comprehensive understanding of HNE and MDA, the formation mechanism, occurrence, and analytical methods for MDA and HNE in food matrix were summarized in this article. Emphasis is focused on formation mechanism including non‐enzymatic pathway and enzymatic pathway, and detection methods including the extraction methods, the new development of sample pre‐treatment technology and the selection of derivative reagents. Impressively, the reaction mechanism of MDA and HNE with myoglobin or myofibrillar protein is also described to explain how MDA and HNE affect food quality.
... Han and his colleagues investigated the formation of HNE in corn oil and soybean oil at 190°C for 3 h, and the final content of HNE in corn and soybean oil was 3.73 and 5.46 μg g −1 , respectively. 9 Guillén and Uriarte investigated the formation of HHE and HNE in sunflower oil and linseed oil after prolonged heating at frying temperature, and significant concentrations of these two toxic aldehydes were found; once they formed, a majority of them existed in the oils. The authors deduced that the presence of HHE and HNE in frying oil was a cause of concern for human health. ...
Article
In this study, the formation of two toxic reactive aldehydes, 4-hydroxy-2-hexenal and 4-hydroxy-2-nonenal, was investigated during frying two different foodstuffs at 180 °C for 7h in three different vegetable oils. Results showed that HHE and HNE content in oil after frying was lower than that in oil fried without foods. It was mainly because of the incorporation of HHE/HNE into fried food. In French fries (FF) HNE content was higher, whereas lower in fried chicken breast meat (FCBM). The bidirectional model systems consisted of model oil frying system and model food frying system were conducted. Result of model oil system showed that content of HNE was higher in FF for the higher hydrophobic property than HHE which would be preferred bounded into the hydrophobic helical structures, whereas lower content of HNE was observed in FCBM for its higher reactivity towards the nucleophilic group, namely protein in FCBM. Furthermore, model food frying system including starch and protein extracted from the corresponding foodstuffs verified the results in model oil system. Finally, the probable migration mechanism of HHE and HNE in different food matrixes was proposed for the first time.
... HHE and HNE are known to originate from the oxidative deterioration of x-3 and x-6 fatty acids respectively (Esterbauer et al., 1991;Long & Picklo, 2010;Spickett, 2013), but the influencing factors and mechanisms underlying their formation remain unknown (Han & Csallany, 2008. Besides, the details of the interactions between oil fractions, such as different kinds of fatty acids in vegetable oils, on the formation of HHE/HNE are still missing. ...
Article
The formation of 4-hydroxy-hexenal (HHE) and 4-hydroxy-nonenal (HNE) in eight vegetable oils was investigated at 180 °C. HHE was only detectable in soybean (SBO), rapeseed (RO) and linseed oils (LO). HNE was measured in all tested oils, but was found mainly in corn (CO), sunflower (SO) and soybean oil (SBO). Oil-dependent formation of HHE/HNE was remarkably observed. Furthermore, different fatty acid methyl esters in tricaprylin, as model oil systems, were constructed to demonstrate their characteristic contribution to HHE/HNE formation. As expected, HHE and HNE originated from the oxidative degradation of methyl linolenate (MLN) and methyl linoleate (ML) respectively. Whereas low concentrations of MLN (<5.0%) and ML (<1.0%) produced no detectable HHE/HNE. The results suggested MLN/ML could induce both HHE/HNE formation and pro-oxidation at higher concentrations. Unexpectedly, methyl stearate and methyl oleate slightly promoted HHE/HNE formation, which might be attributed to free radical transfer mechanisms during thermal oxidation.
... HHE and HNE are known to originate from the oxidative deterioration of x-3 and x-6 fatty acids respectively (Esterbauer et al., 1991;Long & Picklo, 2010;Spickett, 2013), but the influencing factors and mechanisms underlying their formation remain unknown (Han & Csallany, 2008. Besides, the details of the interactions between oil fractions, such as different kinds of fatty acids in vegetable oils, on the formation of HHE/HNE are still missing. ...
Article
Full-text available
The formation of 4‐hydroxy‐hexenal (HHE) and 4‐hydroxy‐nonenal (HNE) in eight vegetable oils was investigated at 180 °C. HHE was only detectable in soybean (SBO), rapeseed (RO) and linseed oils (LO). HNE was measured in all tested oils, but was found mainly in corn (CO), sunflower (SO) and soybean oil (SBO). Oil‐dependent formation of HHE/HNE was remarkably observed. Furthermore, different fatty acid methyl esters in tricaprylin, as model oil systems, were constructed to demonstrate their characteristic contribution to HHE/HNE formation. As expected, HHE and HNE originated from the oxidative degradation of methyl linolenate (MLN) and methyl linoleate (ML) respectively. Whereas low concentrations of MLN (<5.0%) and ML (<1.0%) produced no detectable HHE/HNE. The results suggested MLN/ML could induce both HHE/HNE formation and pro‐oxidation at higher concentrations. Unexpectedly, methyl stearate and methyl oleate slightly promoted HHE/HNE formation, which might be attributed to free radical transfer mechanisms during thermal oxidation.
... As Table 30.1 shows, the incorporation of the toxic 4-hydroxy-(E)-2-nonenal into food fried in thermally degraded soybean oil has been studied, as well as the effect of intermittent and continuous heating at frying temperature on the formation of four 4-hydroxy-(E)-2-alkenals in soybean oil Csallany, 2004, 2006). More recently, the effect of temperature on the formation of 4-hydroxy-(E)-2-nonenal in three oils has been analyzed (Han and Csallany, 2008). The method used to determine these aldehydes involves a very laborious methodology that includes derivatization with DNPH, TLC, extraction and analysis by HPLC-UV/Vis. ...
... As Table 30.1 shows, the incorporation of the toxic 4-hydroxy-(E)-2-nonenal into food fried in thermally degraded soybean oil has been studied, as well as the effect of intermittent and continuous heating at frying temperature on the formation of four 4-hydroxy-(E)-2-alkenals in soybean oil Csallany, 2004, 2006). More recently, the effect of temperature on the formation of 4-hydroxy-(E)-2-nonenal in three oils has been analyzed (Han and Csallany, 2008). The method used to determine these aldehydes involves a very laborious methodology that includes derivatization with DNPH, TLC, extraction and analysis by HPLC-UV/Vis. ...
Chapter
From the beginning of the process, heating an oil at frying temperature brings about its degradation, generating aldehydes and many other compounds. The aldehydes formed can be small molecules or can be supported on truncated acyl groups of triglycerides. Both kinds can also have other functional groups, for which reason some of these aldehydes are very reactive, even showing biological activity. These latter include oxygenated alpha,beta-unsaturated aldehydes, such as 4-hydroxy-2-nonenal and 4-hydroxy-2-hexenal, whose presence in certain heated oils has been recently proved. The composition of the oils in terms of acyl groups decisively influences the aldehydes which may form. As oil heating time increases, so does the content of both aldehydes and other compounds, thus modifying the original sensorial, reactivity and safety characteristics of the oil. The aims of studies related to the presence of aldehydes in heated oils, as well as the methodologies used are also commented on.
... Nevertheless, the carbonyl compounds that remain in the oil after heating are of much greater interest. Specifically in the case of soybean oil, the formation and content of some oxygenated alpha,beta-unsaturated aldehydes after heating at high temperature or after frying have been reported (Gerde, Hammond, & White, 2011;Han & Csallany, 2008;Seppanen & Csallany, 2001, 2002, 2004, 2006. ...
Article
A study of the evolution of the composition of both soybean oil submitted to heating at frying temperature for a prolonged period of time, as well as of soybean oil-frying media used in three different series of deep-frying experiments is carried out by means of 1H nuclear magnetic resonance. The foods involved in the deep-frying processes have very different lipid contents and their lipid composition is also very different. The results obtained allow one to clarify how the nature of the food being fried influences the changes observed in the composition of the soybean oil-frying media throughout the deep-frying process. The study refers both to the evolution of the molar percentage of the different kinds of acyl groups in the frying-media as well as to the nature of the aldehydes formed and the evolution of their concentrations. It is noteworthy that the main aldehydes detected, in both soybean oil and soybean oil-frying media, are the reactive (E,E)-2,4-alkadienals; likewise the genotoxic and cytotoxic 4-hydroxy-(E)-2-alkenals and 4,5-epoxy-2-alkenals are also present. The considerable influence of the food being fried on the occurrence of these reactive and toxic aldehydes in the frying media is shown. Furthermore, the occurrence and evolution of other oxygenated compounds such as alcohols are also addressed, as is the extent of hydrolytic processes. In addition, the evolution of Iodine Value and of the percentage in weight of Polar Compounds is also considered. The influence of the oil nature on all the above mentioned compositional characteristics is also given attention by comparison of these results with those previously obtained using extra virgin olive oil; it is noteworthy that from the toxic aldehyde content point of view the results obtained indicate that the extra virgin olive oil-frying media are much safer than the soybean oil-frying media.
... Culinary oils that have been heated but not used to fry food had reported HNE concentrations ranging from 2.47 [8] to 42 ppm [5]. It should be noted that HNE formation is temperature dependent for many of the oils that have been tested [31,32]. ...
Article
Full-text available
The formation of 4-hydroxy-2-(E)-nonenal (HNE) in a corn–soy oil blend during frying was investigated. Frozen shoestring potatoes were fried once per hour at 180 °C for 8 h/day over a 4-day period. As a control, oil was also heated under identical conditions, except that no product was fried. HNE was quantified by GC–MS using a stable isotope dilution assay with pentaflurobenzyl hydroxylamine hydrochloride (PFBHA) and trimethylsilyl 2,2,2-trifluoro-n-(trimethylsilyl)acetimidate (BSTFA) derivatization. The HNE concentration in the potato fryers increased throughout the first day of frying. On subsequent days the daily maximum HNE concentration was reached after fresh oil was added and the fryer was brought to the frying temperature. The potato fryer oil reached a maximum concentration of 5.6 ppm during the second day of frying. Similarly, the HNE concentration of the oil in the control fryer increased throughout the first day of heating. On subsequent days the daily maximum HNE concentration varied throughout the experimental period. The control fryers reached a maximum concentration of 6.3 ppm at the end of the second day of heating. Throughout the experimental period there was a tendency for the oil in the control fryer to have a greater concentration of HNE than the oil in the potato fryer. Overall time of the experiment and heating with food versus heating without frying food and their interaction were significant in terms of HNE formation.
Article
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4-Hydroxynonenal in petfood HNE (4-hydroxynonenal) is an aldehyde product that can be formed during frying or cooking of foods that contain the polyunsaturated fatty acid, linoleic acid. Published data on HNE in commercial dry and wet petfoods appear to be unavailable. Based on a rat diet containing beef and safflower oil, the maximum HNE level in petfood was estimated to be 7 mg/kg dietary dry matter, or per kg of the food's residue after removal of its moisture (Note 1). There is evidence that ingested HNE is metabolized and then excreted in urine in the form of a wide variety of compounds, mainly mercapturic-acid conjugates. A 4-week rat study showed that the safe upper level of orally administered HNE is lower than the equivalent of 5 mg HNE/kg dietary dry matter. The 5-mg level caused liver and kidney damage as based on indicators measured in blood (Note 2). The estimated, maximum content of HNE in petfood could be toxic. That tentative conclusion calls for further research with regard to HNE. The maximum amount of HNE in dry and wet petfood should be assessed by means of chemical analyses. The safe upper limit of HNE in petfood should also be assessed, preferably on the basis of long-term, HNE-feeding studies in rodents.
Article
The reactivity of hexanal, (E)-hex-2-enal, 4-hydroxyhex-2-enal, and 4-hydroxynon-2-enal in oil-in-water emulsions and its respective compartments, in presence and absence of protein, was studied at 40 °C. In the presence of water, hexanal oxidized to hexanoic acid. In the presence of protein, an additional loss occurred, presumably as a result of adduct formation with cysteine. Similarly, (E)-hex-2-enal oxidized to (E)-hex-2-enoic acid in the presence of water, the results suggested that also this acid is able to form adducts with proteins. 4-Hydroxyalk-2-enals showed the highest reactivity in all models evaluated. Especially in protein containing systems, they were not detectable anymore or their initial concentration was seriously reduced. 4-Hydroxynon-2-enal was the most reactive of the substances studied. The reactivity of the aldehydes was influenced by their partition within emulsions which remarkably was not correlated with their hydrophobicity. These findings need to be considered when using these aldehydes as lipid oxidation markers in foods.
Article
Background Lipid peroxidation yields a large number of aldehydes and carbonyl-containing compounds, of which the reactive and toxic compound 4-hydroxy-2-nonenal (4-HNE) derived from ω-6 polyunsaturated fatty acids (ω-6 PUFAs) is the most extensively studied. The high reactivity of 4-HNE enables this compound to crosslink with various biomolecules and thus contribute to the pathological processes of several diseases, such as atherosclerosis, cancer, diabetes mellitus, and neurodegenerative disorders. Scope and approach From the perspective of food safety, the emergence of lipid peroxidation contaminants in foodstuffs remains a major concern of consumers, health departments, and industries. This review highlights the latest developments regarding the formation pathways, toxicity, analysis methods, occurrence in foodstuff, and mitigation strategies for 4-HNE. Future prospects on measuring and controlling 4-HNE in food are also discussed. Key findings and conclusions The determination of 4-HNE levels in different types of foods indicates that PUFAs-rich vegetable oil and oil-based food are major intake sources of 4-HNE. Considering the toxicity of 4-HNE, sensitive detection techniques combined with feasible control methods should be an effective solution for food quality maintenance and safety assurance. However, current detection methods and 4-HNE control strategies possess inherent advantages and limitations. Therefore, effective 4-HNE detection and new controlling technologies that are practically viable at the industrial level need to be developed.
Article
4‐Hydroxy‐2‐trans‐nonenal (HNE) is a toxic aldehyde produced mostly in oils containing polyunsaturated fatty acid due to heat‐induced lipid peroxidation. The present study examined the effects of the heating time, the degree of unsaturation, and the antioxidant potential on the formation of HNE in two light olive oils (LOO) and two sunflower oils (one high oleic and one regular) at frying temperature. HNE concentrations in these oil samples heated for 0, 1, 3, and 5 hours at 185 °C were measured using high‐performance liquid chromatography. The fatty‐acid distribution and the antioxidant capacity of these four oils were also analyzed. The results showed that all oils had very low HNE concentrations (<0.5 μg g⁻¹ oil) before heating. After 5 hours of heating at 185 °C, HNE concentrations were increased to 17.98, 25.00, 12.51, and 40.00 μg g⁻¹ in the two LOO, high‐oleic sunflower oil (HOSO), and regular sunflower oil (RSO), respectively. Extending the heating time increased HNE formation in all oils tested. It is related to their fatty‐acid distributions and antioxidant capacities. RSO, which contained high levels of linoleic acid (59.60%), a precursor for HNE, was more susceptible to degradation and HNE formation than HOSO and LOO, which contained only 6–8% linoleic acid.
Chapter
Lipid oxidation is still one of the major concerns in food processing, especially in vegetable oils. Fatty acids oxidation leads to primary and secondary oxidation products, such as 4-hydroxy-2-nonenal (HNE) and 4-hydroxy-2-hexenal (HHE). HNE is a secondary oxidation product from the n-6 polyunsaturated fatty acids (PUFA), while HHE formation derives from the oxidation of n-3 PUFA. In recent years, great attention has been devoted to these compounds identified as mutagenic, genotoxic and cytotoxic. Due to their high reactivity with proteins and DNA, they can induce structural damage and changes in the functionality of such molecules. Up to now different factors (e.g. fatty acids composition, effect of temperature, time and type of frying), were studied to understand the behaviour of these compounds, namely HNE, in different food matrices. One of the most researched were vegetable oils, due to their high consumption rates by consumers and food industry. An overview of the current knowledge about HNE and HHE occurrence in vegetable oils, including factors that influence their formation, health effects, analytical approaches, as well as mitigation strategies and challenges are discussed.
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After synthesis of a deuterated 4-HNE standard, the formation of 4-HNE during heating of peanut oil and whole peanuts, respectively, was measured by GC-MS. While a significant increase in 4-HNE levels was observed for peanut oil, the amount of 4-HNE decreased when whole peanuts are roasted due to lipation reactions with amino acid side chains of the proteins. The ɛ-amino group of lysine was identified as the favored reaction partner of 4-HNE. After heating Nα-acetyl-L-lysine and 4-HNE, a Schiff base, a novel pyridinium derivative, a 2-pentylpyrrol derivative and, following reduction and hydrolysis, a reduced, cyclized Michael adduct were identified. 2-Amino-6-(2-pentyl-1H-pyrrol-1-yl)hexanoic acid (2-PPL) was synthesized and quantitated in peanut proteins, which had been incubated with varying amounts of 4-HNE by HPLC-ESI-MS/MS after enzymatic hydrolysis. At low 4-HNE concentrations the modification of lysine could be entirely explained by the formation of 2 PPL. Additionally, 2-PPL was quantified for the first time in peanut samples and an increase depending on the roasting time was observed. 2-PPL represents a suitable marker to evaluate the extent of food protein lipation by 4-HNE.
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Distillers dried grains with solubles (DDGS) from corn contain relatively large amounts of polyunsaturated fatty acids and some yeast components, which may increase oxidative stress and alter immune function, respectively, when fed to pigs. Therefore, indicators of oxidative stress and immune status were determined in pigs (n=24; initial BW 103.8±5.9kg) fed corn soybean meal-based diets or diets containing 35% DDGS for 38days. On day 38, blood samples were collected for plasma and erythrocyte glutathione, 4-hydroxynonenal (4-HNE) protein adduct, nitrite, oxygen radical absorbance capacity, and thiobarbituric acid reactive substances (TBARS) analyses. Peripheral blood mononuclear cells were isolated, and lysates were analyzed for 4-HNE, superoxide dismutase-1 and glutathione-s-transferase-4. Fresh urine was collected and analyzed for F2-isoprostane and TBARS. Plasma immunoglobulin A (IgA), IgG, and fecal IgA were determined, and on day 39, pigs fed each diet were injected intramuscularly with saline (n=6 pigs per diet) or Escherichia coli lipopolysaccharide (LPS; n=6 pigs per diet) and plasma cytokines and metabolites were determined at 4h post LPS injection. There were no differences in basal circulating indicators of oxidative stress between dietary treatment groups, but urinary TBARS were increased (p
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Alzheimer's disease (AD) is characterized by slowly progressive neuronal death, but its molecular cascade remains elusive for over 100 years. Since accumulation of autophagic vacuoles (also called granulo-vacuolar degenerations) represents one of the pathologic hallmarks of degenerating neurons in AD, a causative connection between autophagy failure and neuronal death should be present. The aim of this perspective review is at considering such underlying mechanism of AD that age-dependent oxidative stresses may affect the autophagic-lysosomal system via carbonylation and cleavage of heat-shock protein 70.1 (Hsp70.1). AD brains exhibit gradual but continual ischemic insults that cause perturbed Ca(2+) homeostasis, calpain activation, amyloid ß deposition, and oxidative stresses. Membrane lipids such as linoleic and arachidonic acids are vulnerable to the cumulative oxidative stresses, generating a toxic peroxidation product 'hydroxynonenal' that can carbonylate Hsp70.1. Recent data advocate for dual roles of Hsp70.1 as a molecular chaperone for damaged proteins and a guardian of lysosomal integrity. Accordingly, impairments of lysosomal autophagy and stabilization may be driven by the calpain-mediated cleavage of carbonylated Hsp70.1, and this causes lysosomal permeabilization and/or rupture with the resultant release of the cell degradation enzyme, cathepsins (calpain-cathepsin hypothesis). Here, the author discusses three topics; (1) how age-related decrease in lysosomal and autophagic activities has a causal connection to programmed neuronal necrosis in sporadic AD, (2) how genetic factors such as apolipoprotein E and presenilin 1 can facilitate lysosomal destabilization in the sequential molecular events, and (3) whether a single cascade can simultaneously account for implications of all players previously reported. In conclusion, Alzheimer neuronal death conceivably occurs by the similar 'calpain-hydroxynonenal-Hsp70.1-cathepsin cascade' with ischemic neuronal death. Blockade of calpain and/or extra-lysosomal cathepsins as well as scavenging of hydroxynonenal would become effective AD therapeutic approaches.
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4-Hydroxynonenal (4-HNE) is a major product of the oxidation of ω-6-polyunstaturated lipids and an effector of radical-mediated oxidative damage, whose analytical determination requires chemical derivatization. In this work, its reactivity with fluorinated phenylhydrazines was explored both under preparative and analytical settings. A five-step synthesis of 4-HNE on gram-scale with an overall yield of 30 % is described. Reaction of 4-HNE with ortho-, meta-, or para-CF3-phenylhydrazine, as well as with the 3,5-di-CF3, 2,4-di-CF3, or pentafluoro analogues, in MeCN with 0.5 mM TFA yields the corresponding hydrazones with rate constants kf of 2.8 ± 0.4, 1.7 ± 0.1, 3.0 ± 0.2, 0.6 ± 0.1, 0.5 ± 0.1, and 3.5 ± 0.5 M–1 s–1, respectively at 298 K. At higher temperatures, the hydrazones undergo intramolecular cyclization to form 1,6-dihydropyridazines that, depending on the solvent and temperature, may further react with the hydrazine to yield tetrahydropyridazine adducts and their oxidation products. Other reaction products were isolated, depending on the reaction conditions, and the complex reactivity of 4-HNE with the above nucleophiles is discussed. Due to the good yield and rate of formation of the hydrazone adducts, their stability and favorable UV absorbance, 2-(trifluoromethyl)phenylhydrazine and 2,3,4,5,6-pentafluorophenylhydrazine are the most interesting candidates for the development of rapid and efficient analytical derivatizations of 4-HNE.
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A study is made of the evolution of the composition of sunflower oil kept over prolonged periods of time at high temperature (190 degrees C) in a domestic fryer. The technique used is (1)H NMR spectroscopy. The degradation rate of linoleic acyl groups is determined in this process, as well as the proportions of monounsaturated, of saturated plus modified acyl groups and the iodine values. Intermediate oxidation compounds having hydroperoxide groups and conjugated dienic systems were not detected; however, some secondary oxidation compounds such as aldehydes are generated very early, among them, the genotoxic and cytotoxic 4-hydroxy-trans-2-alkenals. Both concentrations of each kind of aldehyde at different heating times and changes in their concentration were also determined. Simultaneously, the level of oil degradation corresponding to a content of 25% of polar compounds measured by Viscofrit test was analyzed in function of the (1)H NMR spectra derived data.
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Oxidative stress is believed to play important roles in neuronal cell death associated with many different neurodegenerative conditions (e.g., Alzheimer's disease, Parkinson's disease, and cerebral ischemia), and it is believed also that apoptosis is an important mode of cell death in these disorders. Membrane lipid peroxidation has been documented in the brain regions affected in these disorders as well as in cell culture and in vivo models. We now provide evidence that 4-hydroxynonenal (HNE), an aldehydic product of membrane lipid peroxidation, is a key mediator of neuronal apoptosis induced by oxidative stress. HNE induced apoptosis in PC12 cells and primary rat hippocampal neurons. Oxidative insults (FeSO4 and amyloid beta-peptide) induced lipid peroxidation, cellular accumulation of HNE, and apoptosis. Bcl-2 prevented apoptosis of PC12 cells induced by oxidative stress and HNE. Antioxidants that suppress lipid peroxidation protected against apoptosis induced by oxidative insults, but not that induced by HNE. Glutathione, which binds HNE, protected neurons against apoptosis induced by oxidative stress and HNE. PC12 cells expressing Bcl-2 exhibited higher levels of glutathione and lower levels of HNE after oxidative stress. Collectively, the data identify that HNE is a novel nonprotein mediator of oxidative stress-induced neuronal apoptosis and suggest that the antiapoptotic action of glutathione may involve detoxification of HNE.
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The toxic aldehyde 4-hydroxy-2-trans-nonenal (HNE) is an oxidation product of linoleic acid and is formed during the thermal oxidation of soybean oil at frying temperature. This investigation was conducted to determine whether HNE would be incorporated into food fried in thermally oxidized soybean oil. Commercially available liquid soybean oil was heated at 185°C for 5 h prior to frying uniform pieces of potato (1×0.5×7 cm). The oil was sampled prior to and after frying and was analyzed for the presence of HNE and other polar lipophilic aldehydes and related carbonyl compounds by HPLC. The oil was also extracted from the fried potato pieces and was analyzed identically to the frying oil. HNE was found to be a major polar lipophilic compound in the thermally oxidized frying oil, as previously published by this laboratory, and in the oil extracted from the fried potato. Similar concentrations of HNE were found in the oil prior to and after frying and in the oil extracted from the fried potato (57.53±16.31, 52.40±6.10, and 59.64±11.91 mg HNE per 100 g oil, respectively). These results indicate that toxic HNE was readily incorporated into food fried in thermally oxidized oil; extensive consumption of such fried foods could be a health concern.
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Alzheimer's disease (AD) is widely held to be a disorder associated with oxidative stress due, in part, to the membrane action of amyloid β-peptide (Aβ). Aβ-associated free radicals cause lipid peroxidation, a major product of which is 4-hydroxy-2-trans-nonenal (HNE). We determined whether HNE would alter the conformation of synaptosomal membrane proteins, which might be related to the known neurotoxicity of Aβ and HNE. Electron paramagnetic resonance spectroscopy, using a protein-specific spin label, MAL-6(2,2,6,6-tetramethyl-4-maleimidopiperidin-1-oxyl), was used to probe conformational changes in gerbil cortical synaptosomal membrane proteins, and a lipid-specific stearic acid label, 5-nitroxide stearate, was used to probe for HNE-induced alterations in the fluidity of the bilayer domain of these membranes. Synaptosomal membranes, incubated with low concentrations of HNE, exhibited changes in protein conformation and bilayer order and motion (fluidity). The changes in protein conformation were found to be concentration- and time-dependent. Significant protein conformational changes were observed at physiologically relevant concentrations of 1–10 µM HNE, reminiscent of similar changes in synaptosomal membrane proteins from senile plaque- and Aβ-rich AD hippocampal and inferior parietal brain regions. HNE-induced modifications in the physical state of gerbil synaptosomal membrane proteins were prevented completely by using excess glutathione ethyl ester, known to protect neurons from HNE-caused neurotoxicity. Membrane fluidity was found to increase at higher concentrations of HNE (50 µM). The results obtained are discussed with relevance to the hypothesis of Aβ-induced free radical-mediated lipid peroxidation, leading to subsequent HNE-induced alterations in the structure and function of key membrane proteins with consequent neurotoxicity in AD brain.
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Rat and human urine samples were analyzed for lipophilic aldehydes and other carbonyl products of lipid peroxidation. The following compounds were identified as their 2,4-dinitrophenyl hydrazones by cochromatography with pure standards using three solvent systems: butanal, butan-2-one, pentan-2-one, hex-2-enal, hexanal, hepta-2,4-dienal, hept-2-enal, octanal, non-2-enal, deca-2,4-dienal, 4-hydroxyhex-2-enal, and 4-hydroxynon-2-enal. In general, fasted rats excreted less of these compounds than fed rats, indicating they were partially of dietary origin or that the endogenous compounds were excreted in a form not susceptible to hydrazone formation. The compounds excreted in human urine were similar to those excreted in rat urine but were present in lower concentrations. Identification of the conjugated forms fo the lipophilic aldehydes and related carbonyl compounds excreted in urine may be a source of information about their reactions in vivo.
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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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A very sensitive high-performance liquid chromatography (HPLC) method was developed for the simultaneous separation and measurement of nonpolar and polar lipophilic secondary lipid peroxidation products in vegetable oil. Seventeen nonpolar and 13 polar lipophilic aldehydes and related carbonyl compounds, derived from thermally oxidized soybean oil as 2,4-dinitrophenyl hydrazones, were separated simultaneously by reversed-phase HPLC. Detection limit for the individual compounds is 1 ng. Thirteen of the nonpolar carbonyl compounds were identified as: butanal, 2-butanone, pentanal, 2-pentanone, hexenal, hexanal, 2,4-heptadienal, 2-heptenal, octanal, 2-nonenal, 2,4-decadienal, decanal, and undecanal. Three of the polar carbonyl compounds were identified as: 4-hydroxy-2-hexenal, 4-hydroxy-2-octenal, and 4-hydroxy-2-nonenal. The detection of the toxic 4-hydroxy-2-nonenal, a major compound, and 4-hydroxy-2-hexenal, a minor compound, in heated soybean oil is of particular importance because these toxic compounds have been shown to be absorbed from the diet.
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An assay method for the quantification of the cytotoxicities of various agents toward cultured human endothelial cells was developed using Earle's solution as an incubation medium. By this method, the cytotoxicities of a linoleic acid hydroperoxide (LOOH) and its related aliphatic aldehydes toward human umbilical vein endothelial cells were investigated. Saturated aldehydes, pentanal, hexanal and 9-oxononanoic acid, are nontoxic; α,β-unsaturated aldehydes, 2-hexenal, 2-heptenal, 2-octenal and 2-nonenal, are toxic only at high concentrations; LOOH and α,β-unsaturated aldehydes with a hydroxy group or an additional double bond, 4-hydroxy-2-nonenal, 2,4-nonadienal and 2,4-decadienal, are highly toxic. In particular, 2,4-decadienal, whose 50% lethal concentration is 9 μM, is the most injurious. The cytotoxicities of LOOH and its related aldehydes were found to be much reduced in growth medium containing serum, growth factors, heparin, amino acids and vitamins.
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This article describes the chemical nature of α,β-unsaturated aldehydes and some of their toxicological effects based on their ability to function as direct-acting alkylating agents. Selected compounds discussed include α,β-unsaturated aldehydic environmental pollutants, metabolites of xenobiotics and natural products, and lipid peroxidation—and DNA oxidation products derived from cellular constituents. Briefly reviewed are sources and mechanisms of formation of the aldehydes, their reactivity with respect to glutathione and amino-groups, their toxicity based on interaction with sulfhydryl and amino targets in cells, and modulation of their toxicity by metabolism.
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Dietary products of lipid peroxidation cause hepatic dysfunction due to decreases in the activities of some hepatic enzymes and to depletion of CoA. An idea about the decreases and depletion is that the enzymes and CoA could be injured directly by the incorporated products in the liver. Their inactivations in vitro were then examined using a reasonable amount of peroxidation products. The hepatic cytosol, microsomes, and mitochondria were incubated with 10, 15, and 20 micrograms/mg protein of peroxidation products, respectively, and changes in the enzymatic activities were monitored. Glucose-6-phosphate dehydrogenase, mitochondrial NAD-dependent aldehyde dehydrogenase, glucokinase, and glyceradehyde phosphate dehydrogenase were inactivated, and the CoA level was decreased, but the other hepatic enzymes were not. Although glyceraldehyde phosphate dehydrogenase was most sensitive to peroxidation products in vitro, the decrease in activity was not detected by the oral dose of secondary products. On the other hand, among the components of peroxidation products, hydroperoxides and polymers are not incorporated in the liver, but decomposed products of low molecular weight are incorporated. Glucokinase among the above enzymes was not inactivated by the low-molecular-weight products. It was therefore concluded that glucose-6-phosphate dehydrogenase, mitochondrial NAD-dependent aldehyde dehydrogenase, and CoA were targets of the direct attack by incorporated components of peroxidation products in the liver.
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This paper reviews studies relating to the effects of fat unsaturation and fatty acid composition on the development of experimental atherosclerosis in rabbits. The results derived from the feeding of various fats are similar whether one feeds cholesterol or an atherogenic, cholesterol-free semipurified diet. In general, the severity of atherosclerosis is inversely related to the level of fat unsaturation. Two exceptions are cocoa butter which is much less atherogenic than expected, most probably due to its high content of stearic acid, and peanut oil, while relatively unsaturated, is surprisingly atherogenic for rats, rabbits and monkeys. This latter effect is not related to the level (6%) of long-chain saturated fatty acids (arachidic, behenic, lignoceric) present in peanut oil, but rather to its triglyceride structure. Randomization of peanut oil, which modifies its triglyceride structure, significantly reduces its atherogenicity.
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Incorporation of secondary autoxidation products (SP) of linoleic acid into the rat body was investigated. Radioactive SP was administered orally to a group of 5 rats, and excretions of radioactive substances in feces, urine and respiration were measured and compared with excretions from rats fed linoleic acid and its hydroperoxides. The SP-fed group excreted 45% and the other groups about 10% of the administered radioactivity through feces. Urinary excretion accounted for 52% of activity ingested in the SP group and less than 30% in the other groups. The 14CO2 produced in each group was about 25% of the ingested activity. Incorporation of the radioactive substances of SP into tissues and organs was measured periodically after administration of a single dose. The radioactive substances accumulated in the liver between 12-24 hr after administration and accounted for 2.6% of the total amount given, the highest level of all tissues and organs. This accumulation led to an elevation of serum transaminase activities, an increase in hepatic lipid peroxide, as determined by thiobarbituric acid test, and a slight hypertrophy of liver (1.5-fold). Therefore, absorbed SP appeared to contribute to the deleterious condition of the liver.
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Peroxidation of unsaturated lipids, initially studied in the chemistry of oil and fat rancidity, has become a problem of increasing interest in the biological field, because of its proposed role in a variety of pathological conditions. The general mechanism of the process, the formation of toxic aldehydes capable to react with protein and non protein thiols, and the overall effects in cellular membranes are reviewed. The possible implications of lipid peroxidation as one of the main mechanisms of cellular damage in both toxic injury and other pathological conditions are discussed.
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The autoxidation of unsaturated lipids contained in oils, fats, and food and the endogenous oxidative degradation of membrane lipids by lipid peroxidation result in the formation of a very complex mixture of lipid hydroperoxides, chain-cleavage products, and polymeric material. Experimental animal studies and biochemical investigations lend support to the hypothesis that lipid-oxidation products, ingested with food or produced endogenously, represent a health risk. The oral toxicity of oxidized lipids is unexpectedly low. Chronic uptake of large amounts of such materials increases tumor frequency and incidence of atherosclerosis in animals. 4-Hydroxynonenal, a chain-cleavage product resulting from omega 6 fatty acids, disturbs gap-junction communications in cultured endothelial cells and induces several genotoxic effects in hepatocytes and lymphocytes. Although the concentrations of the aldehyde needed to produce these effects are in the range expected to occur in vivo, their pathological significance is far from clear. Recent findings strongly suggest that in vivo modification of low-density lipoprotein by certain lipid-peroxidation products (eg, 4-hydroxynonenal and malonaldehyde) renders this lipoprotein more atherogenic and causes foam-cell formation. Proteins modified by 4-hydroxynonenal and malonaldehyde were detected by immunological techniques in atherosclerotic lesions.
Article
Peroxidation of membrane lipids results in release of the aldehyde 4-hydroxynonenal (HNE), which is known to conjugate to specific amino acids of proteins and may alter their function. Because accumulating data indicate that free radicals mediate injury and death of neurons in Alzheimer's disease (AD) and because amyloid beta-peptide (A beta) can promote free radical production, we tested the hypothesis that HNE mediates A beta 25-35-induced disruption of neuronal ion homeostasis and cell death. A beta induced large increases in levels of free and protein-bound HNE in cultured hippocampal cells. HNE was neurotoxic in a time- and concentration-dependent manner, and this toxicity was specific in that other aldehydic lipid peroxidation products were not neurotoxic. HNE impaired Na+, K(+)-ATPase activity and induced an increase of neuronal intracellular free Ca2+ concentration. HNE increased neuronal vulnerability to glutamate toxicity, and HNE toxicity was partially attenuated by NMDA receptor antagonists, suggesting an excitotoxic component to HNE neurotoxicity. Glutathione, which was previously shown to play a key role in HNE metabolism in nonneuronal cells, attenuated the neurotoxicities of both A beta and HNE. The antioxidant propyl gallate protected neurons against A beta toxicity but was less effective in protecting against HNE toxicity. Collectively, the data suggest that HNE mediates A beta-induced oxidative damage to neuronal membrane proteins, which, in turn, leads to disruption of ion homeostasis and cell degeneration.
Article
Removal of extracellular glutamate at synapses, by specific high-affinity glutamate transporters, is critical to prevent excitotoxic injury to neurons. Oxidative stress has been implicated in the pathogenesis of an array of prominent neurodegenerative conditions that involve degeneration of synapses and neurons in glutamatergic pathways including stroke, and Alzheimer's, Parkinson's and Huntington's diseases. Although cell culture data indicate that oxidative insults can impair key membrane regulatory systems including ion-motive ATPases and amino acid transport systems, the effects of oxidative stress on synapses, and the mechanisms that mediate such effects, are largely unknown. This study provides evidence that 4-hydroxynonenal, an aldehydic product of lipid peroxidation, mediates oxidation-induced impairment of glutamate transport and mitochondrial function in synapses. Exposure of rat cortical synaptosomes to 4-hydroxynonenal resulted in concentration- and time-dependent decreases in [3H]glutamate uptake, and mitochondrial function [assessed with the dye 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)]. Other related aldehydes including malondialdehyde and hexanal had little or no effect on glutamate uptake or mitochondrial function. Exposure of synaptosomes to insults known to induce lipid peroxidation (FeSO4 and amyloid beta-peptide) also impaired glutamate uptake and mitochondrial function. The antioxidants propyl gallate and glutathione prevented impairment of glutamate uptake and MTT reduction induced by FeSO4 and amyloid beta-peptide, but not that induced by 4-hydroxynonenal. Western blot analyses using an antibody to 4-hydroxynonenal-conjugated proteins showed that 4-hydroxynonenal bound to multiple cell proteins including GLT-1, a glial glutamate transporter present at high levels in synaptosomes. 4-Hydroxynonenal itself induced lipid peroxidation suggesting that, in addition to binding directly to membrane regulatory proteins, 4-hydroxynonenal potentiates oxidative cascades. Collectively, these findings suggest that 4-hydroxynonenal plays important roles in oxidative impairment of synaptic functions that would be expected to promote excitotoxic cascades.
Article
The cause of neuronal cell death in Parkinson's disease is unknown but there is accumulating evidence suggesting that oxidative stress may be involved in this process. Current evidence shows that in the substantia nigra there is altered iron metabolism, decreased levels of reduced glutathione and an impairment of mitochondrial complex I activity. However, these changes seem to be unique to the substantia nigra and have not been found in other areas of the brain known to be altered in Parkinson's disease, such as substantia innominata. In addition they do not appear to be related to the presence of Lewy bodies, as other areas of the brain containing Lewy bodies do not show evidence of either oxidative stress or mitochondrial dysfunction. Oxidative stress has now been demonstrated in Alzheimer's disease and its presence appears to be correlated with regions of marked pathological changes.
Composition and characteristics of indi-vidual fats and oils Bailey's industrial oil and fat products
  • Sonntag
  • Nov
Sonntag NOV (1979) Composition and characteristics of indi-vidual fats and oils. In: Stern D (ed) Bailey's industrial oil and fat products. Wiley, New York, pp 289–477