Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux
Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kimura, Akihiko [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2016transfer abstract |
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| Schlagwörter: |
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| Umfang: |
10 |
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| Übergeordnetes Werk: |
Enthalten in: Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery - 2013, an international journal concerned with the effects of chemicals on living systems and immunotoxicology, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:339 ; year:2016 ; day:2 ; month:01 ; pages:9-18 ; extent:10 |
| Links: |
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| DOI / URN: |
10.1016/j.tox.2015.11.005 |
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ELV035264268 |
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| 245 | 1 | 0 | |a Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux |
| 264 | 1 | |c 2016transfer abstract | |
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| 520 | |a Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. | ||
| 520 | |a Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. | ||
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| 700 | 1 | |a Takayasu, Tatsunori |4 oth | |
| 700 | 1 | |a Kondo, Toshikazu |4 oth | |
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10.1016/j.tox.2015.11.005 doi GBV00000000000440.pica (DE-627)ELV035264268 (ELSEVIER)S0300-483X(15)30055-X DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Kimura, Akihiko verfasserin aut Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux 2016transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. NGAL Elsevier Ab Elsevier MRP1 Elsevier PAS Elsevier HO-1 Elsevier MT1 Elsevier p62 Elsevier IL-6 Elsevier NaAsO<ce:inf loc="post">2</ce:inf> Elsevier SOCS3 Elsevier GCL Elsevier CRE Elsevier BUN Elsevier LC3 Elsevier Ishida, Yuko oth Nosaka, Mizuho oth Kuninaka, Yumi oth Hama, Mizuki oth Kawaguchi, Takashi oth Sakamoto, Shoichi oth Shinozaki, Kohei oth Iwahashi, Yumi oth Takayasu, Tatsunori oth Kondo, Toshikazu oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:339 year:2016 day:2 month:01 pages:9-18 extent:10 https://doi.org/10.1016/j.tox.2015.11.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 339 2016 2 0102 9-18 10 |
| spelling |
10.1016/j.tox.2015.11.005 doi GBV00000000000440.pica (DE-627)ELV035264268 (ELSEVIER)S0300-483X(15)30055-X DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Kimura, Akihiko verfasserin aut Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux 2016transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. NGAL Elsevier Ab Elsevier MRP1 Elsevier PAS Elsevier HO-1 Elsevier MT1 Elsevier p62 Elsevier IL-6 Elsevier NaAsO<ce:inf loc="post">2</ce:inf> Elsevier SOCS3 Elsevier GCL Elsevier CRE Elsevier BUN Elsevier LC3 Elsevier Ishida, Yuko oth Nosaka, Mizuho oth Kuninaka, Yumi oth Hama, Mizuki oth Kawaguchi, Takashi oth Sakamoto, Shoichi oth Shinozaki, Kohei oth Iwahashi, Yumi oth Takayasu, Tatsunori oth Kondo, Toshikazu oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:339 year:2016 day:2 month:01 pages:9-18 extent:10 https://doi.org/10.1016/j.tox.2015.11.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 339 2016 2 0102 9-18 10 |
| allfields_unstemmed |
10.1016/j.tox.2015.11.005 doi GBV00000000000440.pica (DE-627)ELV035264268 (ELSEVIER)S0300-483X(15)30055-X DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Kimura, Akihiko verfasserin aut Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux 2016transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. NGAL Elsevier Ab Elsevier MRP1 Elsevier PAS Elsevier HO-1 Elsevier MT1 Elsevier p62 Elsevier IL-6 Elsevier NaAsO<ce:inf loc="post">2</ce:inf> Elsevier SOCS3 Elsevier GCL Elsevier CRE Elsevier BUN Elsevier LC3 Elsevier Ishida, Yuko oth Nosaka, Mizuho oth Kuninaka, Yumi oth Hama, Mizuki oth Kawaguchi, Takashi oth Sakamoto, Shoichi oth Shinozaki, Kohei oth Iwahashi, Yumi oth Takayasu, Tatsunori oth Kondo, Toshikazu oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:339 year:2016 day:2 month:01 pages:9-18 extent:10 https://doi.org/10.1016/j.tox.2015.11.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 339 2016 2 0102 9-18 10 |
| allfieldsGer |
10.1016/j.tox.2015.11.005 doi GBV00000000000440.pica (DE-627)ELV035264268 (ELSEVIER)S0300-483X(15)30055-X DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Kimura, Akihiko verfasserin aut Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux 2016transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. NGAL Elsevier Ab Elsevier MRP1 Elsevier PAS Elsevier HO-1 Elsevier MT1 Elsevier p62 Elsevier IL-6 Elsevier NaAsO<ce:inf loc="post">2</ce:inf> Elsevier SOCS3 Elsevier GCL Elsevier CRE Elsevier BUN Elsevier LC3 Elsevier Ishida, Yuko oth Nosaka, Mizuho oth Kuninaka, Yumi oth Hama, Mizuki oth Kawaguchi, Takashi oth Sakamoto, Shoichi oth Shinozaki, Kohei oth Iwahashi, Yumi oth Takayasu, Tatsunori oth Kondo, Toshikazu oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:339 year:2016 day:2 month:01 pages:9-18 extent:10 https://doi.org/10.1016/j.tox.2015.11.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 339 2016 2 0102 9-18 10 |
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10.1016/j.tox.2015.11.005 doi GBV00000000000440.pica (DE-627)ELV035264268 (ELSEVIER)S0300-483X(15)30055-X DE-627 ger DE-627 rakwb eng 610 VZ 530 VZ 52.56 bkl Kimura, Akihiko verfasserin aut Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux 2016transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. NGAL Elsevier Ab Elsevier MRP1 Elsevier PAS Elsevier HO-1 Elsevier MT1 Elsevier p62 Elsevier IL-6 Elsevier NaAsO<ce:inf loc="post">2</ce:inf> Elsevier SOCS3 Elsevier GCL Elsevier CRE Elsevier BUN Elsevier LC3 Elsevier Ishida, Yuko oth Nosaka, Mizuho oth Kuninaka, Yumi oth Hama, Mizuki oth Kawaguchi, Takashi oth Sakamoto, Shoichi oth Shinozaki, Kohei oth Iwahashi, Yumi oth Takayasu, Tatsunori oth Kondo, Toshikazu oth Enthalten in Elsevier Science Too late or too little? Potential for Alzheimer's disease passive immunotherapy via targeted intracerebroventricular delivery 2013 an international journal concerned with the effects of chemicals on living systems and immunotoxicology Amsterdam [u.a.] (DE-627)ELV011413085 volume:339 year:2016 day:2 month:01 pages:9-18 extent:10 https://doi.org/10.1016/j.tox.2015.11.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_22 GBV_ILN_40 GBV_ILN_105 52.56 Regenerative Energieformen alternative Energieformen VZ AR 339 2016 2 0102 9-18 10 |
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exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux |
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Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux |
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Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. |
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Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. |
| abstract_unstemmed |
Gender is one of the essential factors in the development of various diseases and poisoning. Therefore, we herein examined gender differences in sodium arsenite (NaAsO2)-induced acute renal dysfunction. When male and female BALB/c mice were subcutaneously injected with NaAsO2 (12.5mg/kg), serum and urinary markers for proximal tubular injury were significantly higher in female mice than in male ones. NaAsO2-induced histopathological alterations were consistently more evident in females than in males. Ovariectomy, but not orchiectomy significantly attenuated NaAsO2-induced renal injury. These results imply that the hypersusceptibility of female mice is attributed to estrogen signals. NaAsO2 suppressed the autophagic flux in tubular cells through the activation of ERK. Enhancements in the activation of ERK were significantly greater in females than in males, with the eventual accumulation of LC3-II and P62 in the kidneys, implying that the autophagic flux is impaired in females. The IL-6/STAT3 signaling pathway had protective roles in NaAsO2-induced nephrotoxicity through the suppression of ERK activation. Despite the absence of differences in intrarenal IL-6 expression between male and female mice, STAT3 was less activated with enhanced SOCS3 expression in females than in males. An in vitro study using mProx24 cells revealed that the estrogen treatment induced SOCS3 expression, and eventually suppressed the autophagic flux, as evidenced by greater increases in the accumulation of LC3-II and p62 with ERK activation, which was canceled by the knockdown of Socs3. Collectively, these results indicate that estrogen has a negative impact on the development of NaAsO2 nephrotoxicity through its suppression of the autophagic flux. |
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| title_short |
Exaggerated arsenic nephrotoxicity in female mice through estrogen-dependent impairments in the autophagic flux |
| url |
https://doi.org/10.1016/j.tox.2015.11.005 |
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| author2 |
Ishida, Yuko Nosaka, Mizuho Kuninaka, Yumi Hama, Mizuki Kawaguchi, Takashi Sakamoto, Shoichi Shinozaki, Kohei Iwahashi, Yumi Takayasu, Tatsunori Kondo, Toshikazu |
| author2Str |
Ishida, Yuko Nosaka, Mizuho Kuninaka, Yumi Hama, Mizuki Kawaguchi, Takashi Sakamoto, Shoichi Shinozaki, Kohei Iwahashi, Yumi Takayasu, Tatsunori Kondo, Toshikazu |
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| doi_str |
10.1016/j.tox.2015.11.005 |
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2024-07-06T17:07:16.169Z |
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