The oxidative stability of cholesterol in tallow heated at different frying temperatures (130$\^{C}$, 150$\^{C}$, and 180$\^{C}$) was studied by identifying cholesterol oxides by thin layer chromatography(TLC). And fatty acid compositions in tallow heated were also measured and compared with cholesterol oxides. Unsaturated fatty acid contents slightly decreased as the heating time increased, whereas saturated fatty acid contents increased This phenomenon became excessive especially by heating to higher temperature. It was found that RF value and spot color of the nonsaponifiable lipids from tallow heated on TLC analysis accorded with the synthetic cholesterol oxides in this experiment. Four kinds of cholesterol oxides were detected in tallow heated for 24 hours at three different temperatures. The oxides were identified as 7-$\alpha$-hydroxycholesterol, 7-$\beta$-hydroxycholesterol, 7-ketocholesterol and cholesterol epoxide. It was found that there was a little difference in oxidative pattern of cholesterol between several heating temperatures.
Beef loins that retailed in market were used as experimental samples. Some beef samples in raw state were packaged with PVDC as aerobic and vacuum condition. The other beef samples were cooked until core temperature arrived at 70$^{\circ}C$ and then packaged immediately in the same way of raw samples. After these samples were irradiated by electron beam 6kGy, irradiated samples were stored in refrigerator(2~4$^{\circ}C$). Identify and quantity of cholesterol oxides were analysed stored at 0 and 7 days, respectively. During the early stage of storage, 7$\beta$-hydroxycholesterol and 7-ketocholesterol were respectively produced from the raw meat samples, and the production of these chemicals were significantly higher (P$<$0.05) from the meats with aerobic packaging than those with vacuum packaging. With the passage of storage time, 7$\alpha$-hydroxycholesterol, 20$\alpha$-hydroxycholesterol, $\beta$-epoxide, $\beta$-epoxide and some other chemicals, which were not produced during the early stage of storage, were produced, Also, the production of these chemicals were significantly increased (P$<$0.05) with the passage of storage time. Cooked meat after irradiation and irradiated meat after cooking produced cholesterol on the 7th day of storage, although this chemical was not produced during the early stage of storage. Production of cholesterol oxides was significantly increased (P$<$0.05) with the passage of storage time for all treatments, and showed significantly lower value (P$<$0.05) with the vacuum packaging than aerobic packaging. Summarizing the aforementioned results, it was found that the production of cholesterol oxides was more easily affected by packaging condition than irradiation.
This study investigates the effect of cooking, storage, and reheating conditions on the formation of cholesterol oxidation products (COPs) in pork loin. Samples of pork loin procured 24 h postmortem were initially processed and assessed for total fat and cholesterol content. The cooking methods evaluated were pan roasting, steaming, oven grilling, and microwaving. Cooked pork loin samples were stored at 4℃ and reheated after 3 and 6 d of storage using the original method of preparation or alternately, microwaving. Fat content increased significantly with cooking as a result of the loss in moisture but cholesterol content remained unchanged. Pan roasting and microwave cooking caused a significantly higher production of COPs, as with the process of reheating using microwave, pan roasting, and oven grilling methods. The major COPs found in pork loin were cholestanetriol, 20-hydroxycholesterol, and 25-hydroxycholesterol, whose concentrations varied according to the different cooking and reheating methods used. Moreover, the aerobic storage of cooked pork loin under a refrigerated condition also increased the formation of cholesterol oxides on reheating.
Pork loins that retailed in market were used as experimental samples. Some pork samples in raw state were packaged with PVDC in either aerobic or vacuum condition. The other pork samples were cooked until core temperature reached at 70$\^{C}$ and then packaged immediately in the same way with the raw samples. After these samples were irradiated by electron beam 6 kGy, the samples were stored in a refrigerator (2∼4$\^{C}$). Identification and quantification of cholesterol oxides were performed at 0 and 7 days. The results were following. During the early stage of storage, cholesterol oxides were not produced from the raw meat samples, but with the passage of storage time,7 $\alpha$-hydroxycholesterol, 7$\beta$-hydroxycholesterol, 7-ketocholesterol, 20 $\alpha$-hydroxycholesterol, $\beta$-epoxide and $\alpha$-epoxide, which were not produced during the early stage of storage, were produced. The production of cholesterol and lipid oxidation products were significantly higher (P<0.05) in the meats with aerobic packaging than those with vacuum packaging, Cooked meat after irradiation showed 7 $\alpha$-hydroxycholesterol, 7 $\beta$-hydroxycholesterol, $\alpha$-epoxide and cholestanetriol on the 7th day of storage, although those chemicals were not produced during the early stage of storage. Production of cholesterol oxides was significantly increased (P<0.05) with the passage of storage time for all treatments, and showed significantly lower value (P<0.05) with the vacuum packaging than these for aerobic packaging. Species of cholesterol oxides from irradiated meat after cooking were similar to those from cooked meat after irradiation. Collectively, it was found that the production of cholesterol oxides was more easily affected by packaging condition than irradiation.
Beef, pork and chicken meat that retailed in market were used as experimental samples. Some samples in raw state were packaged with PVDC as aerobic and vacuum condition. The other samples were cooked until internal temperature arrived at $70^{\circ}C$ using electric oven and then packaged immediately in the same way of raw samples. After these samples were irradiated by electron beam (0, 1, 2 kGy), irradiated samples were stored in refrigerator $(2{\sim}4^{\circ}C)$. Identification and quantification of cholesterol oxides were analysed at 0, 7, 14 days. The results were following. The results indicated that raw-vacuum packaged lower detected than that of other treatments. In raw-vacuum packaged, the amounts of $7{\beta}-hydroxycholesterol$ were detected slightly $(below\;0.5\;{\mu}ug/g)$ during storage, and 7-ketocholesterol were detected during every stored time and amounts of this detection were $8.02{\sim}101.30\;{\mu}g/g$. In cooked-aerobic packaged, total amounts of detection were higher than that of other treatments, total amounts of cholesterol oxides were detected about $51.18{\sim}155.90\;{\mu}g/g$ during storage. In all results, pork and chicken samples were similar to the results of beef samples. In all results, total amounts of cholesterol oxides increased significantly as irradiation dose and storage time increased (P<0.05).
Choe, Juhui;Min, Joong-Seok;Lee, Sang-Ok;Khan, Muhammad Issa;Yim, Dong Gyun;Lee, Mooha;Jo, Cheorun
Food Science of Animal Resources
/
v.38
no.3
/
pp.433-441
/
2018
The objective of present study was to investigate the effect of cooking and their combinations with re-heating methods on the formation of cholesterol oxidation products (COPs) in stored chicken thigh meat. Pan roasting, steaming, oven grilling, charcoal grilling, and microwaving were used for cooking. Re-heating of samples was done using the same cooking methods or microwaving after 3 and 6 d of refrigerated storage. Cooking and re-heating resulted in reduction of crude fat and cholesterol contents of chicken thigh meat depending on storage period before re-heating. Cooking and storage period had no influence on the total amount of COPs. The highest total amount of COPs was observed in meat samples cooked by steaming and reheated by microwaving after 6 d of storage, which showed similar value to raw chicken meat stored for 6 days. However, different re-heating methods formed different types of COPs depending on storage period before re-heating. The high amount (p<0.05) of 25-hydroxycholesterol or ${\alpha}-epoxide$ was detected in meat samples reheated by steaming or microwaving at 3 or 6 d of storage after steamed cooking, respectively. As a result, the combination of steaming and re-heating with microwaving could increase the total amount of COPs in chicken thigh meat and different cooking/re-heating methods could form different types of COPs, even though no significant difference in the total amount of COPs depending on storage period.
Cholesterol oxidation products(COPs) such as 7-ketocholesterol, 7 ${\alpha}$, 7 ${\beta}$-hydroxycholesterol and 25-hydroxycholesterol were analyzed for ensuring the safety of squid during its drying and cooking. In addition. changes of malonaldehyde in squid during its drying and cooking were also investigated. Cholesterol was detected 636.4m9/1009 in fresh sample, which was decreased during its drying and cholesterol contents in dried sample were 468.9mg/100g, 486.8mg/100g, respectively, while COPs contents of sun and hot air dried samples increased about 6.2 times more than those contents of fresh sample. Regardless of cooking methods, the contents of COPs in dried products increased after cooking. Especially, those contents were determined 127.3 mg/g in sun dried samples were cooked by microwave oven. The malonaldehyde contents of dried products increased after cooking, its contents in cooked samples by an microwave oven after sun dried were about 4.3 times more than in control products. In general, a small quantity of COPs were formed in dried samples which were cooked by a steam.
Chicken thigh from a retail market were used as experimental samples. Some chicken samples of raw state were packaged with PVDC at an aerobic and vacuum condition. The other samples were cooked until core temperature arrived at 70$^{\circ}C$ and then packaged immediately in the same way of raw samples. After samples were irradiated by electron beam at 6 kGy, they were stored in a refrigerator. Identification and quantity of cholesterol oxides were made at 0 and 7 days of storage, respectively. During the early stage of storage, 7$\beta$-hydroxycholesterol, $\alpha$,$\beta$-epoxide, cholestanetriol and 7-ketocholesterol were produced from the raw meat samples, and the production of these chemicals were significantly higher(P〈0.05) from the samples with aerobic packaging than those with vacuum packaging. With storage time, 7$\alpha$-hydroxycholesterol, 6-ketocholesterol and some other chemicals, which were not found during the early stage of storage, were found. Also, the formation of these chemicals were significantly increased(P〈0.05) with storage time. Cholesterol and lipid oxidation products of cooked meat after irradiation and irradiated meat after cooking were significantly increased(P〈0.05) with storage time for all treatments, and vacuum packaging results in showed significantly lower value(P〈0.05) than aerobic packaging. Summarizing the aforementioned results, it was found that the formation of cholesterol and lipid oxides and lipid oxidation was more easily affected by packaging condition than irradiation.
Some commercial beef loins in raw state were packaged with PVDC as aerobic and vacuum condition. The other beef samples were cooked until core temperature arrived at $70^{\circ}C$ and then packaged immediately in the same way as the raw state. These samples were irradiated by electron beam (0, 1, 2 kGy), and then stored in refrigerator $(2{\sim}4^{\circ}C)$. Identity and quantity of cholesterol oxides were analysed at the 0, 7th, 14th day of storage. In the samples that were raw and packaged aerobically, $7{\alpha}-hydroxycholesterol,\;{\beta}-epoxide,\;7{\beta}-hydroxycholesterol$ and 7-ketocholesterol were detected over $0.5\;{\mu}g/g$. Cholestanetriol and${\alpha}-epoxide$ were detected at levels below $0.5\;{\mu}g/g$ during storage. In the samples that were raw and vacuum-packaged, $7{\alpha}-hydroxycholesterol$, 7-ketocholesterol and cholestanetriol were detected. In the samples that were cooked and packaged aerobically, cholestanetriol and ${\alpha}-epoxide$ were detected below $0.5\;{\mu}g/g$ during storage. $7{\alpha}-hydroxycholesterol,\;{\beta}-epoxide,\;7{\beta}-hydroxycholesterol$and 7-ketocholesterol were detected as $1.53{\sim}26.81,\;1.07{\sim}5.23,\;40.64{\sim}101.30\;and\;7.16{\sim}33.91\;{\mu}g/g$, respectively. In all results, total amounts of cholesterol oxide increased significantly as irradiation dose and storage time increased (P<0.05).
Yonghae Son;Bo-Young Kim;Miran Kim;Jaesung Kim;Ryuk Jun Kwon;Koanhoi Kim
IMMUNE NETWORK
/
v.23
no.5
/
pp.40.1-40.14
/
2023
Glucocorticoids suppress the vascular inflammation that occurs under hypercholesterolemia, as demonstrated in an animal model fed a high-cholesterol diet. However, the molecular mechanisms underlying these beneficial effects remain poorly understood. Because cholesterol is oxidized to form cholesterol oxides (oxysterols) that are capable of inducing inflammation, we investigated whether glucocorticoids affect the immune responses evoked by 7α-hydroxycholesterol (7αOHChol). The treatment of human THP-1 monocytic cells with dexamethasone (Dex) and prednisolone (Pdn) downregulated the expression of pattern recognition receptors (PRRs), such as TLR6 and CD14, and diminished 7αOHChol-enhanced response to FSL-1, a TLR2/6 ligand, and lipopolysaccharide, which interacts with CD14 to initiate immune responses, as determined by the reduced secretion of IL-23 and CCL2, respectively. Glucocorticoids weakened the 7αOHChol-induced production of CCL2 and CCR5 ligands, which was accompanied by decreased migration of monocytic cells and CCR5-expressing Jurkat T cells. Treatment with Dex or Pdn also reduced the phosphorylation of the Akt-1 Src, ERK1/2, and p65 subunits. These results indicate that both Dex and Pdn impair the expression of PRRs and their downstream products, chemokine production, and phosphorylation of signaling molecules. Collectively, glucocorticoids suppress the innate immune response and activation of monocytic cells to an inflammatory phenotype enhanced or induced by 7αOHChol, which may contribute to the anti-inflammatory effects in hypercholesterolemic conditions.
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