• Title/Summary/Keyword: fragmentation

Search Result 1,895, Processing Time 0.036 seconds

Effect of Ginger Extract and Citric Acid on the Tenderness of Duck Breast Muscles

  • He, Fu-Yi;Kim, Hyun-Wook;Hwang, Ko-Eun;Song, Dong-Heon;Kim, Yong-Jae;Ham, Youn-Kyung;Kim, Si-Young;Yeo, In-Jun;Jung, Tae-Jun;Kim, Cheon-Jei
    • Food Science of Animal Resources
    • /
    • v.35 no.6
    • /
    • pp.721-730
    • /
    • 2015
  • The objective of this study was to examine the effect of ginger extract (GE) combined with citric acid on the tenderness of duck breast muscles. Total six marinades were prepared with the combination of citric acid (0 and 0.3 M citric acid) and GE (0, 15, and 30%). Each marinade was sprayed on the surface of duck breasts (15 mL/100 g), and the samples were marinated for 72 h at 4℃. The pH and proteolytic activity of marinades were determined. After 72 h of marination, Warner Bratzler shear force (WBSF), myofibrillar fragmentation index (MFI), pH, cooking loss, moisture content, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and protein solubility were evaluated. There was no significant (p>0.05) difference in moisture content or cooking loss among all samples. However, GE marination resulted in a significant (p<0.05) decrease in WBSF but a significant (p<0.05) increase in pH and MFI. In addition, total protein and myofibrillar protein solubility of GE-marinated duck breast muscles in both WOC (without citric acid) and WC (with citric acid) conditions were significantly (p<0.05) increased compared to non-GE-marinated duck breast muscles. SDS-PAGE showed an increase of protein degradation (MHC and actin) in WC condition compared to WOC condition. There was a marked actin reduction in GE-treated samples in WC. The tenderization effect of GE combined with citric acid may be attributed to various mechanisms such as increased MFI and myofibrillar protein solubility.

Effect of Hypoxia on the Signal Transduction of Apoptosis in Osteoblasts (저산소 상태에서 조골세포 고사의 신호전달 기전)

  • Park, Young-Joo;Oh, Soh-Taek;Kang, Kyung-Hwa;Kim, Sang-Cheol
    • The korean journal of orthodontics
    • /
    • v.33 no.6 s.101
    • /
    • pp.453-463
    • /
    • 2003
  • Mammalian cell is critically dependent on a continuous supply of oxygen. Even brief periods of oxygen deprivation can result in profound cellular damage. The aim of this study was to examine the possible mechanism of apoptosis in response to hypoxia in MC3T3E1 osteoblasts. MC3T3El osteoblasts under hypoxic conditions ($2\%$ oxygen) resulted in apoptosis in a time-dependent manner, determined by DNA fragmentation assay and nuclear morphology, stained with fluorescent dye (Hoechst 33258) Pretreatment with Z-VAD-FMK, a pancaspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, suppressed the DNA ladder in response to hypoxia in a concentration dependent manner. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-l activity (YVADase) was detected. To confirm what caspases were involved in apoptosis, western blot analysis was performed using an anticaspase-3 or 6 antibody. The 17-kDa protein, that corresponds to the active products of caspase-3 and the 20-kDa protein of the active protein of caspase-6 were generated in hypoxia-challenged lysates, in which the full length forms of caspase-3 and 6 were evident. With a time course similar to caspase-3 and 6 activation, hypoxic stress also caused the cleavage of Lamin A, typical of caspase-6 activity. In addition, the hypoxic stress elicited the release of cytochrome c into the cytosol during apoptosis. These findings suggested that the activation of caspases accompanied by a cytochrome c release in response to hypoxia was involved in apoptotic cell death in MC3T3E1 osteoblasts.

Gamma Irradiation Induces a Caspase-dependent Apoptotic Mechanism in Human Prostate Cancer PC-3 Cells (인간 남성호르몬 비의존형 전립선 PC-3 암세포에서 감마선의 Caspase-의존성 세포자멸사 유도 효과)

  • Chang, Jeong-Hyun;Kim, Dong-Hyun;Jeon, Gye-Rok;Kwon, Heun-Young
    • Journal of Life Science
    • /
    • v.18 no.8
    • /
    • pp.1042-1048
    • /
    • 2008
  • Prostate cancer is the most predominant cancer in men and related death rate increases every year. Till date, there is no effective therapy for androgen independent prostate cancer. To investigate the mechanism for cell growth inhibition or apoptosis in human androgen independent prostate cancer PC-3 cells after gamma irradiation. The aim of this study was to examine the potential of gamma irradiation to induce apoptosis in PC-3 cells and to assess the mechanism of gamma irradiation-induced apoptosis. Five different assays were employed in this study: cell proliferation assay, morphological assessments of apoptotic cells, DNA fragmentation analysis, quantification of apoptosis by annexin V (AV) and propidium iodide (PI) staning, and western blot analysis. Cell viability was inversely related to radiation dose. DAPI-positive cells were detected 48 hr after 40 Gy radiation exposure. And nuclear morphological changes of cells were observed by gamma irradiation. DNA ladder patterns in the cells exposed to gamma-radiation were appeared at 24 hr. Also, gamma irradiation induces apoptosis of PC-3 cells via Caspase3, Bax and PARP-dependent fashion.

Potential Involvement of p62, a Phosphotyrosine-independent Ligand of SH2 Domain of $p56^{lck}$, on UV-induced Apoptosis in Jurkat T-cell Line ($p56^{lck}$ SH2 domain 결합 단백질 p62가 Jurkat T-세포주의 세포예정사에 미치는 영향)

  • 정인실
    • Development and Reproduction
    • /
    • v.2 no.2
    • /
    • pp.165-171
    • /
    • 1998
  • p62 is a novel cytoplsmic protein that binds to SH2 domain of p56$^{lck}$, lymphocyte-specific protein tyrosine kinase, and the expression of p62 was observed in most tissues. In addition p62 interacts with various proteins including ubiquitin and atypical PKC isoform, indicating its diverse biological role in different tissues. However, little is known about functional connection between p62 and its binding proteins. In the present study, a novel cellular protein, p62 has been shown to bind to 14-3-3 $\tau$ isoform that is specific for T cells. Moreover, overexpression of p62 in T cells caused to delay onset of UV-induced apoptosis characterized by DNA fragmentation and breakdown of poly (ADP-ribose) polymerase (PARP). Lately, 14-3-3 proteins have been shown to mediate survival signal via interacting proapoptotic Bad protein in the Iymphocyte. These results suggested the presence of p62-mediated regulatory mechanism during apoptosis in T cells, in which activation-induced apoptotic signal could be interfered by p62 and 14-3-3 protein.n.

  • PDF

Nondestructive Interfacial Evaluation and fiber fracture Source Location of Single-Fiber/Epoxy Composite using Micromechanical Technique and Acoustic Emission (음향방출과 미세역학적시험법을 이용한 단일섬유강화 에폭시 복합재료의 비파지적 섬유파단 위치표정 및 계면물성 평가)

  • Park, Joung-Man;Kong, Jin-Woo;Kim, Dae-Sik;Yoon, Dong-Jin
    • Journal of the Korean Society for Nondestructive Testing
    • /
    • v.23 no.5
    • /
    • pp.418-428
    • /
    • 2003
  • Fiber fracture is one of the dominant failure phenomena affecting the total mechanical Performance of the composites. Fiber fracture locations were measured through the conventional optical microscope and the nondestructive acoustic emission (AE) technique and then were compared together as a function of the epoxy matrix modulus and the fiber surface treatment by the electrodeposition method (ED). Interfacial shear strength (IFSS) was measured using tensile fragmentation test in combination of AE method. ED treatment of the fiber surface enlarged the number of fiber fracture locations in comparison to the untreated case. The number of fiber fracture events measured by the AE method was less than optically obtained one. However, fiber fracture locations determined by AE detection corresponded with those by optical observation with small errors. The source location of fiber breaks by AE analysis could be a nondestructive, valuable method to measure interfacial shear strength (IFSS) of matrix in non-, semi- and/or transparent polymer composites.

Genetic Diversity and Population Structure of Codium fragile (SURINGAR) HARlOT in Korea Using Allozymes (알로자임을 이용한 청각의 유전적 다양성과 집단구조)

  • Lee Bok-Kyu;Park So-Hye;Heo Youn-Seong;Ju Mu-Teol;Choi Joo-Soo;Huh Man-Kyu
    • Journal of Life Science
    • /
    • v.16 no.2 s.75
    • /
    • pp.213-218
    • /
    • 2006
  • The study of genetic diversity and population structure was carried out in the Codium fragile using allozyme analysis. Although this species has been regarded as a ecologically and economically important source, there is no report on population structure in Korea. Starch gel electrophoresis was used to investigate the allozyme variation and genetic structure of four Korean populations of this species. Of the 15 genetic loci surveyed, nine (60.0%) was polymorphic in at least one population. Genetic diversity was high at the species level ($H_{ES}$=0.144), and, that of the population level was relatively low ($H_{EP}$=0.128). Nearly 87% of the total genetic diversity in C. fragile was apportioned within populations. The predominant asexual reproduction, population fragmentation, low fecundity, geographic isolation and colonization process are proposed as possible factors contributing to low genetic diversity in this species. The indirect estimated of gene flow based on $G_{ST}$ was 1.69. The moderate level of gene flow in C. fragile populations is mainly caused by thallus developed from isolated utricles dispersal via sea current.

Growth Inhibition and Apoptosis Induction of Sulindac on Human Lung Cancer Cells (비소세포 폐암 세포주에서 Sulindac의 성장억제와 세포고사 유도)

  • Kim, Hak Ryul;Yang, Sei Hoon;Jeong, Eun Taik
    • Tuberculosis and Respiratory Diseases
    • /
    • v.56 no.5
    • /
    • pp.514-522
    • /
    • 2004
  • Background : Non-steroidal anti-inflammatory drugs (NSAID) are useful in chemoprevention of colorectal cancers. Continuous NSAID administation causes 40% to 50% reduction in relative risk for colorectal cancer. Sulindac possesses an antiproliferative effect and induces apoptosis and tumor regression on colon cancer and other types of cancers. We intended to analyze the effects of sulindac in three non-small cell lung cancer cell lines. Materials and Methods : The human lung cancer cell lines, A549, NCI-H157 and NCI-H460 were used for this study. Viability was tested by MTT assay, and cell death rate was measured by lactate dehydrogenase(LDH) release. Apoptosis was estimated by flow cytometric analysis and nuclear staining. Results: Sulindac was able to decrease the viability of non-small cell lung cancer cells in a dose- and time- dependent manner. In a parallel effect of sulindac on cell death rate, LDH release was increased in sulindac-treated lung cancer cells. Sulindac significantly increased apoptosis characterized by an increase of $sub-G_0/G_1$ fraction and morphological change of nuclei. The rate of apoptotic cells after sulindac treatment in lung cancer cells increased in a time- and dose- dependent manner in flow cytometric analysis. Apoptotic cells were defined as nuclear shrinkage, chromatin condensation and nuclear fragmentation of cells. Conclusion : Sulindac decreases viability and induces the apoptosis of lung cancer cells. Further studies will be needed to elucidate the potential mechanism of sulindac-induced apoptosis in lung cancer cells.

Cytotoxic Effects of Decursin from Angelica gigas Nakai in Human Cancer Cells (당귀로부터 정제한 Decursin의 인체암세포주에 대한 세포독성)

  • Park, Kyung-Wuk;Choi, Sa-Ra;Shon, Mi-Yae;Jeong, Il-Yun;Kang, Kap-Suk;Lee, Sung-Tae;Shim, Ki-Hwan;Seo, Kwon-Il
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.36 no.11
    • /
    • pp.1385-1390
    • /
    • 2007
  • Anticarcinogenic-active compound was isolated and purified from Angelica gigas Nakai. The compound was identified as decursin ($C_{19}H_{20}O_5$; molecular weight 328) by mass, IR spectrophotometry $^1H-NMR$ and $^{13}C-NMR$. The proliferation decreased in a dose dependant fashion in the MCF-7 cells treated with decursin for 24 hours over the concentration of $20{\mu}g/mL$. The $IC_{50}$ value of the decursin treatment for 24 hours were 31.04, 33.60, 27,24, $20.45{\mu}g/mL$ in the SW480, 293, HepG2 and MCF-7 cells, respectively, The growth inhibitory effect was stronger in the MCF-7 cells compared to other cells including 293 of human normal cells. The chromatin condensation, apoptotic body formation and DNA fragmentation were examined in the cells treated with decursin. These results suggest that decursin from Angelica gigas Nakai inhibited the growth through apoptosis in MCF-7 cells.

PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression

  • Kim, Duk-Soo;Sohn, Eun-Jeong;Kim, Dae-Won;Kim, Young-Nam;Eom, Seon-Ae;Yoon, Ga-Hyeon;Cho, Sung-Woo;Lee, Sang-Hyun;Hwang, Hyun-Sook;Cho, Yoon-Shin;Park, Jin-Seu;Eum, Won-Sik;Choi, Soo-Young
    • BMB Reports
    • /
    • v.45 no.9
    • /
    • pp.532-537
    • /
    • 2012
  • P18, a member of the INK4 family of cyclin-dependent kinase inhibitors, is a tumor suppressor protein and plays a key cell survival role in a variety of human cancers. Under pathophysiological conditions, the INK4 group proteins participate in novel biological functions associated with neuronal diseases and oxidative stress. Parkinson's disease (PD) is characterized by loss of dopaminergic neurons, and oxidative stress is important in its pathogenesis. Therefore, we examined the effects of PEP-1-p18 on oxidative stress-induced SH-SY5Y cells and in a PD mouse model. The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenyl pyridinium-induced SH-SY5Y cell death by inhibiting Bax expression levels and DNA fragmentation. Additionally, PEP-1-p18 prevented dopaminergic neuronal cell death in the substantia nigra of a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PD mouse model. These results indicate that PEP-1-p18 may be a useful therapeutic agent against various diseases and is a potential tool for treating PD.

Cytosolic prion protein induces apoptosis in human neuronal cell SH-SY5Y via mitochondrial disruption pathway

  • Wang, Xin;Dong, Chen-Fang;Shi, Qi;Shi, Song;Wang, Gui-Rong;Lei, Yan-Jun;Xu, Kun;An, Run;Chen, Jian-Ming;Jiang, Hui-Ying;Tian, Chan;Gao, Chen;Zhao, Yu-Jun;Han, Jun;Dong, Xiao-Ping
    • BMB Reports
    • /
    • v.42 no.7
    • /
    • pp.444-449
    • /
    • 2009
  • Different neurodegenerative disorders like prion disease, is caused by protein misfolding conformers. Reverse-transfected cytosolic prion protein (PrP) and PrP expressed in the cytosol have been shown to be neurotoxic. To investigate the possible mechanism of neurotoxicity due to accumulation of PrP in cytosol, a PrP mutant lacking the signal and GPI (CytoPrP) was introduced into the SH-SY5Y cell. MTT and trypan blue assays indicated that the viability of cells expressing CytoPrP was remarkably reduced after treatment of MG-132. Obvious apoptosis phenomena were detected in the cells accumulated with CytoPrP, including loss of mitochondrial transmembrane potential, increase of caspase-3 activity, more annexin V/PI-double positive-stained cells and reduced Bcl-2 level. Moreover, DNA fragmentation and TUNEL assays also revealed clear evidences of late apoptosis in the cells accumulated CytoPrP. These data suggest that the accumulation of CytoPrP in cytoplasm may trigger cell apoptosis, in which mitochondrial relative apoptosis pathway seems to play critical role.