• BMB Reports
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• v.42 no.10
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• pp.648-654
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• 2009

Overexpression of phospholipid hydroperoxide glutathione peroxidase (PHGPx) genes has been reported to play an important role in protecting host cells from oxidative injury in several model systems. A radish phospholipid hydroperoxide glutathione peroxidase (RsPHGPx) known to have high catalytic activity was applied to mouse 3T3 fibroblasts to determine the protective effects of PHGPx against oxidative injury triggered by hydroperoxides such as hydrogen peroxide ($H_2O_2$), tert-butyl hydroperoxide (t-BHP) and phosphatidylcholine hydroperoxide (PCOOH). We observed that preincubation of cells with RsPHGPx significantly increased cell viability, reduced levels of malondialdehyde (MDA), inhibited generation of reactive oxygen species (ROS), and maintained natural cell shapes after treatment with $H_2O_2$, t-BHP or PCOOH, indicating that the exogenous RsPHGPx can act as an effective hydroperoxide-scavenger and may also protect target cells from oxidative damage. These results suggest the possibility for use of RsPHGPx as a therapeutic protectant.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.20 no.1
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• pp.63-68
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• 1987

The results of previous paper(Lee et al, 1987), indicated that the role of polyunsaturated carbonyls from the polar lipid seemed more important than those of the nonpolar lipid in the browning reaction. In this study, the role of phosphoipid in lipid oxidative browning reaction was investigated. In fatty acid composition of hair tail fish, neutral lipid and glycolipid contained the higher percent of saturated and monoenic acids while phospholipid contained more of polyenoic acids. When this fish was dried and stored, polyunsaturated fatty acids of phospholipid and glycolipid more rapidly decreased than that of neutral lipid. The browning was developed more rapidly in phospholipid than in glycolipid and neutral lipid. In the test of phospholipids, the phosphatidylcholine which fractionated by $CHCl_3-MeOH(1:1)$ solution was the largest in quantity, tut the phosphatidylethanolamine which fractionated by $CHCl_3-MeOH(4:1)$ was more active in the development of browning.

• Korean Journal of Veterinary Research
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• v.35 no.4
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• pp.713-727
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• 1995

The present study was investigated fatty acid composition of the phospholipid in the RBC membrane, liver and microsomal fraction after vitamin E and/or insulin treatment to evaluate the effect of vitamin E on the oxidative stress in STZ-treated rat and BB rat. Results obtained through the experiments were summarized as follows; 1. Effect of vitamin E and/or insulin treatment in STZ-treated rat 1) In the insulin treated group and the combination treated groups of vitamin E with insulin, body weights were increased compared to STZ-treated rat(STZ control group). Especially it was more significantly increased in the combination treated group of high dose vitamin E with insulin. 2) The composition of fatty acids of the phospholipid in RBC membrane, liver and microsomal fractions was shown a decreased C16:1, C18:1, C20:4 and an increased C16:0, C18:0, C18:2 in STZ control group compared to normal control group. In RBC membrane, liver and microsomal fractions after vitamin E with insulin treatment in STZ-treated rat, effect on the composition of fatty acids of the phospholipid was shown the result of a decreased C16:0, C18:0, C18:2 and an increased C16:1, C18:1, C20:4. 3) Hemolysis rate of the RBC to $H_2O_2$ was increased in the STZ control group and it was decreased below the hemolysis level of normal control group by vitamin E treatment. 2. Effect of vitamin E and/or insulin treatment in BB rat 4) Only in microsomal fraction, fatty acid composition was different between insulin treatment group and vitamin E with insulin treatment group. It was increased C16:0 and C18:1, and decreased C18:0 and C18:2 in vitamin E with insulin treatment group: But C20:4 was not different in two groups. These results suggest that the combination treatment of vitamin E and insulin could prevent the oxidative change of fatty acids in P-lipid of the RBC membrane, liver and microsomal fraction in STZ-treated rats and BB rats.

• Archives of Pharmacal Research
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• v.26 no.7
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• pp.554-558
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• 2003

Platelet activating factor acetylhydrolase (PAF-AH) activity has been identified in cerebrospinal fluid (CSF) samples taken from children with meningitis. We reported that PAF-AH activity is significantly increased, by about 3 fold, in patients with meningitis compared to control subjects. Because of limited knowledge about this enzyme in CSF, we examined the biochemical properties of CSF PAF-AH. PAF-AH of CSF was calcium independent, showed a broad pH spectrum and was relatively heat stable. In addition, this enzyme activity was strongly inhibited by phenylmethanesulfonyl fluoride (PMSF), partially inhibited by p-bromophenacylbromide (p-BPB), uninhibited by iodoacetamide, and moderately stimulated by dithiothreitol (DTT). PAF-AH of CSF did not degrade phospholipid with a long chain fatty acyl group at sn-2 position. This enzyme hydrolyzed PAF and oxidatively modified phosphatidylcholine. Furthermore, we identified a monomeric polypeptide with a molecular weight of approximately 45 kDa by Western blot using human plasma PAF-AH antibody. These results suggested that plasma type PAF-AH activity exist in CSF taken from children with meningitis.

• Nutritional Sciences
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• v.6 no.1
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• pp.20-24
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• 2003

The effect of a-tocopherol on the formation and accumulation of phospholipid hydroperoxides, especially of phosphatidylcholine hydroperoxides, in the tissues of 2, 2 -azobis Hydrochloride (AAPH) - dosed rats was investigated. In a-tocopherol supplemented rats, the activities of glutathione peroxidase, catalase and superoxide dismutase were significantly inhibited, compared with the AAPH group. AAPH treatment led to oxidation of phospholipids in the liver, lungs, brain, plasma and red blood cells (RBC), resulting in a notable increase in phosphatidylcholine hydroperoxide (PCOOH). All tissues of the rats given an $\alpha$-tocopherol supplement showed an attenuation of the stimulating effect of AAPH, leading to low levels of formation of PCOOH. Also, the rats injected with AAPH and a-tocopherol showed relatively normal-appearing hepatocytes, except for a little loss of the granules. With regards to the morphological appearance of the liver, it was observed that oral intakes of a -tocopherol resulted in an antioxidant defense against attacks of peroxyl radicals. Thus, we suggest that a-tocopherol is potentially helpful in protecting membrane phospholipids against oxidative damage in vivo.

• Preventive Nutrition and Food Science
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• v.8 no.1
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• pp.36-39
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• 2003

Many defined cell culture media were formulated over 3() years ago and may be deficient in certain micronutrients whose essentiality has only subsequently been recognised. The objective of this study was to evaluate whether alpha-minimal essential medium (MEM) supplemented with 10% foetal bovine serum contained sufficient selenium for optimal activity of the selenium containing enzymes cytosolic glutathione peroxidase (cGPx) and phospholipid hydroperoxide glutathione peroxidase (PHGPx) in cultured Chinese hamster ovary (CHO) cells. Additionally, the effect of zinc deficiency and metallothionein (MT) overexpression on cGPx and PHGPx activity was studied. The addition of 100 nM of selenous acid to the culture medium increased cGPx expression by 10-fold and PHGPx by about 2-fold in both wild-type CHO-K1 cells and CHO-K1 cells overexpressing mouse MT-1. Zinc deficiency had no significant effect on enzyme activity, but cells overexpressing mouse MT-1 had higher levels of cGPx activity. Zinc deficiency decreased cell survival but overexpression of MT-1 was partially protective, probably because its presence in quantity favoured the uptake, sequestration and cellular retention of any remaining zinc. This study demonstrates that selenium in complete alpha-MEM is insufficient for optimal cGPx and PHGPx activity and may compromise the cellular response to oxidative stress.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.617-628
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• 1998

In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.

• Korean Journal of Veterinary Research
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• v.59 no.2
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• pp.59-67
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• 2019

We investigated whether ${\beta}$-carotene (${\beta}-CA$) or ellagic acid (EA), originating from various fruits and vegetables, has a preventive effect against male infertility induced by exogenous scrotal hyperthermia. ICR adult mice were intraperitoneally treated with 10 mg/kg of ${\beta}-CA$ or EA daily for 13 days consecutively. During this time, mice were subjected to transient scrotal heat stress in a water bath at $43^{\circ}C$ for 20 min on day 7, and their testes and blood were obtained on day 14 for histopathologic and biochemical analyses. Heat stress induced significant testicular weight reduction, germ cell loss and degeneration, as well as abnormal localization of phospholipid hydroperoxide glutathione peroxidase (PHGPx) and manganese superoxide dismutase (MnSOD) in spermatogenic and Leydig cells. Heat stress also altered the levels of oxidative stress (lipid peroxidation, SOD activity, and PHGPx, MnSOD, and $HIF-1{\alpha}$ mRNAs), apoptosis (Bax, Bcl-xL, caspase 3, $NF-{\kappa}B$, and $TGF-{\beta}1$ mRNAs), and androgen biosynthesis (serological testosterone concentration and $3{\beta}$-hydroxysteroid dehydrogenase mRNA) in testes. These changes were all improved significantly by ${\beta}-CA$ treatment, but only slightly improved by EA treatment. These findings indicate that ${\beta}-CA$, through modulations of oxidative stress, apoptosis, and androgen biosynthesis, is a potent preventive agent against testicular injuries induced by scrotal hyperthermia.

• Journal of Microbiology and Biotechnology
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• v.33 no.8
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• pp.992-997
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• 2023

Ferroptosis is a new kind of programmed cell death of which occurrence in microorganisms is not clearly verified. The elevated level of reactive oxygen species (ROS) influences cellular metabolisms through highly reactive hydroxyl radical formation under the iron-dependent Fenton reaction. Iron contributes to ROS production and acts as a cofactor for lipoxygenase to catalyze poly unsaturated fatty acid (PUFA) oxidation, exerting oxidative damage in cells. While ferroptosis is known to take place only in mammalian cells, recent studies discovered the possible ferroptosis-like death in few specific microorganisms. Capacity of integrating PUFA into intracellular membrane phospholipid has been considered as a key factor in bacterial or fungal ferroptosis-like death. Vibrio species in bacteria and Saccharomyces cerevisiae in fungi exhibited certain characteristics. Therefore, this review focus on introducing the occurrence of ferroptosis-like death in microorganisms and investigating the mode of action underlying the cells based on contribution of lipid peroxidation and iron-dependent reaction.

• Journal of the Korean Society of Food Science and Nutrition
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• v.30 no.6
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• pp.1220-1226
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• 2001

This study was conducted to investigate the effect of water-soluble extract from roasted chicory on the lipid metabolism and oxidative stress in male Sprague-Dawley rats. The experimental groups were divided into three groups ; the normal group, the cholesterol group and the chicory group. Roasted chicory extract was supplemented at 5.0% (w/w) level in the cholesterol diet. Concentration of total cholesterol in serum was significantly higher in the cholesterol group than in the normal group, but this increase in the cholesterol group was significantly decreased by the cholesterol diet supplemented with chicory extract. Concentration of HDL-cholesterol in serum was significantly lower in the cholesterol group than in the normal group, but this decrease in the cholesterol group tended to increase in the chicory group. However, concentrations of triglyceride, phospholipid and nonesterified fatty acid in serum were not significantly different among the groups. Concentrations of triglyceride and cholesterol in liver were significantly higher in the cholesterol and chicory groups than in the normal group. Feces weight and the excretion of cholesterol and bile acid into feces were significantly higher in the chicory group than in other groups. Concentrations of thiobarbituric acid reactive substances (TBARS) in homogenates and microsomal fractions of liver were not significantly different among the groups. On the other hand, concentration of 8-hydroxydeoxyguanosine (8-OHdG) as an useful marker of oxidative stress in urine was lower in the chicory group than in other groups. Concentration of serum glucose was signnificantly lower in the cholesterol group than in the normal group, but that of the chicory group was significantly higher than in the normal group. These results demonstrated that dietary chicory extract exerted the decreasing effect of cholesterol level and oxidative stress in cholesteral-fed rats.