• Asian-Australasian Journal of Animal Sciences
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• v.20 no.10
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• pp.1606-1611
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• 2007

The experiment was conducted to investigate the effects of dihydropyridine on laying performance and fat metabolism of laying hens. Five hundred and forty laying hens, 40 weeks old, were randomly allotted to three groups, each of which included four replicates of 45 hens. The groups were given a basal corn-soybean meal diet supplemented with 0, 150 mg/kg and 300 mg/kg dihydropyridine. Results showed that compared with the control group (0 mg/kg dihydropyridine), supplements of 150 and 300 mg/kg dihydropyridine increased egg production rate by 9.39% (p<0.01) and 12.97% (p<0.01), increased mean egg weight by 3% (p>0.05) and 4.8% (p>0.05), and improved feed efficiency by 9.54% (p<0.05) and 7.25% (p<0.05), respectively; The addition of 150 and 300 mg/kg dihydropyridine decreased percentage of abdominal fat by 35.4% (p<0.05) and 46.9% (p<0.05), decreased liver fat content by 32.4% (p<0.05) and 10.5% (p<0.05), increased HSL activity of abdominal fat by 39.64% (p<0.05) and 48.48% (p<0.05), increased HSL activity of liver by 9.4% (p>0.05) and 47.34% (p<0.05) and increased the content of cAMP in adenohypophysis by 14.67% (p<0.05) and 10.91% (p<0.05), respectively; The inclusion of 150 mg/kg dihydropyridine increased liver superoxide dismutase activity by 69.61% (p<0.05), and increased hepatic apoB concentration by 53.96% (p<0.05); The supplementation of 150 or 300 mg/kg dihydropyridine decreased malondialdehyde concentration of hepatic mitochondria by 30.90% (p<0.01) and 10.39% (p<0.05), respectively; Supplemented dihydropyridine had no significant effects on TG, Ch HDL-C and VLDL-C concentrations in serum; addition of 150 or 300 mg/kg dihydropyridine increased T3 levels in serum by 15.34% (p<0.05) and 11.88% (p<0.05) and decreased insulin concentration by 40.44% (p<0.05) and 54.37% (p<0.05), respectively. The results demonstrated that adding dihydropyridine had the tendency of improving very low density lipoprotein receptor (VLDLR) content in the ovary. It was concluded that dihydropyridine could improve laying performance and regulate the fat metabolism of laying hens and that 150 mg/kg dihydropyridine is the optimum dose for laying birds in practical conditions.

• Journal of Microbiology and Biotechnology
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• v.27 no.3
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• pp.633-643
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• 2017

To examine the pro-apoptotic role of the human ortholog (YPEL5) of the Drosophila Yippee protein, the cell viability of Saccharomyces cerevisiae mutant strain with deleted MOH1, the yeast ortholog, was compared with that of the wild-type (WT)-MOH1 strain after exposure to different apoptogenic stimulants, including UV irradiation, methyl methanesulfonate (MMS), camptothecin (CPT), heat shock, and hyperosmotic shock. The $moh1{\Delta}$ mutant exhibited enhanced cell viability compared with the WT-MOH1 strain when treated with lethal UV irradiation, 1.8 mM MMS, $100{\mu}M$ CPT, heat shock at $50^{\circ}C$, or 1.2 M KCl. At the same time, the level of Moh1 protein was commonly up-regulated in the WT-MOH1 strain as was that of Ynk1 protein, which is known as a marker for DNA damage. Although the enhanced UV resistance of the $moh1{\Delta}$ mutant largely disappeared following transformation with the yeast MOH1 gene or one of the human YPEL1-YPEL5 genes, the transformant bearing pYES2-YPEL5 was more sensitive to lethal UV irradiation and its UV sensitivity was similar to that of the WT-MOH1 strain. Under these conditions, the UV irradiation-induced apoptotic events, such as FITC-Annexin V stainability, mitochondrial membrane potential (${\Delta}{\psi}m$) loss, and metacaspase activation, occurred to a much lesser extent in the $moh1{\Delta}$ mutant compared with the WT-MOH1 strain and the mutant strain bearing pYES2-MOH1 or pYES2-YPEL5. These results demonstrate the functional conservation between yeast Moh1 and human YPEL5, and their involvement in mitochondria-dependent apoptosis induced by DNA damage.

• Current Research on Agriculture and Life Sciences
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• v.3
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• pp.92-98
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• 1985

The experiments were conducted to investigate the activity changes of peroxidase, existence of isoenzyme and the changes of reserved substances in tomato under subatmospheric pressure storage condition. The results obtained were as follows: 1. Soluble fraction showed the highest peroxidase activity and followed by cell wall fraction, mitochondria fraction and ribosome fraction in that order. 2. Peroxidase activity was decreased during the ripening and senescence period in tomato. Especially, peroxidase activity in tomato was higher at a room temperature ($25^{\circ}C$) than at a low temperature ($15^{\circ}C$). The decreasing inclination was similar in both treatment. The peroxidase activity was higher in 380 Torr, than in 570 Torr. 3. At least, two isoperoxidases(Soluble or solubilized) were identified from different extraction procedures. Three of four isoenzymes were recognized from a vertical slab of polyacrylamide gel electrophoresis. 4. The changes of components in tomato under SAP were generally affected by temperature and pressure. Especially, quality of tomato stored at a low temperature ($15^{\circ}C$) and SAP (380 Torr.) was best during storage.

• Journal of the Korean Applied Science and Technology
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• v.37 no.4
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• pp.744-754
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• 2020

We investigated the whether endurance exercise and MitoQ intake mediated neuroprotection are associated with mitochondrial function in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine(MPTP) -induced mice model of Parkinson's disease. C57BL/6 male mice were randomly assigned to five groups: Normal Conrol(NC, n=10), MPTP Control(MC, n=10), MPTP +MitoQ(MQ, n=10), MPTP + Exercise(ME, n=10) and MPTP + MitoQ + Exercise(MQE, n=10). Exercise intervention groups performed the treadmill exercise for 5days/week for 5 weeks with gradual increase of intensity. MitoQ intake groups consumed the MitoQ at a concentration of 250μmol by dissolving with water during experiment period. Our data demonstrated that ME and MQE group restored MPTP-induced motor dysfunction. In addition, treatment groups(MQ, ME and MQE) increased tyrosine hydroxylase levels, and suppressed the accumulation of α-synuclein levels. Futhermore, treatment groups modulated the mitochondrial function such as upregulated mitochondrial biogenesis, increased antioxidant enzyme, enhanced a anti-apoptotic protein(e.g., BCL2), and reduced a pro-apoptotic protein(e.g., BAX). Taken together, these results suggested that endurance exercise and MitoQ intake-mediated increase in mitochondrial function contributes to improvement of aggravated dopaminergic neuronal, resulting in attenuation of motor function of Parkinson's disease.

• Journal of Nutrition and Health
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• v.20 no.6
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• pp.432-441
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• 1987

This study was undertaken to investigate effects of alcohol and fat content in a balanced diet on growth, hepatic function and some biochemical indices of blood in growing rats. Fourty eight male rats of Sprague-Dawley strain weighing about 160g were divided into 4 groups ; high fat diet group, alcohol-adminstered high fat diet group, low fat diet group and alcohol-administered low fat diet group. High and low fat diet supplied 30% and 12%, respectively, of total calorie intake from fat and alcohol-treated groups received water containing 10% ethanol. Diets contained adequate amounts of all nutrients required for rats, including lipotropic agents(choline and methionine) to minimize effects of factors other than alcohol on liver function. Growth rate was lowest in alcohol-administered low-fat diet group, despite that their energy intake was equivalent to the others. For a 3-week study period, 21.86% and 23.61% of total calorie intake were derived from alcohol in alcohol-adminitered high fat diet group and low fat diet group, respectively. There was no influenced on vitamin B$_1$ status by alcohol consumption. Concentration of triglyceride in plasma increased with alcohol comsumption, and the effect was greater after 6 weeks than after 3 weeks of alcohol consumption . Difference of dietary fat content did not affect the level of triglyceride . The levels of total cholesterol and HDL-cholesterol in plasma were not influenced by alcohol consumption. Serum glutamate pyruvate transaminase activity and hepatic mitochondrial respiration rate did not differ between groups. The results indicate that neither moderate alcohol drinking for 6 weeks nor fat content with a balanced diet caused any dramatic change of metabolism and liver function in rats. However they suggest that even moderate alcohol consumption can affect growth of animals dramatically and the effect may be lessened with relatively high fat content in diet.

• The Korean Journal of Malacology
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• v.26 no.1
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• pp.63-78
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• 2010

The purpose of this study was to investigate the effect of tributyltin (TBT) on histopathological and ultrastructural changes in the digestive gland structure of the equilateral venus, Gomphina veneriformis. Experimental period was 36 weeks. Experimental groups consist of control condition and 3 TBTCl exposure conditions (0.4, 0.6, $0.8\;TBTC\;{\mu}g\;L^{-1}$). Outer envelop of the visceral mass of G. veneriformis exposed to TBTCl was observed disappearance of microvilli and cilia, decrease of mucous cell and partially destruction of epithelium. In the digestive gland showed an increase of number of hemocyte and mucopolysaccaride near the digestive tubule at early time of the exposure. Especially, in $0.8\;TBTC\;{\mu}g\;L^{-1}$ group, collapse of digestive tubule with modification of epithelium was observed. TEM observation revealed the numerous glycogen granules in epithelium of the outer envelop and connective tissue. In the ciliated cell of the primary duct formed the cilia in cytoplasm. Basophilic cell was observed destruction of the rough endoplasmic reticulum and mitochondria. Also, nucleus in the epithelium of the digestive tubule was disappeared heterochromatin and nucleolus, and condense. As the concentration of TBTCl increased, the accumulation of lipofucin increased in the digestive gland, but the collapse of digestive tubule induced a decrease of accumulation of lipofuscin.

• Applied Biological Chemistry
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• v.43 no.4
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• pp.236-240
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• 2000

Correlations between mitochondrial respiration, glycolysis activity and overall growth activity of rice (Oryza sativa: cv. Dasan) seedlings during low temperature exposure were studied in order to provide insights into the underlying mechanism for the primary phase of chilling injury in plants. Among cellular membranes involved in energy metabolism, only the mitochondrial inner membrane showed not only physical phase transition at ca. $13^{\circ}C$, as monitored by ESR spin label, but also functional phase transition at the same temperature, as assessed by cytochrome c oxidase activity. The main regulatory enzyme of glycolysis, phosphofructokinase, in situ did not suffer phase transition of its activity at least in the $4{\sim}27^{\circ}C$ range. Low temperature caused a significant accumulation of glucose 6-phosphate (G6P) and fructose 6-phosphate (F6P), which disappeared almost completely on rewarming of the seedlings. Temperature profiles of the steady state levels of G6P and F6P revealed the inflection point appearing at around phase transition temperature of the mitochondrial membrane. The results conform to our previous proposition on the mechanism for the early stage events of chilling injury that the accumulation of glycolytic metabolites in cells due to metabolic imbalance at low temperature gives rise to an excess supply of electrons during rewarming period, which, in turn, results in overproduction of active oxygen in mitochondria.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.325-331
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• 2003

3-Nitropropionic acid (3-NP) inhibits electron transport in mitochondria, leading to a metabolic failure. In order to elucidate the mechanism underlying this toxicity, we examined a few biochemical changes possibly involved in the process, such as metabolic inhibition, generation of reactive oxygen species (ROS), DNA strand breakage, and activation of Poly(ADP-ribose) polymerase (PARP). Exposure of SK-N-BE(2)C neuroblastoma cells to 3-NP for 48 h caused actual cell death, while inhibition of mitochondrial function was readily observed when exposed for 24 h to low concentrations (0.2${\sim}$2 mM) of 3-NP. The earliest biochemical change detected with low concentration of 3-NP was an accumulation of ROS (4 h after 3-NP exposure) followed by degradation of DNA. PARP activation by damaged DNA was also detectable, but at a later time. The accumulation of ROS and DNA strand breakage were suppressed by the addition of glutathione or N-acetyl-L-cysteine (NAC), which also partially restored mitochondrial function and cell viability. In addition, inhibition of PARP also reduced the 3-NP-induced DNA strand breakage and cytotoxicity. These results suggest that oxidative stress and activation of PARP are the major factors in 3-NP-induced cytotoxicity, and that the inhibition of these factors may be useful in protecting neuroblastoma cells from 3-NP-induced toxicity.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.2
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• pp.213-220
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• 2016

Mast cells are primary mediators of allergic inflammation. Beta-1,3-glucan (BG) protects against infection and shock by activating immune cells. Activation of the BG receptor induces an increase in intracellular $Ca^{2+}$, which may induce exocytosis. However, little is known about the precise mechanisms underlying BG activation of immune cells and the possible role of mitochondria in this process. The present study examined whether BG induced mast cell degranulation, and evaluated the role of calcium transients during mast cell activation. Our investigation focused on the role of the mitochondrial calcium uniporter (MCU) in BG-induced degranulation. Black mouse (C57) bone marrow-derived mast cells were stimulated with $0.5{\mu}g/ml$ BG, $100{\mu}g/ml$ peptidoglycan (PGN), or $10{\mu}M$ A23187 (calcium ionophore), and dynamic changes in cytosolic and mitochondrial calcium and membrane potential were monitored. BG-induced mast cell degranulation occurred in a time-dependent manner, and was significantly reduced under calcium-free conditions. Ruthenium red, a mitochondrial $Ca^{2+}$ uniporter blocker, significantly reduced mast cell degranulation induced by BG, PGN, and A23187. These results suggest that the mitochondrial $Ca^{2+}$ uniporter has an important regulatory role in BG-induced mast cell degranulation.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.2
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• pp.201-211
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• 2016

Although the antioxidant and cardioprotective effects of NecroX-5 on various in vitro and in vivo models have been demonstrated, the action of this compound on the mitochondrial oxidative phosphorylation system remains unclear. Here we verify the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity during hypoxia-reoxygenation (HR). Necrox-5 treatment ($10{\mu}M$) and non-treatment were employed on isolated rat hearts during hypoxia/reoxygenation treatment using an ex vivo Langendorff system. Proteomic analysis was performed using liquid chromatography-mass spectrometry (LC-MS) and non-labeling peptide count protein quantification. Real-time PCR, western blot, citrate synthases and mitochondrial complex activity assays were then performed to assess heart function. Treatment with NecroX-5 during hypoxia significantly preserved electron transport chain proteins involved in oxidative phosphorylation and metabolic functions. NecroX-5 also improved mitochondrial complex I, II, and V function. Additionally, markedly higher peroxisome proliferator-activated receptor-gamma coactivator-$1{\alpha}$ ($PGC1{\alpha}$) expression levels were observed in NecroX-5-treated rat hearts. These novel results provide convincing evidence for the role of NecroX-5 in protecting mitochondrial oxidative phosphorylation capacity and in preserving $PGC1{\alpha}$ during cardiac HR injuries.