• Title/Summary/Keyword: Oxidation Mechanism

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Biodegradation of Phthalic acid by White rot Fungus, Polyporus brumalis (백색부후균 Polyporus brumalis에 의한 프탈산의 분해)

  • Lee, Soo-Min;Park, Ki-Ryung;Lee, Sung-Suk;Kim, Myung-Kil;Choi, In-Gyu
    • Journal of the Korean Wood Science and Technology
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    • v.33 no.1 s.129
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    • pp.48-57
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    • 2005
  • Phthalate esters are known as plasticizers and some of them suspected as endocrine disrupting chemicals. In this study, in order to identify the mechanism of phthalate esters degradation by white rot fungus, phthalic acid, which is major metabolite in the biodegradation of phthalate esters, was used. Phthalic acid 50 ppm was treated in culture medium with Polyporus brumalis. The availability of ABTS oxidation was different from control and phthalic acid treated group after 4 days of incubation. The activity was gradually increased in control group, but not in phthalic acid treated group. Especially, esterase activity of control group was maximized at 10 days of incubation, and then decreased while the activity of phthalic acid treated group was increased. Glucose was used as a carbon source, and the difference of glucose consumption by control and phthalic acid treated group was not significant. However, after 6 days of incubation the residual glucose in culture medium was rapidly decreased. The consumption rate of phthalic acid treated group was lower than control. These results might indicate that the absorption of phthalic acid in culture medium was occurred by mycelium and metabolized through some pathways as that of glucose was. To clearify the chemical modification of phthalic acid in culture medium, phthalic acid was reacted under in vitro condition which mycelium was excluded. The metabolites were analyzed by GC/MS. The results showed that phthalic acid was converted to phthalic acid anhydride by the extracellular enzymes of P. brumalis.

Small molecule natural compound agonist of SIRT3 as a therapeutic target for the treatment of intervertebral disc degeneration

  • Wang, Jianle;Nisar, Majid;Huang, Chongan;Pan, Xiangxiang;Lin, Dongdong;Zheng, Gang;Jin, Haiming;Chen, Deheng;Tian, Naifeng;Huang, Qianyu;Duan, Yue;Yan, Yingzhao;Wang, Ke;Wu, Congcong;Hu, Jianing;Zhang, Xiaolei;Wang, Xiangyang
    • Experimental and Molecular Medicine
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    • v.50 no.11
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    • pp.5.1-5.14
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    • 2018
  • Oxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of intervertebral disc degeneration (IVDD). Sirtuin 3 (SIRT3), a sirtuin family protein located in mitochondria, is essential for mitochondrial homeostasis; however, the role of SIRT3 in the process of IVDD has remained elusive. Here, we explored the expression of SIRT3 in IVDD in vivo and in vitro; we also explored the role of SIRT3 in senescence, apoptosis, and mitochondrial homeostasis under oxidative stress. We subsequently activated SIRT3 using honokiol to evaluate its therapeutic potential for IVDD. We assessed SIRT3 expression in degenerative nucleus pulposus (NP) tissues and oxidative stress-induced nucleus pulposus cells (NPCs). SIRT3 was knocked down by lentivirus and activated by honokiol to determine its role in oxidative stress-induced NPCs. The mechanism by which honokiol affected SIRT3 regulation was investigated in vitro, and the therapeutic potential of honokiol was assessed in vitro and in vivo. We found that the expression of SIRT3 decreased with IVDD, and SIRT3 knockdown reduced the tolerance of NPCs to oxidative stress. Honokiol ($10{\mu}M$) improved the viability of NPCs under oxidative stress and promoted their properties of anti-oxidation, mitochondrial dynamics and mitophagy in a SIRT3-dependent manner. Furthermore, honokiol activated SIRT3 through the AMPK-PGC-$1{\alpha}$ signaling pathway. Moreover, honokiol treatment ameliorated IVDD in rats. Our study indicated that SIRT3 is involved in IVDD and showed the potential of the SIRT3 agonist honokiol for the treatment of IVDD.

Effects of Piperine on Insulin Resistance and Lipid Accumulation in Palmitate-treated HepG2 Cells (Palmitate처리된 인간 간세포주 HepG2 세포에서 piperine의 지질 축적과 인슐린 저항성 기전에 대한 연구)

  • Jung, Hee Jin;Bang, EunJin;Jeong, Seong Ho;Kim, Byeong Moo;Chung, Hae Young
    • Journal of Life Science
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    • v.29 no.9
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    • pp.964-971
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    • 2019
  • Hepatic lipid accumulation and insulin resistance increases in patients with non-alcoholic fatty liver disease. Piperine is a major compound found in black pepper (Piper nigrum) and long pepper (P. longum). Piperine has been used in fine chemical for its anti-cancer, anti-obesity, anti-diabetic, anti-inflammatory and anti-oxidant properties. However, the signaling-based mechanism of piperine and its role as an inhibitor of lipogenesis and insulin resistance in human hepatocyte cells remains ill-defined. In the present study, we explored the effects of piperine on lipid accumulation and insulin resistance, and explored the potential underlying molecular mechanisms in palmitate-treated HepG2 cells. Piperine treatment resulted in a significant reduction of triglyceride content. Furthermore, piperine treatment decreased palmitate-treated intracellular lipid deposition by inhibiting the lipogenic target genes, sterol-regulatory-element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS); whereas the expression of carnitine palmitoyl transferase (CPT-1) and phosphorylation of acetyl coenzyme A carboxylase (ACC) gene involved in fatty acid oxidation was increased. Moreover, piperine also inhibited the phosphorylation of insulin receptor substrate (IRS)-1 (Ser307). Piperine treatment modulated palmitate-treated lipid accumulation and insulin resistance in HepG2 cells with concomitant reduction of lipogenic target genes, such as SREBP-1 and FAS, and induction of CPT-1-ACC and phosphorylation of IRS-1 (Tyr632)-Akt pathways. Therefore, piperine represents a promising treatment for the prevention of lipid accumulation and insulin resistance.

Development of Cucumber Cotyledon in View of Metabolic Pathways and Organelle (세포내 소기관과 물질대사의 관점에서 오이 떡잎의 발달)

  • Kim, Dae-Jae
    • Journal of Life Science
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    • v.31 no.8
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    • pp.778-785
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    • 2021
  • The germination of cucumber seeds begins with the degradation of reserved oil to fatty acids within the lipid body, which are then further metabolized to acyl-CoA. The acyl-CoA moves from the lipid body to the glyoxysome following β-oxidation for the production of acetyl-CoA. As an initial carbon source supplier, acetyl-CoA is an essential molecule in the glyoxylate cycle within the glyoxysome, which produces the metabolic intermediates of citrate and malate, among others. The glyoxylate cycle is a necessary metabolic pathway for oil seed plant germination because it produces the metabolic intermediates for the tricarboxylic acid (TCA) cycle and for gluconeogenesis, such as the oxaloacetate, which moves to the cytosol for the initiation of gluconeogenesis by phophoenolpyruvate carboxykinase (PEPCK). Following reserved oil mobilization, the production and transport of various metabolic intermediates are involved in the coordinated operation and activation of multiple metabolic pathways to supply directly usable carbohydrate in the form of glucose. Furthermore, corresponding gene expression regulation compatibly transforms the microbody to glyoxysome, which contains the organelle-specific malate synthase (MS) and isocitrate lyase (ICL) enzymes during oil seed germination. Together with glyoxylate cycle, carnitine, which mediates the supplementary route of the acetyl-CoA transport mechanism via the mitochondrial BOU (A BOUT DE SOUFFLE) system, possibly plays a secondary role in lipid metabolism for enhanced plant development.

Effects of taurine and ginseng extracts on energy metabolism during exercise and their anti-fatigue properties in mice

  • Kim, Jisu;Beak, Suji;Ahn, Sanghyun;Moon, Byung Seok;Kim, Bom Sahn;Lee, Sang Ju;Oh, Seung Jun;Park, Hun-Young;Kwon, Seung Hae;Shin, Chul Ho;Lim, Kiwon;Lee, Kang Pa
    • Nutrition Research and Practice
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    • v.16 no.1
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    • pp.33-45
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    • 2022
  • BACKGROUND/OBJECTIVES: Ginseng extract (GSE) and taurine (TR) are widely used antifatigue resources in functional foods. However, the mechanism underlying the antifatigue effects of GSE and TR are still unclear. Hence, we investigated whether GSE and TR have synergistic effects against fatigue in mice. MATERIALS/METHODS: L6 cells were treated with different concentrations of TR and GSE, and cell viability was determined using 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium. Oxidative stress was analyzed by immunocytochemistry using MitoTrackerTM Red FM and an anti-8-oxoguanine antibody. Respiratory gas analysis was performed to investigate metabolism. Expression of an activated protein kinase was analyzed using immunohistochemistry. Gene expression of cluster of differentiation 36 and pyruvate dehydrogenase lipoamide kinase isozyme 4 was measured using reverse transcription-polymerase chain reaction. Mice were orally administered TR, GSE, or their combination for 30 days, and then fatigue-related parameters, including lactate, blood urea nitrogen, and glycogen, were measured after forced swimming. RESULTS: TR and GSE reduced oxidative stress levels in hydrogen peroxide-stimulated L6 cells and enhanced the oxygen uptake and lipid metabolism in mice after acute exercise. After oral administration of TR or GSE for 30 days, the fatigue-related parameters did not change in mice. However, the mice administered GSE (400 mg/kg/day) alone for 30 days could swim longer than those from the other groups. Further, no synergistic effect was observed after the swimming exercise in mice treated with the TR and GSE combination for 30 days. CONCLUSIONS: Taken together, our data suggest that TR and GSE may exert antifatigue effects in mice after acute exercise by enhancing oxygen uptake and lipid oxidation.

Ultrasonic Immersion-steam Cleaning and High Temperature Drying Process for Removing Cutting Oil on Titanium Turning Scraps (타이타늄 터닝 스크랩 내 절삭유 제거를 위한 초음파 침지-스팀 및 고온 건조 공정)

  • Chae, Jikwang;Yoo, Suhwan;Oh, Jung-Min;Lim, Jae-Won
    • Resources Recycling
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    • v.30 no.1
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    • pp.60-65
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    • 2021
  • The recycling of titanium turning scraps requires the removal of cutting oil and other contaminants remaining on the surface. In this study, an experiment was conducted in which titanium scraps were cleaned by a combination of ultrasonic immersion-steam cleaning and subsequent drying at high temperature. To determine the removal mechanism of cutting oil, the contact angle between titanium surface and cutting oil was measured. The result confirmed the optimum condition of the immersion solution of the titanium turning scraps. In the case of immersion cleaning of Na4P2O7 aqueous solution, the degree of carbon removed in the cutting oil was the highest at 50℃, and it was confirmed that the carbon content obtained from the combination of steam cleaning and ultrasonic immersion-steam cleaning was lower than that from steam cleaning after ultrasonic immersion. The oxidation and decomposition behaviors of cutting oil were investigated using Thermogravimetric analysis (TGA) and the result was applied in the high temperature drying process. From the results of the high temperature drying tests, it was concluded that 200℃ is the optimal drying temperature.

Anti-melanogenic Effects of Cnidium japonicum in B16F10 Murine Melanoma Cells (B16F10 피부 흑색종세포에서 갯사상자 추출물의 멜라닌 합성 저해 효과)

  • Jo, Hyun Jin;Karadeniz, Fatih;Oh, Jung Hwan;Seo, Youngwan;Kong, Chang-Suk
    • Journal of Life Science
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    • v.32 no.5
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    • pp.331-339
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    • 2022
  • Melanin is a pigment produced by melanocytes to protect the skin from external stimuli, mainly ultraviolet (UV) rays. However, abnormal and excessive production of melanin causes hyperpigmentation disorders, such as freckles, age spots, and discoloration. Natural cosmeceuticals are a new trend for treating or preventing hyperpigmentation due to fewer side effects and biocompatibility. In this context, the current study focused on Cnidium japonicum, a halophyte with several uses in folk medicine, to evaluate its potential as a skin-whitening agent. The effect of C. japonicum extract (CJE) on melanin production was analyzed in melanogenesis-stimulated B16F10 melanoma cells. The results showed that CJE successfully inhibited the oxidation of tyrosine and L-DOPA by tyrosinase and subsequently decreased the production of the key enzymes responsible for melanin production: tyrosinase, tyrosinase-related protein-1, and protein-2. This effect was confirmed by decreased intracellular and extracellular melanin levels in B16F10 melanoma cells after CJE treatment. Further experiments to elucidate the action mechanism revealed that CJE treatment suppressed melanin production by inhibiting the activation of glycogen synthase kinase 3 β (GSKβ)/β-catenin and protein kinase A (PKA)/cAMP-response element binding protein (CREB) pathways, which are the upstream activators of melanogenesis. In conclusion, the present study suggests that C. japonicum is a potential natural source of bioactive substances for the development of novel cosmeceuticals that can act against hyperpigmentation.

Experiment on the effect of Artemisia sieversiana extract on hair loss prevention and cell growth

  • Yang, Seungbo;Jin, Chul;Kwon, Seungwon;Cho, Seung-Yeon;Park, Seong-Uk;Jung, Woo-Sang;Moon, Sang-Kwan;Park, Jung-Mi;Cho, Ki-Ho;Ko, Chang-Nam
    • The Journal of Korean Medicine
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    • v.43 no.1
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    • pp.18-32
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    • 2022
  • Objectives: This study aimed to examine the safety, effects on proliferation of hair papilla cells, and anti-inflammatory and antioxidant mechanisms of Artemisia sieversiana Ehrh. ex Willd. (AS) extract. Methods: Safety tests through purity testing, acute toxicity tests, and repeated toxicity tests were performed using AS extract (ASE) which had been dried for over two years. Cell culture and proliferation tests were conducted; VEGF (vascular endothelial growth factor), bFGF (basic fibroblast growth factor), and EGF (epidermal growth factor) and protein expression analyses were performed for mechanistic evaluation; and inhibitory effects of ASE on the RNA expression of testosterone, 5𝛼-reductase, and aromatase was assessed. The anti-inflammatory and antioxidant efficacy of ASE was confirmed by measuring the levels of nitric oxide, inflammatory mediators (TNF-𝛼 and PGE2), inflammatory cytokines (IL-1𝛽, IL-6, and IL-8), and chemokine MCP-1. Results: The safety of ASE was confirmed. The mechanism of cell proliferation in human hair follicle dermal papilla cells involved the promotion of VEGF, bFGF, and EGF expression. ASE decreased mRNA expression of testosterone, 5𝛼-reductase, and aromatase-1 in a concentration-dependent manner. PGE2 and TNF-𝛼 production by inflammatory mediators was also significantly decreased in a concentration-dependent manner, and inflammatory cytokine and chemokine expression was inhibited. Conclusions: ASE is suggested to promote papillary cell growth at the cellular level, to suppress expression of various enzymes involved in hair cycle and cell death, and to inhibit hair loss through anti-androgen, anti-inflammatory, and antioxidant effects.

Effect of L-carnitine on Field Potential and ATP-dependent K+ Channel of Rat Cardiac Muscles (L-carnitine 투여가 흰쥐의 심근 Field Potential과 ATP-dependent K+ channel에 미치는 영향)

  • Kim, Jee-Youn;Sim, Young-Je;Chang, Hyun-Kyung;Kim, Chang-Ju
    • Korean Journal of Exercise Nutrition
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    • v.13 no.1
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    • pp.15-21
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    • 2009
  • Ergogenic aids are substances, devices, and practices that enhance an individual's energy use and production, and recovery from fatigue. L-carnitine increases enhance performance and aerobic capacity by stimulating lipid oxidation in muscle cells during long term exercise. L-carnitine is a well known and widely used ergogenic aid. In the present study, the effect of L-carnitine at concentrations of 100 nM, 1 μM, 10 μM, and 100 μM on the amplitude of field potential in rat cardiac muscle slices was measured using multi-channel extracellular recording (MED 64) system. In the present result, L-carnitine was shown to enhance field potential as a does-dependent manner. The increasing effect of the L-carnitine on field potential was not affected by application of the glibenclamide, an ATP-dependant K+ channel antagonist. The increasing effect of L-carnitine on field potential was suppressed by application of the diazoxide, an ATP-dependent K+ channel agonist. Present data show that L-carnitine potentiates field potentials by inhibition on ATP-dependant K+ channel in cardiac muscles. The enhancing effect of the L-carnitine on the field potential in cardiac muscles can be suggested as one of the underlying mechanism of ergogenic aid of the L-carnitine.

ATHEROSCLEROSIS, CHOLESTEROL AND EGG - REVIEW -

  • Paik, I.K.;Blair, R.
    • Asian-Australasian Journal of Animal Sciences
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    • v.9 no.1
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    • pp.1-25
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    • 1996
  • The pathogenesis of atherosclerosis can not be summarized as a single process. Lipid infiltration hypothesis and endothelial injury hypothesis have been proposed and investigated. Recent developments show that there are many points of potential interactions between them and that they can actually be regarded as two phases of a single, unifying hypothesis. Among the many risk factors of atherosclerosis, plasma homocysteine and lipoprotein(a) draw a considerable interest because they are independent indicators of atherogenicity. Triglyceride (TG)-rich lipoproteins (chylomicron and VLDL) are not considered to be atherogenic but they are related to the metabolism of HDL cholesterol and indirectly related to coronary heart disease (CHD). LDL can of itself be atherogenic but the oxidative products of this lipoprotein are more detrimental. HDL cholesterol has been considered to be a favorable cholesterol. The so-called 'causalist view' claims that HDL traps excess cholesterol from cellular membranes and transfers it to TG-rich lipoproteins that are subsequently removed by hepatic receptors. In the so-called 'noncausalist view', HDL does not interfere directly with cholesterol deposition in the arterial wall but instead reflects he metabolism of TG-rich lipoproteins and their conversion to atherogenic remnants. Approximately 70-80% of the human population shows an effective feedback control mechanism in cholesterol homeostasis. Type of dietary fat has a significant effect on the lipoprotein cholesterol metabolism and atherosclerosis. Generally, saturated fatty acids elevate and PUFA lower serum cholesterol, whereas MUFA have no specific effect. EPA and DHA inhibit the synthesis of TG, VLDL and LDL, and may have favourable effects on some of the risk factors. Phospholipids, particularly lecithin, have an antiatherosclerotic effect. Essential phospholipids (EPL) may enhance the formation of polyunsaturated cholesteryl ester (CE) which is less sclerotic and more easily dispersed via enhanced hydrolysis of CE in the arterial wall. Also, neutral fecal steroid elimination may be enhanced and cholesterol absorption reduced following EPL treatment. Antioxidants protect lipoproteins from oxidation, and cells from the injury of toxic, oxidized LDL. The rationale for lowering of serum cholesterol is the strong association between elevation of plasma or serum cholesterol and CHD. Cholesterol-lowing, especially LDL cholesterol, to the target level could be achieved using diet and combination of drug therapy. Information on the link between cholesterol and CHD has decreased egg consumption by 16-25%. Some clinical studies have indicated that dietary cholesterol and egg have a significant hypercholesterolemic effect, while others have indicated no effect. These studies differed in the use of purified cholesterol or cholesterol in eggs, in the range of baseline and challenge cholesterol levels, in the quality and quantity of concomitant dietary fat, in the study population demographics and initial serum cholesterol levels, and clinical settings. Cholesterol content of eggs varies to a certain extent depending on the age, breed and diet of hens. However, egg yolk cholesterol level is very resistant to change because of the particular mechanism involved in yolk formation. Egg yolk contains a factor of factors responsible for accelerated cholesterol metabolism and excretion compared with crystalline cholesterol. One of these factors could be egg lecithin. Egg lecithin may not be as effective as soybean lecithin in lowering serum cholesterol level due probably to the differences of fatty acid composition. However, egg lecithin may have positive effects in hypercholesterolemia by increasing serum HDL level and excretion of fecal cholesterol. The association of serum cholesterol with egg consumption has been widely studied. When the basal or control diet contained little or no cholesterol, consumption of 1 or 2 eggs daily increased the concentration of plasma cholesterol, whereas that of the normolipemic persons on a normal diet was not significantly influenced by consuming 2 to 3 eggs daily. At higher levels of egg consumption, the concentration of HDL tends to increase as well as LDL. There exist hyper-and hypo-responders to dietary (egg) cholesterol. Identifying individuals in both categories would be useful from the point of view of nutrition guidelines. Dietary modification of fatty acid composition has been pursued as a viable method of modifying fat composition of eggs and adding value to eggs. In many cases beneficial effects of PUFA enriched eggs have been demonstrated. Generally, consumption of n-3 fatty acids enriched eggs lowered the concentration of plasma TG and total cholesterol compared to the consumption of regular eggs. Due to the highly oxidative nature of PUFA, stability of this fat is essential. The implication of hepatic lipid accumulation which was observed in hens fed on fish oils should be explored. Nutritional manipulations, such as supplementation with iodine, inhibitors of cholesterol biosynthesis, garlic products, amino acids and high fibre ingredients, have met a limited success in lowering egg cholesterol.