• Toxicological Research
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• v.20 no.3
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• pp.213-223
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• 2004

This work aimed to study the effectiveness of cellular oxidative parameter (malondial-dehyde, protein carbonyl, and 8-hydroxy-2'deoxyguanosine). The experimental groups were aluminum treated rats and control rats. Aluminum treatd rats were given intraperitoneally aluminum nitrate nonahydrate ($Al^{3+}$, 0.2 mmol/kg) daily for 30 days except Sunday. Control rats were injected 1 ml of saline. After the dose, rats were decapitated and hippocampus and cerebral cortex were removed. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation), protein carbonyl (index of protein oxidation), 8-hydroxy-2'-deoxy-guanosine (8-OHdG, index of DNA oxidation), reduced glutathione (GSH) levels as well as glutathione reductase (GR) and catalase. AI concentrations in the tissues were also measured. All results were corrected by tissue protein levels. The results were as followed; 1. The concentrations of AI in the cortex and hippocampus were significantly higher in the AI-treated rats than in the control rats. 2. Antioxidative enzyme's activity, catalase and GR, were significantly higher in the AI-treated rats than the control rats. GSH levels were also higher in the AI-treated rats. 3. MDA, protein carbonyl, and 8-OHdG concentration of AI-treated rats were significantly higher than those of control rats. 4. The concentrations of antioxidants, and oxidative stress parameter were correlated with the concentrations of AI in hippocampus and cerebral cortex. Catalase and GR activity were also correlated with the concentration of AI. Based on these results, it can be suggested that intraperitoneally injected AI was accumulated in the brain and induced the increase of antioxidant levels and antioxidative enzyme activity. Also, the oxidative products of cellular macromolecules are significantly related to tissue AI concentration. Therefore MDA, protein carbonyl, and 8-OHdG are useful markers for oxidative stress on cellular macromolecules.

• Asian-Australasian Journal of Animal Sciences
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• v.30 no.8
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• pp.1135-1142
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• 2017

Objective: The objective of this study was to evaluate effects of heat treatment and soybean oil inclusion on protein oxidation of soy protein isolate (SPI) and of oxidized protein on redox status of broilers at an early age. Methods: SPI mixed with soybean oil (SPIO) heated at $100^{\circ}C$ for 8 h was used to evaluate protein oxidation of SPI. A total of two hundred and sixteen 1-day-old Arbor Acres chicks were divided into 3 groups with 6 replicates of 12 birds, receiving basal diet (CON), heat-oxidized SPI diet (HSPI) or mixture of SPI and 2% soybean oil diet (HSPIO) for 21 d, respectively. Results: Increased protein carbonyl, decreased protein sulfhydryl of SPI were observed as heating time increased in all treatments (p<0.05). Addition of 2% soybean oil increased protein carbonyl of SPI at 8 h heating (p<0.05). Dietary HSPI and HSPIO decreased the average daily gain of broilers as compared with the CON (p<0.05). Broilers fed HSPI and HSPIO exhibited decreased glutathione (GSH) in serum, catalase activity and total sulfhydryl in liver and increased malondialdehyde (MDA) and protein carbonyl in serum, advanced oxidation protein products (AOPPs) in liver and protein carbonyl in jejunal mucosa as compared with that of the CON (p<0.05). Additionally, broilers receiving HSPIO showed decreased glutathione peroxidase activity (GSH-Px) in serum, GSH and hydroxyl radical scavenging capacity in liver, GSH-Px activity in duodenal mucosa, GSH-Px activity and superoxide anion radical scavenging capacity in jejunal mucosa and increased AOPPs in serum, MDA and protein carbonyl in liver, MDA and AOPPs in jejunal mucosa (p<0.05). Conclusion: Protein oxidation of SPI can be induced by heat and soybean oil and oxidized protein resulted in redox imbalance in broilers at an early age.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.42 no.2
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• pp.104-108
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• 2009

Glycation and oxidation induce formation of carbonyl (CO) groups in proteins, which can be used to develop an index of cellular aging. Methyl glyoxal (MG) and hypochlorite anions are deleterious products of oxygen free-radical reaction. The effects of eel carnosine on protein modification mediated by MG and hypochlorite were studied. MG and hypochlorite induced formation of carbonyl groups with high molecular weight and cross-linked forms of ovalbumin. The presence of eel carnosine effectively inhibited these modifications in a concentration-dependent manner. Imidazole ring in eel carnosine might have a primary role in inhibition of protein glycation. Our data suggests that the eel carnosine may be useful as a "natural" anti-glycating agents.

• Nutrition Research and Practice
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• v.2 no.3
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• pp.158-164
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• 2008

This study investigated that the antioxidative effect of freeze-dried cranberry powder against protein and lipid oxidation and ameliorative effect of serum lipid profile in rat fed atherogenic diet. Six weeks old male Sprague-Dawley rats were divided into the following four groups: normal diet group with 5% com oil(control), atherogenic diet group with 5% com oil, 10% lard, 1% cholesterol, and 0.5% sodium cholate(HFC), atherogenic plus 2% cranberry powder diet group(HFC+C2), and atherogenic plus 5% cranberry powder diet group(HFC+C5), and respective diet and water were fed daily for 6 weeks. After the experimental period, the serum lipid profile, such as total cholesterol, HDL-cholesterol, LDL-cholesterol, and triglyceride, ferric reducing ability of plasma(FRAP), plasma phenolics content, superoxide dismutase(SOD) activity, serum protein carbonyl and thiobarbituric acid reactive substances(TBARS) levels were examined. Total phenolic compound and total flavonoid levels in freeze-dried cranberry powder were 9.94 mg/g and 8.12 mg/g, respectively. Serum total cholesterol and LDL-cholesterol levels were not significantly different for cranberry powder treatment, but serum HDL-cholesterol level was significantly increased in HFC+C5 group compared with HFC group. Plasma FRAP value tended to be increased by cranberry powder treatment though there was no significant difference. Plasma total phenol concentrations and SOD activities were not significantly different among all groups. Serum protein carbonyl and TBARS levels were significantly decreased in HFC+C5 group compared with HFC group. Overall results suggested that freeze-dried cranberry powder might have the serum lipid improving effect, as well as anti oxidative effect demonstrated by its protective effect against protein and lipid oxidation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.6
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• pp.899-907
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• 1994

Accumulation of peroxidized lipid, fed or injected in the body of rats was investigated and the effect of peroxidized lipid on the antioxidative system was studied also. Three groups each having six of Sprague-dawley rats were raised for 8 weeks. the peroxide value(POV) of diet fed to the control and the peroxidized group was 5.47 and 22.14meq/kg , respectively. Injected group was given the control diet and peroxidized linoleic acid(POV 31.81meq/kg) was injected into the peritoneal area three times a week. The POV, MDA, and protein carbonyl values of the peroxidized and the injected group (experimental groups) were significantly higher (p<0.05) than those of the control group. Cu, Zn-SOD and M-SOD activity of the experimentla groups increased 1.6 times that of control group at 4 th week. and decreased by 60% of their activityafter 8 weeks of feeding (p<0.05) . Catalase activity, glutathione and Vt, E contents of the experimental groups were significantly lower (p<0.05) than those of the control group during 8 weeks. The accumulation of peroxidcized lipid in liver were ovserved both in the fed or the injected group. The increased of enzyme activity of the experimental group during 4 weeks suggests ianadaptation of antioxidative system to get rid of the peroxidized lipid. Decrease of enzyme activity and glutathione observed as the peroxidized lipid lipid accumulation proceeded further, however, seems to indicate the oxdiative damage of enzyme and protein . Determination of the protein carbonyl content may be used as a method for measuring the oxidative damaging effect of peroxidized lipid.

• Korean Journal of Veterinary Research
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• v.36 no.4
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• pp.809-819
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• 1996

This study was conducted to identify the effects of caffeine or combinations of caffeine and iron or vitamin E on the lipid and protein components in the MDBK(Mardin-Darby Bovine Kidney) cells. For the In vitro test, MDBK cells in ${\alpha}$-MEM(Minimum Essential Medium) were divided into 4 treatment groups according to drug types and dosages as follows; the control(group A), group B was treated with 0.3mM caffeine, group C was treated with 0.3mM caffeine and 0.3mM ferric chloride, group D was treated with 0.3mM caffeine and 0.3mM vitamin E. Those groups were further divided into 5 subgroups according to the time lapsed(control, 4hrs, 8hrs, 24hrs and 48hrs lapsed group). The concentrations of the carbonyl group and malondialdehyde(MDA) and the patterns of the SDS-PAGE(Sodium Dodecyl Sulfate-Polyacrylamide Gel Electrophoresis) and fatty acid compositions were analyzed to determine the oxidative damages and metabolic changes on the lipid and protein components in the MDBK cells. The results obtained from this study were summarized as follows; 1. The concentrations of carbonyl group and malondialdehyde in MDBK cells of group C were significantly higher(p<0.01) in comparison to the control, and increased according to the time lapsed. But the results of groups B and D were little different in comparison to the group C. 2. As the analytical results of fatty acid compositions in MDBK cells, the proportions of palmitoleic acid and linoleic acid in groups B, C and D were lower in comparison to the control, while the proportion of arachidonic acid in groups B, C and D were significantly higher(p<0.01) in comparison to the control. 3. In order to determine the oxidative damages to the protein in MDBK cells, the patterns of the SDS-PAGE were examined and the patterns of SDS-PAGE in groups C and D were significantly different between 43kd and 200kd of molecular weight.

• Bulletin of the Korean Chemical Society
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• v.34 no.2
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• pp.406-410
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• 2013

Tetrahyropapaveroline (THP) is compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegenerative disorder, such as Parkinson's disease (PD). The aim of this study was to evaluate the potential of THP to cause oxidative damage on the structure of cytochrome c (cyt c). Our data showed that THP led to protein aggregation and the formation of carbonyl compound in protein aggregates. THP also induced the release of iron from cyt c. Reactive oxygen species (ROS) scavengers and iron specific chelator inhibited the THP-mediated cyt c modification and carbonyl compound formation. The results of this study show that ROS may play a critical role in THP-induced cyt c modification and iron releasing of cyt c. When cyt c that has been exposed to THP was subsequently analyzed by amino acid analysis, lysine, histidine and methionine residues were particularly sensitive. It is suggested that oxidative damage of cyt c by THP might induce the increase of iron content in cells and subsequently led to the deleterious condition. This mechanism is associated with the deterioration of organs under neurodegenerative disorder such as PD.

• Bulletin of the Korean Chemical Society
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• v.34 no.11
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• pp.3295-3300
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• 2013

Acrolein (ACR) is a well-known carbonyl toxin produced by lipid peroxidation of polyunsaturated fatty acids, which is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). In Alzheimer's brain, ACR was found to be elevated in hippocampus and temporal cortex where oxidative stress is high. In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with ACR. When cytochrome c was incubated with ACR, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in ACR-treated cytochrome c. Reactive oxygen species scavengers and iron specific chelator inhibited the ACR-mediated cytochrome c modification and carbonyl compound formation. Our data demonstrate that oxidative damage of cytochrome c by ACR might induce disruption of cyotochrome c structure and iron mishandling as a contributing factor to the pathology of AD.

• Proceedings of the Korea Society of Environmental Toocicology Conference
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• 2002.10a
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• pp.169-169
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• 2002

The mobilizable amount of transition metals is a fraction of the total amount of the metal from urban particulate matter. Although the fraction is small, some metals (Fe, Cu) are the major participants in a reaction that generates reactive oxygen species (ROS), which can damage various biomolecules. Damaging effects of the metals can be measured by the single strand breakage (SSB) of X174 RFI DNA or the carbonyl formation of protein. In another study, we have shown that more metals are mobilized by PM2.5 than by PM10 in general. DNA SSB of >20% for PM2.5 and >15% for PM10 was observed in the presence of chelator (EDTA or citrate)/reductant (ascorbate), compared to the control (<3%) only with the chelator. The carbonyl formation by both PMs was very similar in the presence of the chelator, regardless of the kind of proteins. Compared to the control in the absence of chelator/reductant, 3.3 times and 4.9 times more carbonyl formation for PM2.5 and PM10, respectively, was obtained with BSA in the presence of chelator/reductant, showing that PM10 induced 33% more damage than PM2.5. However, 4.8 times and 1.9 times more carbonyl formation for PM2.5 and PM10, respectively, was observed with lysozyme in the presence of chelator/reductant, showing that PM2.5 induced 250% more damage than PM10. Although different proteins showed different sensitivities toward ROS, all these results indicate that the degrees of the oxidation of or damage to the biomolecules by the mobilized metals were higher with PM2.5 than with PM10. Therefore, it is expected that more metals mobilized from PM2.5 than from PM10, more damage to the biomolecules by PM2.5 than by PM10. We suggest that when the toxicity of the dust particle is considered, the particle size as well as the mobilizable fraction of the metal should be considered in place of the total amounts.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.13
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• pp.5343-5348
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• 2015

Promoter hypermethylation of the runt-related transcription factor 3 (RUNX3) gene is associated with increased risk of hepatocellular carcinoma (HCC). Oxidative stress plays a vital role in both carcinogenesis and progression of HCC. However, whether oxidative stress and RUNX3 hypermethylation in HCC have a cause-and-effect relationship is not known. In this study, plasma protein carbonyl and total antioxidant capacity (TAC) in patients with hepatitis B virus (HBV)-associated HCC (n=60) and age-matched healthy subjects (n=80) was determined. RUNX3 methylation in peripheral blood mononuclear cells (PBMC) of subjects was measured by methylation-specific PCR. Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Plasma protein carbonyl content was significantly higher, whereas plasma TAC was significantly lower, in HCC patients than healthy controls. Based on logistic regression, increased plasma protein carbonyl and decreased plasma TAC were independently associated with increased risk for HCC. PBMC RUNX3 methylation in the patient group was significantly greater than in the healthy group. RUNX3 methylation in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells was significantly higher than in untreated control cells. In conclusion, increase in oxidative stress in Thai patients with HBV-associated HCC was demonstrated. This oxidative increment was independently associated with an increased risk for HCC development. RUNX3 in PBMC was found to be hypermethylated in the HCC patients. In vitro, RUNX3 hypermethylation was experimentally induced by $H_2O_2$. Our findings suggest that oxidative stress is a cause of RUNX3 promoter hypermethylation in HCC cells.