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Hypoallergenic and Physicochemical Properties of the A2 β-Casein Fraction of Goat Milk
Tae-Hwan Jung,Hyo-Jeong Hwang,Sung-Seob Yun,Won-Jae Lee,Jin-Wook Kim,Ji-Yun Ahn,Woo-Min Jeon,Kyoung-Sik Han2.6* 한국축산식품학회 2017 한국축산식품학회지 Vol.37 No.6
Goat milk has a protein composition similar to that of breast milk and contains abundant nutrients, but its use in functional foods is rather limited in comparison to milk from other sources. The aim of this study was to prepare a goat A2 β-casein fraction with improved digestibility and hypoallergenic properties. We investigated the optimal conditions for the separation of A2 β-casein fraction from goat milk by pH adjustment to pH 4.4 and treating the casein suspension with calcium chloride (0.05 M for 1 h at 25°C). Selective reduction of β- lactoglobulin and αs-casein was confirmed using sodium dodecyl sulphate-polyacrylamide gel electrophoresis and reverse-phase high-performance liquid chromatography. The hypoallergenic property of A2 β-casein fraction was examined by measuring the release of histamine and tumor necrosis factor alpha from HMC-1 human mast cells exposed to different proteins, including A2 β-casein fraction. There was no significant difference in levels of both indicators between A2 β-casein treatment and the control (no protein treatment). The A2 β-casein fraction is abundant in essential amino acids, especially, branched-chain amino acids (leucine, valine, and isoleucine). The physicochemical properties of A2 β-casein fraction, including protein solubility and viscosity, are similar to those of bovine whole casein which is widely used as a protein source in various foods. Therefore, the goat A2 β-casein fraction may be useful as a food material with good digestibility and hypoallergenic properties for infants, the elderly, and people with metabolic disorders.
Park, Jong Il,Han, sang seop,Jeong, Tae Cheon,Roh, Jung Koo,Kim, Hyoung Chin,Kim, Jeong Hwan,Jeon, Yeong Joong,Kim, Dal Hyun,Kim,Je Hak,Park, Kwan Ha 한국응용약물학회 1997 Biomolecules & Therapeutics(구 응용약물학회지) Vol.5 No.1
The antigenic potential of CFA-001, cefazolin, a cephalosporin derivative produced by an enzymatic semisynthesis, was determined in Hartley guinea pigs. A battery of tests employed consisted of active systemic anaphylaxis (ASA), passive cutaneous anaphylaxis (PCA), and indirect hemagglutination test (IHA). The results were as follows: 1) In ASA, no signs attributable to anaphylaxis was observed in guinea pigs sensitized with CFA-001, whereas OVA-sensitized animals induced severe anaphylactic symptoms; 2) guinea pigs did not produce antibodies against CFA-001 when sensitized with or without Freund's complete adjuvant (FCA) in homologous PCA tests. Meanwhile, antibodies against ovalbumin (OVA) were clearly detected; 3) No CFA-001-specific hemagglutination was observed in the IHA using sera obtained from CFA-001-sensitized guinea pigs. These results suggest that CFA-001 has no antigenicity potential in guinea pigs.
Induction of apoptosis in arsenic trioxide-treated lung cancer A549 cells by buthionine sulfoximine.
Han, Yong Hwan,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun Korean Society for Molecular Biology 2008 Molecules and cells Vol.26 No.2
<P>Arsenic trioxide (ATO) affects many biological processes such as cell proliferation, apoptosis, differentiation and angiogenesis. L-buthionine sulfoximine (BSO) is an inhibitor of GSH synthesis. We tested whether ATO reduced the viability of lung cancer A549 cells in vitro, and investigated the in vitro effect of the combination of ATO and BSO on cell viability in relation to apoptosis and the cell cycle. ATO caused a dose-dependant decrease of viability of A549 cells with an IC50 of more than 50 microM. Low doses of ATO or BSO (1 approximately 10 microM) alone did not induce cell death. However, combined treatment depleted GSH content and induced apoptosis, loss of mitochondrial transmembrane potential (DeltaPsi(m)) and cell cycle arrest in G2. Reactive oxygen species (ROS) increased or decreased depending on the concentration of ATO. In addition, BSO generally increased ROS in ATO-treated A549 cells. ROS levels were at least in part related to apoptosis in cells treated with ATO and/or BSO. In conclusion, we have demonstrated that A549 lung cells are very resistant to ATO, and that BSO synergizes with clinically achievable concentration of ATO. Our results suggest that combination treatment with ATO and BSO may be useful for treating lung cancer.</P>
Preparation of Recycled Polyvinyl Alcohol) (PVA)/Iodine Polarizing Film
Han, Man Ho,Shin, Jae Kyun,Oh, Kyeong Il,Lee, Young Jae,Song, Du Hyun,Chung, Yong Sik,Lee, Yong Rok,Choi, Han Gon,Oh, Tae Hwan,Han, Sung Soo,Noh, Seok Kyun,Lyoo, Won Seok SAGE Publications 2010 POLYMERS AND POLYMER COMPOSITES Vol.18 No.7
Suppression of arsenic trioxide-induced apoptosis in HeLa cells by N-acetylcysteine.
Han, Yong Hwan,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun Korean Society for Molecular Biology 2008 Molecules and cells Vol.26 No.1
<P>Arsenic trioxide (ATO) can affect many biological functions such as apoptosis and differentiation in various cells. We investigated the involvement of ROS and GSH in ATO-induced HeLa cell death using ROS scavengers, especially N-acetylcysteine (NAC). ATO increased intracellular O(2)(*-) levels and reduced intracellular GSH content. The ROS scavengers, Tempol, Tiron and Trimetazidine, did not significantly reduce levels of ROS or GSH depletion in ATO-treated HeLa cells. Nor did they reduce the apoptosis induced by ATO. In contrast, treatment with NAC reduced ROS levels and GSH depletion in the ATO-treated HeLa cells and prevented ATO-induced apoptosis. Treatment with exogenous SOD and catalase reduced the depletion of GSH content in ATO-treated cells. Catalase strongly protected the cells from ATO-induced apoptosis. In addition, treatment with SOD, catalase and NAC slightly inhibited the G1 phase accumulation induced by ATO. In conclusion, NAC protects HeLa cells from apoptosis induced by ATO by up-regulating intracellular GSH content and partially reducing the production of O(2)(*-).</P>
Han, Yong Hwan,Moon, Hwa Jin,You, Bo Ra,Yang, Yeon Mi,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun Potamitis Press 2010 Anticancer research Vol.30 No.3
<P>MG132, a proteasome inhibitor, has been shown to induce apoptotic cell death through formation of reactive oxygen species (ROS). Here, we evaluated the effects of MG132 on the growth of endothelial cells, especially calf pulmonary artery endothelial cells (CPAECs). MG132 dose-dependently inhibited the growth of CPAECSs and human umbilical vein endothelial cells (HUVECs) at 24 hours. MG132 also induced apoptosis in both cell lines, which was accompanied by the loss of mitochondrial membrane potential. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 and -9 inhibitor) significantly rescued CPAECs from MG132-induced cell death. MG132 increased ROS level and GSH depleted cell numbers of CPAECs. None of the caspase inhibitors reduced ROS level in MG132-treated CPAECs but did reduce apoptosis in these cells. In conclusion, MG132 inhibited the growth of endothelial cells, especially CPAECs via caspase-dependent apoptosis. MG132-induced CPAEC death was related to GSH depletion rather than a change in ROS level.</P>