• Title/Summary/Keyword: Vitamin E-succinate

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Induction of Apoptosis by Vitamin E Succinate in Human Erythroleukemia K562 Cells (인간 만성백혈병 세포주에서의 Vitamin E Succinate에 의한 세포사멸 유도)

  • Jang, Chang-Deug;Kim, Jong-Myoung;An, Won-Geun;Park, Hye-Ryoun
    • Journal of Life Science
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    • v.17 no.7 s.87
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    • pp.896-904
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    • 2007
  • Regulation mechanism of apoptosis has been known to be important for understanding the pathogenesis of a number of human diseases including cancers. The effects of $RRR-{\alpha}-tocopheryl$ succinate(vitamin E succinate, VES) on the cell viability, generation of ROS, expression of proteins involved in apoptosis, and growth of human chronic myelogenous leukemia K562 cells were analyzed in this study. VES treatment not only induced the generation of the ROS but also increased the levels of $NF-{\kappa}B$, COX-2, and $p21^{WAF1/CIP1}$ in K562 cells. It modulates the levels of pro-apoptotic proteins such as Bax provoking the apoptosis in K562 cells. The cleavage of PARP into 89 kDa was also increased upon VES treatment in a dosage-dependent manner. Induction of an apoptosis was evident by the increase of sub-Gl peak and cell shrinkage condensed chromatin in K562 cells treated with VES. It also resulted in an inhibition of tumor growth by 50% and prolonged survival of the Iymphoma-induced mice. This potentiation of VES obtained in vitro and in vivo may indicate the feasibility of more effective chemotherapy in chronic myelogenous leukemia.

Activation of PKC-$\beta$II-is Required for Vitamin E-Succinate-Induced Apoptosis of U937 Cells

  • Kim, Song-Ja;Park, Jae-Han;Lee, Sun-Ryung;Bang, Ok-Sun;Kang, Shin-Sung
    • Animal cells and systems
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    • v.4 no.3
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    • pp.279-285
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    • 2000
  • Vitamin E-succinate (VES) treatment of U937 human monoblasts induced cells to undergo apoptosis. After 96 h of VES treatment at 10 $\mu$/ml, more than 80% of cells appeared apoptotic. Evidence for apoptosis by VES was based on propidium iodide staining for detection of chromatin condensational fragmentation and electrophoretic DNA ladder formation. Western blot analyses showed a transient increase in Fas and p21 protein levels up to 48 h alter the VES treatment. Protein expression and activity of CDK1 and lamin B degradation were remarkably induced by VES, following the cleavage of caspase-3 after 48 h. The VES-induced apoptosis was found to involve activation of PKC as shown by increases in membrane translocation of PKC$\beat$II and PKC activity. Pretreatment of GF109203X (PKC inhibitor) prior to VES treatment almost completely inhibited the induction of apoptosis as assessed by blockage of VES-induced caspase-3 activity and DNA fragmentation. However, GF109203X h8d no effect on the VES-induced nitric oxide synthesis, which was required for monocvtic differentiation in our previous report (J Cell Sci 111, 435, 1998). Taken together, our data suggest that induction of apoptosis by VES in U937 cells occurs through activation of PKC-$\beat$II resulting in the activation of caspase-3 cascade and is independent of nitric oxide.

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Toxic Activities of the Oxidant Chromate in Culture Cells (산화성 크롬의 배양세포에서의 독성작용)

  • 박형숙
    • Environmental Analysis Health and Toxicology
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    • v.13 no.1_2
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    • pp.1-9
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    • 1998
  • The ROS-producing potency of chromium compounds of several oxidation states were determined in the H4 cells. $K_2Cr_2O_7$ as Cr (VI), synthetic Cr (V) compounds and Cr (III) as TPP produced high level of ROS. However, ROS values of Cr-picolinate as Cr (III), CrCl$_2$, CrCI$_2$, were almost equal to the control. The effects of physiological antioxidants compounds which react with free radicals were examined for their effects on chromate-induced production of reactive oxygen species (ROS) in A549 cells after the addition of $K_2Cr_2O_7$. The compounds used were vitamin C (ascorbate), vitamin E ($\alpha$-tocopherol), superoxide dismutase (SOD) and catalase. The preincubation of ascorbate (200uM) with A549 cells for 20hr resulted in a significant reduction of hexavalent chromate(100uM) induced ROS. However, there is no effects of preincubation of the cells with vitamin E succinate (10 and 20uM, 20hr) on the ROS production. Also, the effects of Cr (VI) on the cell cycle of A549 cells was measured by adding the DNA intercalating agent, propidium iodide. S phase of the cell cycle was increased by the chromium (VI) compounds up to 20uM indicating toxicity or possible mitogenic action of the cell. The shoulder in Go/G1 phase at 20uM Cr (VI) with 24 hr treatment indicates apoptosis.

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Comparison of the fecal microbiota with high- and low performance race horses

  • Taemook Park;Jungho Yoon;YoungMin Yun;Tatsuya Unno
    • Journal of Animal Science and Technology
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    • v.66 no.2
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    • pp.425-437
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    • 2024
  • Exercise plays an important role in regulating energy homeostasis, which affects the diversity of the intestinal microbial community in humans and animals. To the best of the authors' knowledge, few studies have reported the associations between horse gut microbiota along with their predicted metabolic activities and the athletic ability of Jeju horses and Thoroughbreds living in Korea. This study was conducted to investigate the association between the gut microbiota and athletic performance in horses. This study sequenced the V3 and V4 hypervariable regions of the partial 16S rRNA genes obtained from racehorse fecal samples and compared the fecal microbiota between high- and low-performance Jeju horses and Thoroughbreds. Forty-nine fecal samples were divided into four groups: high-performance Jeju horses (HJ, n = 13), low-performance Jeju horses (LJ, n = 17), high-performance Thoroughbreds (HT, n = 9), and low-performance Thoroughbreds (LT, n = 10). The high-performance horse groups had a higher diversity of the bacterial community than the low-performance horse groups. Two common functional metabolic activities of the hindgut microbiota (i.e., tryptophan and succinate syntheses) were observed between the low-performance horse groups, indicating dysbiosis of gut microbiota and fatigue from exercise. On the other hand, high-performance horse groups showed enriched production of polyamines, butyrate, and vitamin K. The racing performance may be associated with the composition of the intestinal microbiota of Jeju horses and Thoroughbreds in Korea.

Evans' Syndrome Induced by Rabies Vaccination in a Dog

  • Yeji Kim;Jihyun Kim;Yunji Song;Songju Oh;Ha-Jung Kim
    • Journal of Veterinary Clinics
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    • v.40 no.4
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    • pp.288-293
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    • 2023
  • A 11-year-old neutered male Maltese dog was vaccinated with a rabies vaccine (Rabisin®, Boehringer Ingelheim International GmbH, Germany) subcutaneously at a local animal hospital. One hour after vaccination, purpura with edema was observed at the injection site and severe thrombocytopenia (0 K/μL) was noted on a complete blood count (CBC). No specific findings were found in serum chemistry, electrolyte, blood gas analysis, and coagulation tests. The patient was hospitalized and administered antihemorrhagic agents (vitamin K, desmopressin), antihistamines (chlorpheniramine) and corticosteroids (methylprednisolone sodium succinate). On a repeat CBC, mild anemia had developed, thrombocytopenia was still noted, and autoagglutination was observed on a saline agglutination test (SAT). A polymerase chain reaction panel for infectious agents (e.g., Babesia spp.) was negative. The diagnosis was secondary immune-mediated thrombocytopenia (IMT) with immune-mediated hemolytic anemia (IMHA) associated with vaccination. Therefore, the immunosuppressants (prednisolone, and mycophenolate mofetil) were administered. Six days after drug administration, new lesion was not observed, and the previous lesions were significantly improved. It gradually improved and 4 weeks after hematocrit and platelet recovered to normal levels. It was maintained for 6 months without recurrence of related symptoms. Based on patient's history and test results, the patient was diagnosed with Evans' syndrome associated with rabies vaccine.