8 Quinolinol Derivative

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 21 Experts worldwide ranked by ideXlab platform

Kenichi Akiba - One of the best experts on this subject based on the ideXlab platform.

  • selective transport of platinum iv from a palladium ii mixture across a liquid membrane impregnated with an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport of Pt(IV) and Pd(II) through a supported liquid membrane (SLM) has been investigated by using an alkylated Derivative of 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) and Pd(II) were highly extractable with LIX 26 from the mineral acid solutions of H 2 SO 4 , HNO 3 and HCl. Platinum(IV) was completely stripped by a weakly acidic solution, but Pd(II) entirely retained in the organic phase. In liquid membrane transport, Pt(IV) was completely transported through a LIX 26-SLM from mineral acid solutions into weakly acidic solutions. Palladium(II) was also extracted into the SLM from the HCl feed solution, while only a small portion of Pd(II) was stripped into the product solution. In the cases of H 2 SO 4 and HNO 3 feed solutions, no Pd(II) was stripped into the product solution. The recovery and separation of Pt(VI) from a Pd(II)Pt(IV) solution were accomplished through an SLM impregnated with 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a 1 M H 2 SO 4 or HNO 3 feed solution into a 0.5 M (H,Na) Cl 2 CHCOO product solution, in which Pt(IV) was transported into the product solution while Pd(II) was built up in the LIX 26-SLM.

  • carrier mediated transport of platinum iv through a supported liquid membrane impregnating an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport behavior of Pt(IV) has been studied through a supported liquid membrane (SLM) containing a long-chain 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) was extracted with LIX 26 from an HCl solution via an anion exchange reaction and stripped from the loaded organic phase by a weakly acidic solution (pH>1). Platinum(IV) was nearly quantitatively transported across an SLM impregnating 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a feed solution of 1–2 M HCl into a weakly acidic product solution. The transport rate of Pt(IV) was related to the distribution ratio on the feed side. Platinum(IV) was efficiently enriched in the product solution with high recovery.

Jianshun Fu - One of the best experts on this subject based on the ideXlab platform.

  • selective transport of platinum iv from a palladium ii mixture across a liquid membrane impregnated with an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport of Pt(IV) and Pd(II) through a supported liquid membrane (SLM) has been investigated by using an alkylated Derivative of 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) and Pd(II) were highly extractable with LIX 26 from the mineral acid solutions of H 2 SO 4 , HNO 3 and HCl. Platinum(IV) was completely stripped by a weakly acidic solution, but Pd(II) entirely retained in the organic phase. In liquid membrane transport, Pt(IV) was completely transported through a LIX 26-SLM from mineral acid solutions into weakly acidic solutions. Palladium(II) was also extracted into the SLM from the HCl feed solution, while only a small portion of Pd(II) was stripped into the product solution. In the cases of H 2 SO 4 and HNO 3 feed solutions, no Pd(II) was stripped into the product solution. The recovery and separation of Pt(VI) from a Pd(II)Pt(IV) solution were accomplished through an SLM impregnated with 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a 1 M H 2 SO 4 or HNO 3 feed solution into a 0.5 M (H,Na) Cl 2 CHCOO product solution, in which Pt(IV) was transported into the product solution while Pd(II) was built up in the LIX 26-SLM.

  • carrier mediated transport of platinum iv through a supported liquid membrane impregnating an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport behavior of Pt(IV) has been studied through a supported liquid membrane (SLM) containing a long-chain 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) was extracted with LIX 26 from an HCl solution via an anion exchange reaction and stripped from the loaded organic phase by a weakly acidic solution (pH>1). Platinum(IV) was nearly quantitatively transported across an SLM impregnating 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a feed solution of 1–2 M HCl into a weakly acidic product solution. The transport rate of Pt(IV) was related to the distribution ratio on the feed side. Platinum(IV) was efficiently enriched in the product solution with high recovery.

Shigeto Nakamura - One of the best experts on this subject based on the ideXlab platform.

  • selective transport of platinum iv from a palladium ii mixture across a liquid membrane impregnated with an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport of Pt(IV) and Pd(II) through a supported liquid membrane (SLM) has been investigated by using an alkylated Derivative of 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) and Pd(II) were highly extractable with LIX 26 from the mineral acid solutions of H 2 SO 4 , HNO 3 and HCl. Platinum(IV) was completely stripped by a weakly acidic solution, but Pd(II) entirely retained in the organic phase. In liquid membrane transport, Pt(IV) was completely transported through a LIX 26-SLM from mineral acid solutions into weakly acidic solutions. Palladium(II) was also extracted into the SLM from the HCl feed solution, while only a small portion of Pd(II) was stripped into the product solution. In the cases of H 2 SO 4 and HNO 3 feed solutions, no Pd(II) was stripped into the product solution. The recovery and separation of Pt(VI) from a Pd(II)Pt(IV) solution were accomplished through an SLM impregnated with 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a 1 M H 2 SO 4 or HNO 3 feed solution into a 0.5 M (H,Na) Cl 2 CHCOO product solution, in which Pt(IV) was transported into the product solution while Pd(II) was built up in the LIX 26-SLM.

  • carrier mediated transport of platinum iv through a supported liquid membrane impregnating an 8 Quinolinol Derivative
    Journal of Membrane Science, 1995
    Co-Authors: Jianshun Fu, Shigeto Nakamura, Kenichi Akiba
    Abstract:

    Abstract The transport behavior of Pt(IV) has been studied through a supported liquid membrane (SLM) containing a long-chain 8-Quinolinol, LIX 26, as a mobile carrier. Platinum(IV) was extracted with LIX 26 from an HCl solution via an anion exchange reaction and stripped from the loaded organic phase by a weakly acidic solution (pH>1). Platinum(IV) was nearly quantitatively transported across an SLM impregnating 15% (v/v) LIX 26 and 10% (v/v) 1-octanol in kerosene from a feed solution of 1–2 M HCl into a weakly acidic product solution. The transport rate of Pt(IV) was related to the distribution ratio on the feed side. Platinum(IV) was efficiently enriched in the product solution with high recovery.

高橋 一平 - One of the best experts on this subject based on the ideXlab platform.

  • The mechanism of a novel radioprotector, 8-Quinolinol Derivative KH-3
    2019
    Co-Authors: 高橋 一平, 森田 明典, 青木 伸, 王 冰, 細井 義夫, 兼安 祐子, 権丈 雅浩, 木村 智樹, 村上 雄二, 永田 靖
    Abstract:

    Purpose/Objective (s): Radiation therapy for cancer often has severe side effects that limit its efficacy. Because these side effects are in part determined by p53-mediated apoptosis, temporary suppression of p53 has been suggested as a therapeutic strategy to relieve the damage of normal tissues during treatment of p53-deficient tumors. On the other hand, it is known that dissociation of a zinc ion, which is coordinated to metal ion binding site of p53, could induce p53 denaturation, hence we evaluated some zinc chelators as radioprotective p53 inhibitor. As a result, we found 5-chloro-8-Quinolinol (KH-3) as a radioprotector that can protect mice from a sublethal dose of 7.5 Gy total-body irradiation (TBI). In this study, we investigated the effects and mechanism of KH-3 comparatively to a known radioprotective p53 inhibitor, PFTm. Materials /Methods: Imprinting control region (ICR) female mice, aged 8-week old, were total-body irradiated with an X-ray generator (Pantak-320S, Shimadzu) operated at 200 kV at a dose rate of 0.66 Gy/min. KH-3 (35 mg/kg) or vehicle was ip injected 30 minutes before 7.5 Gy TBI. In cell analysis, highly radiosensitive cell line MOLT-4, derived from human T-cell leukemia, was used and 10 Gy-irradiated. The suppressive effect of KH-3 and the reference compound PFTm on radiation-induced MOLT-4 apoptosis was evaluated using Annexin V-FITC or MitoTracker Red staining. To examine the specificity of KH-3 for p53-mediated apoptosis, we used MOLT-4 cells and their Derivatives, namely, p53-knockdown transformant and p53 revertant which re-expressed p53 using shRNA-resistant FLAG-tagged p53-expressing plasmid. To elucidate the mechanism of action of KH-3 in p53-mediated apoptotic pathway, we mainly investigated the expression of p53 target-genes, p21 and PUMA, using quantitative real-time PCR and immunoblotting analyses. Results: For the 30-day survival study, half of the animals in the KH-3-treated group survived, whereas all the mice receiving only TBI died within 14 days (P < 0.01). Cell death analysis revealed that KH-3 had a higher inhibitory effect on cell death and lower toxicity than that of PFTm in the MOLT-4 cells. KH-3 was ineffective against the radiation-induced apoptosis of p53-knockdown transformant, but suppressed that of p53 revertant. Results indictated that suppression of radiation-induced apoptosis by KH-3 was specifically mediated through p53 signaling pathways. Furthermore, KH-3 modulated p53 target-gene expression without affecting p53 expression. In particular, p21, which has anti-apoptotic activity, was markedly up-regulated by KH-3. Conclusion: KH-3 is a novel kind of radioprotector that modulates p53 transcription. The radioprotective effect of KH-3 may be associated with its ability to up-regulate p21 expression.American Society for Radiation Oncology (ASTRO) Annual Meetin

  • KH-3, a Transcriptional Modulator of p53, Protects Mice from Radiation-Induced Gastrointestinal Syndrome
    2019
    Co-Authors: 高橋 一平, 森田 明典, 青木 伸, 王 冰, 細井 義夫, 笹谷 めぐみ, 有安 真也, 神谷 研二, 稲葉 俊哉
    Abstract:

    Purpose/Objective(s): In a previous study, we reported that some zinc (II) chelators suppress radiation-induced p53-dependent apoptosis through inhibition of p53-dependent apoptotic pathways. As a result of further screening, we found an 8-Quinolinol Derivative KH-3 as a radioprotector that has an ability to modulate p53 transcription resulting in the up-regulation of p21, and that can protect mice from a sublethal dose of 7.5 Gy total-body irradiation (TBI), but not of a higher dose of TBI (8.0 Gy). These data indicate that KH-3 is effective only in a narrow range of radiation dose that causes sublethal hematopoietic syndrome in mouse TBI. In this study, we further investigated the effects and mechanism of KH-3, including RNA interference-mediated silencing analysis of p21. In addition, p53 and p21 have been reported as resistant factors in radiation-induced gastrointestinal (GI) syndrome in mice. The fact raises the possibility that KH-3 protects mice from GI syndrome by up-regulating p21. We then tested the possibility using the technique of abdominal subtotal-body irradiation (SBI) to avoid the hematopoietic syndrome.\n Materials /Methods: In cell analysis, highly radiosensitive cell line MOLT-4, derived from human T-cell leukemia, was used and 10 Gy-irradiated. The suppressive effect of KH-3 and the reference compound PFTm on radiation-induced MOLT-4 apoptosis was evaluated using Annexin V-FITC or MitoTracker Red staining, and WST-8 colorimetric assay. To examine the specificity of KH-3 for p21 in the p53-mediated apoptosis, we used MOLT-4 cells and its p21-knockdown transformant. In mouse SBI model, ICR female mice, aged 8-week old, were irradiated with a gamma-ray generator with shielding lead walls at least 3.0 cm thick. KH-3 (60 mg/kg) or vehicle was ip injected 30 minutes before 18 or 24 Gy SBI, and the mice were anesthetized 5-10 minutes before SBI. The abdomen of the anesthetized mice was exposed to gamma rays at a dose rate of 0.70 Gy/min.\n Results: RNA interference-mediated silencing of p21 revealed that KH-3 was ineffective against the radiation-induced apoptosis of p21-knockdown transformant, indictating that suppression of radiation-induced apoptosis by KH-3 was specifically mediated through p53-p21 signaling pathways. For the 30-day survival study, survival rates of mice in KH-3-treated groups were 90% (18 Gy-SBI) and 40% (24-Gy SBI) respectively, whereas those of the control vehicle-injected groups were 40% (18 Gy-SBI) and 0% (24-Gy SBI) respectively. The dose-reduction factor (DRF) of KH-3 in the SBI was about 1.3. Conclusion: KH-3 is a novel kind of radioprotector that upregulates p53-p21 pathway and protects mice from GI death. KH-3 may serve as a therapeutic radioprotector for protecting normal tissues against adverse side effects of radiation/chemotherapy in abdominal cancer.ASTRO\u27s 56th Annual Meeting(第56回米国放射線治療学会議

  • KH-3, a Transcriptional Modulator of p53, Protects Mice from Radiation-Induced Gastrointestinal Syndrome
    'Elsevier BV', 2014
    Co-Authors: 高橋 一平, 森田 明典, 青木 伸, 王 冰, 細井 義夫, 笹谷 めぐみ, 有安 真也, 神谷 研二, 稲葉 俊哉
    Abstract:

    Purpose/Objective(s): In a previous study, we reported that some zinc (II) chelators suppress radiation-induced p53-dependent apoptosis through inhibition of p53-dependent apoptotic pathways. As a result of further screening, we found an 8-Quinolinol Derivative KH-3 as a radioprotector that has an ability to modulate p53 transcription resulting in the up-regulation of p21, and that can protect mice from a sublethal dose of 7.5 Gy total-body irradiation (TBI), but not of a higher dose of TBI (8.0 Gy). These data indicate that KH-3 is effective only in a narrow range of radiation dose that causes sublethal hematopoietic syndrome in mouse TBI. In this study, we further investigated the effects and mechanism of KH-3, including RNA interference-mediated silencing analysis of p21. In addition, p53 and p21 have been reported as resistant factors in radiation-induced gastrointestinal (GI) syndrome in mice. The fact raises the possibility that KH-3 protects mice from GI syndrome by up-regulating p21. We then tested the possibility using the technique of abdominal subtotal-body irradiation (SBI) to avoid the hematopoietic syndrome.\n Materials /Methods: In cell analysis, highly radiosensitive cell line MOLT-4, derived from human T-cell leukemia, was used and 10 Gy-irradiated. The suppressive effect of KH-3 and the reference compound PFTm on radiation-induced MOLT-4 apoptosis was evaluated using Annexin V-FITC or MitoTracker Red staining, and WST-8 colorimetric assay. To examine the specificity of KH-3 for p21 in the p53-mediated apoptosis, we used MOLT-4 cells and its p21-knockdown transformant. In mouse SBI model, ICR female mice, aged 8-week old, were irradiated with a gamma-ray generator with shielding lead walls at least 3.0 cm thick. KH-3 (60 mg/kg) or vehicle was ip injected 30 minutes before 18 or 24 Gy SBI, and the mice were anesthetized 5-10 minutes before SBI. The abdomen of the anesthetized mice was exposed to gamma rays at a dose rate of 0.70 Gy/min.\n Results: RNA interference-mediated silencing of p21 revealed that KH-3 was ineffective against the radiation-induced apoptosis of p21-knockdown transformant, indictating that suppression of radiation-induced apoptosis by KH-3 was specifically mediated through p53-p21 signaling pathways. For the 30-day survival study, survival rates of mice in KH-3-treated groups were 90% (18 Gy-SBI) and 40% (24-Gy SBI) respectively, whereas those of the control vehicle-injected groups were 40% (18 Gy-SBI) and 0% (24-Gy SBI) respectively. The dose-reduction factor (DRF) of KH-3 in the SBI was about 1.3. Conclusion: KH-3 is a novel kind of radioprotector that upregulates p53-p21 pathway and protects mice from GI death. KH-3 may serve as a therapeutic radioprotector for protecting normal tissues against adverse side effects of radiation/chemotherapy in abdominal cancer

稲葉 俊哉 - One of the best experts on this subject based on the ideXlab platform.

  • KH-3, a Transcriptional Modulator of p53, Protects Mice from Radiation-Induced Gastrointestinal Syndrome
    2019
    Co-Authors: 高橋 一平, 森田 明典, 青木 伸, 王 冰, 細井 義夫, 笹谷 めぐみ, 有安 真也, 神谷 研二, 稲葉 俊哉
    Abstract:

    Purpose/Objective(s): In a previous study, we reported that some zinc (II) chelators suppress radiation-induced p53-dependent apoptosis through inhibition of p53-dependent apoptotic pathways. As a result of further screening, we found an 8-Quinolinol Derivative KH-3 as a radioprotector that has an ability to modulate p53 transcription resulting in the up-regulation of p21, and that can protect mice from a sublethal dose of 7.5 Gy total-body irradiation (TBI), but not of a higher dose of TBI (8.0 Gy). These data indicate that KH-3 is effective only in a narrow range of radiation dose that causes sublethal hematopoietic syndrome in mouse TBI. In this study, we further investigated the effects and mechanism of KH-3, including RNA interference-mediated silencing analysis of p21. In addition, p53 and p21 have been reported as resistant factors in radiation-induced gastrointestinal (GI) syndrome in mice. The fact raises the possibility that KH-3 protects mice from GI syndrome by up-regulating p21. We then tested the possibility using the technique of abdominal subtotal-body irradiation (SBI) to avoid the hematopoietic syndrome.\n Materials /Methods: In cell analysis, highly radiosensitive cell line MOLT-4, derived from human T-cell leukemia, was used and 10 Gy-irradiated. The suppressive effect of KH-3 and the reference compound PFTm on radiation-induced MOLT-4 apoptosis was evaluated using Annexin V-FITC or MitoTracker Red staining, and WST-8 colorimetric assay. To examine the specificity of KH-3 for p21 in the p53-mediated apoptosis, we used MOLT-4 cells and its p21-knockdown transformant. In mouse SBI model, ICR female mice, aged 8-week old, were irradiated with a gamma-ray generator with shielding lead walls at least 3.0 cm thick. KH-3 (60 mg/kg) or vehicle was ip injected 30 minutes before 18 or 24 Gy SBI, and the mice were anesthetized 5-10 minutes before SBI. The abdomen of the anesthetized mice was exposed to gamma rays at a dose rate of 0.70 Gy/min.\n Results: RNA interference-mediated silencing of p21 revealed that KH-3 was ineffective against the radiation-induced apoptosis of p21-knockdown transformant, indictating that suppression of radiation-induced apoptosis by KH-3 was specifically mediated through p53-p21 signaling pathways. For the 30-day survival study, survival rates of mice in KH-3-treated groups were 90% (18 Gy-SBI) and 40% (24-Gy SBI) respectively, whereas those of the control vehicle-injected groups were 40% (18 Gy-SBI) and 0% (24-Gy SBI) respectively. The dose-reduction factor (DRF) of KH-3 in the SBI was about 1.3. Conclusion: KH-3 is a novel kind of radioprotector that upregulates p53-p21 pathway and protects mice from GI death. KH-3 may serve as a therapeutic radioprotector for protecting normal tissues against adverse side effects of radiation/chemotherapy in abdominal cancer.ASTRO\u27s 56th Annual Meeting(第56回米国放射線治療学会議

  • KH-3, a Transcriptional Modulator of p53, Protects Mice from Radiation-Induced Gastrointestinal Syndrome
    'Elsevier BV', 2014
    Co-Authors: 高橋 一平, 森田 明典, 青木 伸, 王 冰, 細井 義夫, 笹谷 めぐみ, 有安 真也, 神谷 研二, 稲葉 俊哉
    Abstract:

    Purpose/Objective(s): In a previous study, we reported that some zinc (II) chelators suppress radiation-induced p53-dependent apoptosis through inhibition of p53-dependent apoptotic pathways. As a result of further screening, we found an 8-Quinolinol Derivative KH-3 as a radioprotector that has an ability to modulate p53 transcription resulting in the up-regulation of p21, and that can protect mice from a sublethal dose of 7.5 Gy total-body irradiation (TBI), but not of a higher dose of TBI (8.0 Gy). These data indicate that KH-3 is effective only in a narrow range of radiation dose that causes sublethal hematopoietic syndrome in mouse TBI. In this study, we further investigated the effects and mechanism of KH-3, including RNA interference-mediated silencing analysis of p21. In addition, p53 and p21 have been reported as resistant factors in radiation-induced gastrointestinal (GI) syndrome in mice. The fact raises the possibility that KH-3 protects mice from GI syndrome by up-regulating p21. We then tested the possibility using the technique of abdominal subtotal-body irradiation (SBI) to avoid the hematopoietic syndrome.\n Materials /Methods: In cell analysis, highly radiosensitive cell line MOLT-4, derived from human T-cell leukemia, was used and 10 Gy-irradiated. The suppressive effect of KH-3 and the reference compound PFTm on radiation-induced MOLT-4 apoptosis was evaluated using Annexin V-FITC or MitoTracker Red staining, and WST-8 colorimetric assay. To examine the specificity of KH-3 for p21 in the p53-mediated apoptosis, we used MOLT-4 cells and its p21-knockdown transformant. In mouse SBI model, ICR female mice, aged 8-week old, were irradiated with a gamma-ray generator with shielding lead walls at least 3.0 cm thick. KH-3 (60 mg/kg) or vehicle was ip injected 30 minutes before 18 or 24 Gy SBI, and the mice were anesthetized 5-10 minutes before SBI. The abdomen of the anesthetized mice was exposed to gamma rays at a dose rate of 0.70 Gy/min.\n Results: RNA interference-mediated silencing of p21 revealed that KH-3 was ineffective against the radiation-induced apoptosis of p21-knockdown transformant, indictating that suppression of radiation-induced apoptosis by KH-3 was specifically mediated through p53-p21 signaling pathways. For the 30-day survival study, survival rates of mice in KH-3-treated groups were 90% (18 Gy-SBI) and 40% (24-Gy SBI) respectively, whereas those of the control vehicle-injected groups were 40% (18 Gy-SBI) and 0% (24-Gy SBI) respectively. The dose-reduction factor (DRF) of KH-3 in the SBI was about 1.3. Conclusion: KH-3 is a novel kind of radioprotector that upregulates p53-p21 pathway and protects mice from GI death. KH-3 may serve as a therapeutic radioprotector for protecting normal tissues against adverse side effects of radiation/chemotherapy in abdominal cancer