Accumulation Of Lipid Oxidation Products Research Articles

Deep‐frying impact on food and oil chemical composition: Strategies to reduce oil absorption in the final product

AbstractDuring frying, oils can deteriorate due to autoxidation and hydrolytic alterations, processes influenced by the oil's fatty acid composition (FAC) and antioxidant content. However, there are different techniques to improve fried food quality and reduce oil absorption. This review aims to assess existing literature on the interactions between frying methods, oil selection, and the chemical composition of foods. To achieve this goal, the article examines the impact of oil FAC, antioxidants, pretreatments, and alternative frying technologies. A literature search was conducted from 2016 to 2023. The keywords used were (AND/OR) frying, fried foods, oil, oil absorption, and fatty acids. Oils rich in monounsaturated fatty acids and antioxidants, such as olive oil, are recommended for their nutritional benefits and improved oil stability. The water content and structure of the food also play a significant role in oil absorption. Pretreatments to diminish food moisture content contribute to a lower oil absorption in the fried food while mitigating excessive accumulation of lipid oxidation products. Proper selection of frying oils, incorporation of antioxidants, and the use of pretreatments could help prevent chemical changes and minimize oil absorption during frying. These measures contribute to maintaining the nutritional quality and safety of fried foods while also enhancing their overall sensory appeal.

Disturbed electron transport beyond PSI changes metabolome and transcriptome in Zn-deficient soybean

Low Zn availability in soils is a problem in many parts of the world, with tremendous consequences for food and feed production because Zn deficiency affects the yield and quality of plants. In this study we investigated the consequences of Zn-limitation in hydroponically cultivated soybean (Glycine max L.) plants. Parameters of photosynthesis biophysics were determined by spatially and spectrally resolved Kautsky and OJIP fluorescence kinetics and oxygen production at two time points (V4 stage, after five weeks, and pod development stage, R5–R6, after 8–10 weeks). Lower NPQ at 730 nm and lower quantum yield of electron transport flux until PSI acceptors were observed, indicating an inhibition of the PSI acceptor side. Metalloproteomics showed that down-regulation of Cu/Zn-superoxide dismutase (CuZnSOD) and Zn‑carbonic anhydrase (CA) were primary consequences of Zn-limitation. This explained the effects on photosynthesis in terms of decreased use of excitons, which consequently led to oxidative stress. Indeed, untargeted metabolomics revealed an accumulation of lipid oxidation products in the Zn-deficient leaves. Further response to Zn deficiency included up-regulation of gene expression of cell wall metabolism, response to (a)biotic stressors and antioxidant activity, which correlated with accumulation of antioxidants, Vit B6, (iso)flavonoids and phytoalexins.

Effects of citrate-stabilized gold and silver nanoparticles on some safety parameters of Porphyridium cruentum biomass.

Introduction: Our research raises the question of how realistic and safe it is to use gold and silver nanoparticles in biotechnologies to grow microalgae, which will later be used to obtain valuable products. To this purpose, it was necessary to assess the influence of 10 and 20nm Au and Ag nanoparticles stabilized in citrate on the growth of microalga Porphyridium cruentum in a closed cultivation system, as well as some safety parameters of biomass quality obtained under experimental conditions. Methods: Two types of experiments were conducted with the addition of nanoparticles on the first day and the fifth day of the cultivation cycle. Changes in productivity, lipid content, malondialdehyde (MDA), as well as antioxidant activity of microalgae biomass have been monitored in dynamics during the life cycle in a closed culture system. Results: The impact of nanoparticles on the growth curve of microalgae culture was marked by delaying the onset of the exponential growth phase. A significant increase in the content of lipids and MDA in biomass was noted. Excessive accumulation of lipid oxidation products within the first 24h of cultivation resulted in altered antioxidant activity of red algae extracts. Discussion: Citrate-stabilized gold and silver nanoparticles proved to be a stress factor for red microalga Porphyridium cruentum, causing significant changes in both biotechnological and biomass safety parameters. Addition of Au and Ag nanoparticles during the exponential growth phase of porphyridium culture led to an enhanced lipid accumulation and reduced MDA values in biomass.

The Influence of Cooking Parameters and Chilled Storage Time on Quality of Sous-Vide Atlantic Mackerel (Scomber scombrus)

ABSTRACTThe aim of the present study was to evaluate the effects of various sous-vide time–temperature regimes and their interactions on quality parameters of Atlantic mackerel (Scomber scombrus) during chilled storage. The mackerel fillets were exposed to sous-vide treatment at 60, 75, and 90°C for 10, 15, and 20 min and further stored for 1, 3, and 7 days at 4 ± 1°C before analysis. Changes in pH, water content and cook loss, amount of water- and salt-soluble proteins, texture, and color parameters, as well as accumulation of lipid oxidation products in sous-vide-cooked mackerel were assessed. Sous-vide cooking time and temperature had the lowest contribution to the formation of primary and secondary products of lipid oxidation, as well as increase in yellowness of the fish flesh due to their accumulation; whereas duration of chilled storage led to a significant increase in oxidation and yellowness (p < 0.05). Duration of chilled storage also affected structural and textural properties of the fish muscle, leading to a decreased cook loss. At the same time, sous-vide cooking decreased the firmness of the fish muscle. Duration of chilled storage was found to have the highest significant effect (p < 0.001) on all physicochemical characteristics of sous-vide-cooked mackerel.

Neuroprotective effects of the gliopeptide ODN in an in vivo model of Parkinson's disease.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive loss of dopamine (DA) neurons through apoptotic, inflammatory and oxidative stress mechanisms. The octadecaneuropeptide (ODN) is a diazepam-binding inhibitor (DBI)-derived peptide, expressed by astrocytes, which protects neurons against oxidative cell damages and apoptosis in an in vitro model of PD. The present study reveals that a single intracerebroventricular injection of 10ng ODN 1h after the last administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) prevented the degeneration of DA neurons induced by the toxin in the substantia nigra pars compacta of mice, 7days after treatment. ODN-mediated neuroprotection was associated with a reduction of the number of glial fibrillary acidic protein-positive reactive astrocytes and a strong inhibition of the expression of pro-inflammatory genes such as interleukins 1β and 6, and tumor necrosis factor-α. Moreover, ODN blocked the inhibition of the anti-apoptotic gene Bcl-2, and the stimulation of the pro-apoptotic genes Bax and caspase-3, induced by MPTP in the substantia nigra pars compacta. ODN also decreased or even in some cases abolished MPTP-induced oxidative damages, overproduction of reactive oxygen species and accumulation of lipid oxidation products in DA neurons. Furthermore, DBI knockout mice appeared to be more vulnerable than wild-type animals to MPTP neurotoxicity. Taken together, these results show that the gliopeptide ODN exerts a potent neuroprotective effect against MPTP-induced degeneration of nigrostriatal DA neurons in mice, through mechanisms involving downregulation of neuroinflammatory, oxidative and apoptotic processes. ODN may, thus, reduce neuronal damages in PD and other cerebral injuries involving oxidative neurodegeneration.

Changes in volatile aroma compounds of organic fragrant rice during storage under different conditions

Aroma of fragrant rice greatly affects palatability as well as consumer acceptability. Loss of desirable volatile compounds such as 2-acetyl-1-pyrroline (2-AP) and increase in volatile lipid oxidation products in aged rice have been reported. The aim of this study was to monitor the changes in key volatile compounds of organic red fragrant rice cv. Hom Daeng during storage. Effects of packaging material, storage temperature and time were evaluated using solid phase microextraction/gas chromatography/mass spectrometry. Thirteen key volatile compounds including ten lipid oxidation products were monitored. For samples vacuum packed in Nylon/LLDPE pouches at ambient temperature, significant increases in hexanal, 2-pentylfuran, 1-octanol and 4-vinyl guaiacol and significant decreases in 2-AP and geranyl acetone were found after the second month (P< or =0.05). Vacuum packing in OPP/Al/LLDPE pouches or storage at 15 degrees C better retarded the formation of volatile lipid oxidation products and greater retained desirable odorants, including 2-AP. However, accumulation of lipid oxidation products and 4-vinyl guaiacol was apparent after the sixth month under these storage conditions. A greater extent and higher rate of undesirable changes in volatile compounds were found in samples stored under Nylon/LLDPE/ambient temperature condition. Nevertheless, this condition is acceptable for the retail trade of organic rice in Thailand. Storage conditions using reduced temperature or better packaging materials may be more appropriate for exported rice or superior-grade fragrant rice to better maintain the desirable rice aroma.

Olive phenols efficiently inhibit the oxidation of serum albumin-bound linoleic acid and butyrylcholine esterase

Background Olive phenols are widely consumed in the Mediterranean diet and can be detected in human plasma. Here, the capacity of olive phenols and plasma metabolites to inhibit lipid and protein oxidations is investigated in two plasma models. Methods The accumulation of lipid oxidation products issued from the oxidation of linoleic acid bound to human serum albumin (HSA) by AAPH-derived peroxyl radicals is evaluated in the presence and absence of phenolic antioxidants. Phenol binding to HSA is addressed by quenching of the Trp214 fluorescence and displacement of probes (quercetin, dansylsarcosine and dansylamide). Next, the esterase activity of HSA-bound butyrylcholine esterase (BChE) is used as a marker of protein oxidative degradation. Results Hydroxytyrosol, oleuropein, caffeic and chlorogenic acids inhibit lipid peroxidation as well as HSA-bound BChE as efficiently as the potent flavonol quercetin. Hydroxycinnamic derivatives bind noncompetitively HSA subdomain IIA whereas no clear site could be identified for hydroxytyrosol derivatives. General significance In both models, olive phenols and their metabolites are much more efficient inhibitors of lipid and protein oxidations compared to vitamins C and E. Low postprandial concentrations of olive phenols may help to preserve the integrity of functional proteins and delay the appearance of toxic lipid oxidation products.

Abstract 421: Aldose Reductase Protects Against the Early Atherosclerotic Lesion Formation InApoe-null Mice

Atherosclerotic lesion formation is associated with extensive oxidation of unsaturated lipids and the accumulation of lipid oxidation products. Products of lipid oxidation, particularly aldehydes, stimulate cytokine production and enhance monocyte adhesion. Aldehydes generated by oxidized lipids are metabolized by several biochemical pathways, of which aldose reductase (AR)-catalyzed reduction represents a metabolic fate common to both free and phospholipid esterified aldehydes. Herein, we tested the hypothesis that inhibition of AR could aggravate atherosclerotic lesion formation by preventing the removal and the detoxification of aldehydes generated by oxidized lipids. In atherosclerotic lesions of apoE-null mice, AR protein was associated with macrophage-rich regions and its abundance increased with lesion progression. Treatment of 8 week old apoE-null mice with AR inhibitors sorbinil or tolrestat for 4 weeks increased lesion formation in the aortic arch (P&lt;0.01) and the aortic sinus (P&lt;0.01). No change in lesion formation was observed when 24 week old mice were fed AR inhibitors for 12 weeks. To probe the role of AR in atherogenesis further, we generated AR −/− /apoE −/− mice. Lesions of 8 week old AR −/− /apoE −/− mice maintained on high fat diet for 4 or 12 weeks were significantly larger throughout the aortic tree (P&lt;0.01 for both the groups) when compared with age-matched AR +/+ /apoE −/− mice. Lesions in AR −/− /apoE −/− mice exhibited increased collagen (P&lt;0.01) and macrophage content (P&lt;0.01) and a decrease in smooth muscle cells (P&lt;0.01). GC-MS analysis showed that the concentration of AR substrates HNE and hexanal was increased by 2.5–3 fold (P&lt;0.01) in the plasma of AR −/− /apoE −/− mice as compared with AR +/+ /apoE −/− mice. Immunohistochemical analysis showed greater accumulation of protein-HNE adducts in arterial lesions of AR −/− /apoE −/− mice. These observations suggest that AR is up regulated during atherosclerosis and that this protein protects against early stages of atherosclerotic lesion formation by removing aldehydes generated by lipid oxidation.

Vitamin C preserves the cardio-protective paraoxonase activity of high-density lipoprotein during oxidant stress

HDL-associated paraoxonase (PON) antioxidant enzyme activity is cardio-protective. We investigated whether vitamin C prevented loss of PON activity from HDL during oxidant stress. HDL was incubated with either hydrophilic or lipophilic peroxyl radical initiators in the absence (control) or presence of vitamin C (50 and 100 μmol/L). Regardless of the type of radical, accumulation of lipid oxidation products in HDL was similar in incubations lacking vitamin C. Loss of PON activity was greater in HDL exposed to hydrophilic, in contrast to lipophilic, radicals, but addition of vitamin C maintained enzyme activity. Vitamin C’s capacity to attenuate loss of the HDL ability to prevent atherogenic modification of LDL (assessed as electrophoretic mobility) was, however, modest, and appeared limited only to those incubations in which HDL was exposed to lipophilic radicals. Our results indicate that vitamin C may, under some conditions, prevent loss of cardio-protective function from HDL during oxidant stress.

Loss of Redness (a*) as a Tool To Follow Hemoglobin-Mediated Lipid Oxidation in Washed Cod Mince

Instrumental measurement of redness loss (decrease in a* value) was evaluated as a tool to follow hemoglobin (Hb)-mediated lipid oxidation in fish muscle. Two washed cod mince model systems were used (prepared at pH 6.5 and 5.5), both fortified with 15 micromol/kg of trout Hb and adjusted to pH 6.5 and 81% moisture. The rate of oxidation was varied through pH alterations (pH 6.1 and 6.9) and addition of an antioxidative cod muscle press juice. During ice storage, TBARS, painty odor, and a* values were followed. In all "oxidizing" samples, a* values correlated well with TBARS and painty odor development; r = -0.95 and -0.77, respectively. In press juice containing samples, the correlation was lower (0.55 for a vs TBARS) because there was a slight a* value decrease even in the absence of measurable lipid oxidation. a* values distinguished between "oxidizing" and stable samples within 1 day, before any lipid oxidation products could be chemically detected. It was confirmed in an aqueous phosphate buffer model system that the redness loss corresponded to a buildup of brownish met-Hb at the expense of oxy- and deoxy-Hb. The a* value data were best used as a lipid oxidation index by calculating the rate of decrease (k value) in the "initial phase" of the redness loss (before accumulation of lipid oxidation products) or in the "differentiation phase" (during the exponential raise in TBARS/painty odor). Calibration to lipid oxidation products must, however, be made for each specific sample type. Washing method, pH, Hb-type, etc., all affected both k values and absolute a* readings. Small yellowness (b*) increases also occurred along with a value losses, possibly the result of polymerized Schiff bases.

Hyperbaric oxygen reduces the progression and accelerates the regression of atherosclerosis in rabbits.

We studied the effect of hyperbaric oxygen (HBO) treatment on the extent of diet-induced accumulation of lipid oxidation products in rabbit plasma and tissues, on plasma paraoxonase activity, and on the extent of progression and regression of atherosclerotic lesions in the rabbit aorta. HBO treatment of cholesterol-fed rabbits dramatically reduces the development of arterial lesions despite having little or no effect on plasma or individual lipoprotein cholesterol concentrations. Compared with no treatment in cholesterol-fed animals, HBO treatment also substantially reduces the accumulation of lipid oxidation products (conjugated dienes, trienes, and thiobarbituric acid-reactive substances) in plasma, in the low density lipoprotein and high density lipoprotein fractions of plasma, in the liver, and in the aortic tissues. In addition, HBO treatment prevents the decrease in plasma paraoxonase activity observed in rabbits fed cholesterol-rich diets. Similarly, in regression studies, HBO treatment has no effect on the rate of plasma (or lipoprotein) cholesterol decline but significantly accelerates aortic lesion regression compared with no treatment. Direct measures of aortic cholesterol content support these morphological observations. On the basis of these results, we conclude that repeated, but relatively short, exposure to HBO induces an antioxidant defense mechanism(s) that is responsible for retarding the development or accelerating the regression of atherosclerotic lesions.

Dietary α‐Tocopheryl Acetate Contributes to Lipid Stability in Cooked Beef

ABSTRACTLipid oxidation was investigated in cooked gluteus medius from Holstein steers fed diets including four levels of α‐tocopheryl acetate (0, 250, 500 and 2,000 mg/steer daily) for 42 or 126 days. Alpha‐tocopherol (vitamin E) concentrations increased in fresh and cooked muscle due to level and duration of supplementation (P&lt;0.01). Cooking did not affect α‐tocopherol concentration in the muscle. Dietary α‐tocopheryl acetate delayed (P&lt;0.01) accumulation of lipid oxidation products in cooked muscle during 6 days of display at 4°. Daily supplementation of 500 mg α‐tocopheryl acetate for 126 days resulted in 3.4 μg α‐tocopherol/g cooked gluteus medius.

Decreased concentration of hemoglobin, accumulation of lipid oxidation products and unchanged skeletal muscle in Atlantic salmon (Salmo salar) fed low dietary vitamin E

Atlantic salmon (Salmo salar) fry, initial weight 0.16 g, were fed a semipurified diet with 0, 15, 30, 60 or 120 mg dl-α-tocopheryl acetate/kg. After 24 weeks, the first two of these groups were extinct, and the fish receiving 30 mg/kg were clearly vitamin E deficient. Vitamin E deficient fish had low hemoglobin levels, characterized by a combination of reduced cellular hemoglobin concentration, red cell volume and red cell number, and an increased number and fraction of immature red blood cells. The hemoglobin concentration decreased over the decreasing range of experimental dl-ga-tocopheryl acetate levels. Therefore, even if 60 mg dl-α-tocopheryl acetate/kg gave good survival, this level was clearly physiologically suboptimal. Ceroid accumulated in the liver of fish fed 30 mg vitamin E/kg, and autofluorescent inclusions were found in the red blood cells of fish fed 30 and 60 mg vitamin E/kg. Degeneration of skeletal muscle was not observed in the present study.

Effect of long- or short-term feeding of alpha-tocopheryl acetate to Holstein and crossbred beef steers on performance, carcass characteristics, and beef color stability.

Three experiments were conducted to examine the effects of vitamin E supplementation on feedlot cattle. Vitamin E supplementation did not affect feedlot performance or carcass characteristics of cattle fed a high-concentrate diet (P greater than .1). The major finding was the effectiveness of vitamin E in extending the color stability of displayed beef (P less than .01). Color stability during display of longissimus lumborum steaks from cattle supplemented with 300 IU/d for 266 d, 1,140 IU/d for 67 d, or 1,200 IU/d for 38 d was extended by 2.5 to 4.8 d. Gluteus medius steaks had an extended color display life of 1.6 to 3.8 d. The accumulation of lipid oxidation products, but not aerobic microbes, associated with displayed longissimus lumborum was suppressed for muscle from vitamin E-supplemented steers. Taste panelists detected no difference among longissimus lumborum steaks from control and vitamin E-supplemented steers but found (P less than .01) steaks aged for 21 d to be more tender than steaks aged for 7 d. Supplementing cattle with vitamin E should reduce economic losses associated with discolored beef during retail display.