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2-Butoxyethanol

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James E. Klaunig – 1st expert on this subject based on the ideXlab platform

  • Kupffer cells participate in 2-Butoxyethanol-induced liver hemangiosarcomas
    Toxicology, 2010
    Co-Authors: Lisa M. Kamendulis, Stacy M Corthals, James E. Klaunig

    Abstract:

    Abstract 2-Butoxyethanol increases hemangiosarcomas selectively in male mouse liver after chronic inhalation through mechanisms that have not fully been elucidated. Hemolysis, a primary toxic effect associated with 2-Butoxyethanol exposure in rodents, increased hemosiderin (iron) deposition in Kupffer cells in the liver. These findings, along with the induction of hepatic neoplastic lesions, led to our hypothesis that the induction hemangiosarcomas by 2-Butoxyethanol is due to the activation of Kupffer cells, subsequent to hemolysis, that results in the induction of DNA synthesis in target cells (endothelial cells); allowing for the selective proliferation of preneoplastic target cells and/or the promotion of new initiated cells. The present studies were conducted to determine whether Kupffer cells contributed to 2-Butoxyethanol-induced endothelial DNA synthesis in the liver, thereby determining whether a linkage exists between these events. Male B6C3F1 mice were treated with 450 and 900 mg/kg 2-Butoxyethanol (via daily gavage; 5×/week) for 7 days in the presence or absence of Kupffer cell depletion (via clodronate-encapsulated liposomes). 2-Butoxyethanol (450 and 900 mg/kg/day) increased the number of F4/80 stained cells (Kupffer cells) compared to controls (∼1.3- and ∼1.6-fold over control, respectively). Clodronate liposome treatment reduced the number of Kupffer cells by >90%, as assessed by F4/80 immunohistochemistry. Increased hemolysis, measured by increases in relative spleen weights and decreased hematocrit was confirmed in 2-Butoxyethanol treated mice. The percentage of iron-stained endothelial cells increased by ∼11-fold over control, and endothelial cell DNA synthesis increased ∼1.7-fold over control in 2-Butoxyethanol exposed mice. Importantly, Kupffer cell depletion reduced 2-Butoxyethanol-induced iron staining and hepatic endothelial cell DNA synthesis. These studies provide evidence supporting the hypothesis that the Kupffer cell modulates 2-Butoxyethanol-induced endothelial cell DNA synthesis, and therefore may contribute to hemangiosarcoma induction by 2-Butoxyethanol.

  • Kupffer cells participate in 2-Butoxyethanol-induced liver hemangiosarcomas.
    Toxicology, 2010
    Co-Authors: Lisa M. Kamendulis, Stacy M Corthals, James E. Klaunig

    Abstract:

    2-Butoxyethanol increases hemangiosarcomas selectively in male mouse liver after chronic inhalation through mechanisms that have not fully been elucidated. Hemolysis, a primary toxic effect associated with 2-Butoxyethanol exposure in rodents, increased hemosiderin (iron) deposition in Kupffer cells in the liver. These findings, along with the induction of hepatic neoplastic lesions, led to our hypothesis that the induction hemangiosarcomas by 2-Butoxyethanol is due to the activation of Kupffer cells, subsequent to hemolysis, that results in the induction of DNA synthesis in target cells (endothelial cells); allowing for the selective proliferation of preneoplastic target cells and/or the promotion of new initiated cells. The present studies were conducted to determine whether Kupffer cells contributed to 2-Butoxyethanol-induced endothelial DNA synthesis in the liver, thereby determining whether a linkage exists between these events. Male B6C3F1 mice were treated with 450 and 900 mg/kg 2-Butoxyethanol (via daily gavage; 5x/week) for 7 days in the presence or absence of Kupffer cell depletion (via clodronate-encapsulated liposomes). 2-Butoxyethanol (450 and 900 mg/kg/day) increased the number of F4/80 stained cells (Kupffer cells) compared to controls (approximately 1.3- and approximately 1.6-fold over control, respectively). Clodronate liposome treatment reduced the number of Kupffer cells by >90%, as assessed by F4/80 immunohistochemistry. Increased hemolysis, measured by increases in relative spleen weights and decreased hematocrit was confirmed in 2-Butoxyethanol treated mice. The percentage of iron-stained endothelial cells increased by approximately 11-fold over control, and endothelial cell DNA synthesis increased approximately 1.7-fold over control in 2-Butoxyethanol exposed mice. Importantly, Kupffer cell depletion reduced 2-Butoxyethanol-induced iron staining and hepatic endothelial cell DNA synthesis. These studies provide evidence supporting the hypothesis that the Kupffer cell modulates 2-Butoxyethanol-induced endothelial cell DNA synthesis, and therefore may contribute to hemangiosarcoma induction by 2-Butoxyethanol.

  • Mechanisms of 2-Butoxyethanol-induced hemangiosarcomas.
    Toxicological Sciences, 2006
    Co-Authors: Stacy M Corthals, Lisa M. Kamendulis, James E. Klaunig

    Abstract:

    Chronic exposure to 2-Butoxyethanol increased liver hemangiosarcomas in male mice. The mechanism for the selective induction of hemangiosarcomas by 2-Butoxyethanol is unknown but has been suggested to occur through non–DNA-reactive mechanisms. The occurrence of liver hemangiosarcomas in male mice has been linked to oxidative damage subsequent to RBC hemolysis and iron deposition and activation of macrophages (Kupffer cells) in the liver, events that exhibit a threshold in both animals and humans. 2-Butoxyethanol is metabolized to 2-butoxyacetaldehyde and 2butoxyacetic acid, and although the aldehyde metabolite is short lived, the potential exists for this metabolite to cause DNA damage. The present study examined whether 2-Butoxyethanol and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, damaged mouse endothelial cell DNA using the comet assay. No increase in DNA damage was observed following 2-Butoxyethanol (1–10mM), 2-butoxyacetaldehyde (0.1–1.0mM), or 2-butoxyacetic acid (1–10mM) in endothelial cells after 2, 4, or 24 h of exposure. Additional studies examined the involvement of hemolysis and macrophage activation in 2-Butoxyethanol carcinogenesis. DNA damage was produced by hemolyzed RBCs (10 3 10 6 , 4 h), ferrous sulfate (0.1–1.0mM; 2–24 h), and hydrogen peroxide (50–100mM; 1–4 h) in endothelial cells. Hemolyzed RBCs also activated macrophages, as evidenced by increased tumor necrosis factor (TNF) a, while neither 2-Butoxyethanol nor butoxyacetic acid increased TNF-a from macrophages. The effect of activated macrophages on endothelial cell DNA damage and DNA synthesis was also studied. Coculture of endothelial cells with activated macrophages increased endothelial cell DNA damage after 4 or 24 h and increased endothelial cell DNA synthesis after 24 h. These data demonstrate that 2-Butoxyethanol and related metabolites do not directly cause DNA damage. Supportive evidence also demonstrated that damaged RBCs, iron, and/or products from macrophage activation (possibly reactive oxygen species) produce DNA damage in endothelial cells and that activated macrophages stimulate endothelial cell proliferation. These events coupled together provide the events necessary for the induction of hemangiosarco

Lisa M. Kamendulis – 2nd expert on this subject based on the ideXlab platform

  • Kupffer cells participate in 2-Butoxyethanol-induced liver hemangiosarcomas
    Toxicology, 2010
    Co-Authors: Lisa M. Kamendulis, Stacy M Corthals, James E. Klaunig

    Abstract:

    Abstract 2-Butoxyethanol increases hemangiosarcomas selectively in male mouse liver after chronic inhalation through mechanisms that have not fully been elucidated. Hemolysis, a primary toxic effect associated with 2-Butoxyethanol exposure in rodents, increased hemosiderin (iron) deposition in Kupffer cells in the liver. These findings, along with the induction of hepatic neoplastic lesions, led to our hypothesis that the induction hemangiosarcomas by 2-Butoxyethanol is due to the activation of Kupffer cells, subsequent to hemolysis, that results in the induction of DNA synthesis in target cells (endothelial cells); allowing for the selective proliferation of preneoplastic target cells and/or the promotion of new initiated cells. The present studies were conducted to determine whether Kupffer cells contributed to 2-Butoxyethanol-induced endothelial DNA synthesis in the liver, thereby determining whether a linkage exists between these events. Male B6C3F1 mice were treated with 450 and 900 mg/kg 2-Butoxyethanol (via daily gavage; 5×/week) for 7 days in the presence or absence of Kupffer cell depletion (via clodronate-encapsulated liposomes). 2-Butoxyethanol (450 and 900 mg/kg/day) increased the number of F4/80 stained cells (Kupffer cells) compared to controls (∼1.3- and ∼1.6-fold over control, respectively). Clodronate liposome treatment reduced the number of Kupffer cells by >90%, as assessed by F4/80 immunohistochemistry. Increased hemolysis, measured by increases in relative spleen weights and decreased hematocrit was confirmed in 2-Butoxyethanol treated mice. The percentage of iron-stained endothelial cells increased by ∼11-fold over control, and endothelial cell DNA synthesis increased ∼1.7-fold over control in 2-Butoxyethanol exposed mice. Importantly, Kupffer cell depletion reduced 2-Butoxyethanol-induced iron staining and hepatic endothelial cell DNA synthesis. These studies provide evidence supporting the hypothesis that the Kupffer cell modulates 2-Butoxyethanol-induced endothelial cell DNA synthesis, and therefore may contribute to hemangiosarcoma induction by 2-Butoxyethanol.

  • Kupffer cells participate in 2-Butoxyethanol-induced liver hemangiosarcomas.
    Toxicology, 2010
    Co-Authors: Lisa M. Kamendulis, Stacy M Corthals, James E. Klaunig

    Abstract:

    2-Butoxyethanol increases hemangiosarcomas selectively in male mouse liver after chronic inhalation through mechanisms that have not fully been elucidated. Hemolysis, a primary toxic effect associated with 2-Butoxyethanol exposure in rodents, increased hemosiderin (iron) deposition in Kupffer cells in the liver. These findings, along with the induction of hepatic neoplastic lesions, led to our hypothesis that the induction hemangiosarcomas by 2-Butoxyethanol is due to the activation of Kupffer cells, subsequent to hemolysis, that results in the induction of DNA synthesis in target cells (endothelial cells); allowing for the selective proliferation of preneoplastic target cells and/or the promotion of new initiated cells. The present studies were conducted to determine whether Kupffer cells contributed to 2-Butoxyethanol-induced endothelial DNA synthesis in the liver, thereby determining whether a linkage exists between these events. Male B6C3F1 mice were treated with 450 and 900 mg/kg 2-Butoxyethanol (via daily gavage; 5x/week) for 7 days in the presence or absence of Kupffer cell depletion (via clodronate-encapsulated liposomes). 2-Butoxyethanol (450 and 900 mg/kg/day) increased the number of F4/80 stained cells (Kupffer cells) compared to controls (approximately 1.3- and approximately 1.6-fold over control, respectively). Clodronate liposome treatment reduced the number of Kupffer cells by >90%, as assessed by F4/80 immunohistochemistry. Increased hemolysis, measured by increases in relative spleen weights and decreased hematocrit was confirmed in 2-Butoxyethanol treated mice. The percentage of iron-stained endothelial cells increased by approximately 11-fold over control, and endothelial cell DNA synthesis increased approximately 1.7-fold over control in 2-Butoxyethanol exposed mice. Importantly, Kupffer cell depletion reduced 2-Butoxyethanol-induced iron staining and hepatic endothelial cell DNA synthesis. These studies provide evidence supporting the hypothesis that the Kupffer cell modulates 2-Butoxyethanol-induced endothelial cell DNA synthesis, and therefore may contribute to hemangiosarcoma induction by 2-Butoxyethanol.

  • Mechanisms of 2-Butoxyethanol-induced hemangiosarcomas.
    Toxicological Sciences, 2006
    Co-Authors: Stacy M Corthals, Lisa M. Kamendulis, James E. Klaunig

    Abstract:

    Chronic exposure to 2-Butoxyethanol increased liver hemangiosarcomas in male mice. The mechanism for the selective induction of hemangiosarcomas by 2-Butoxyethanol is unknown but has been suggested to occur through non–DNA-reactive mechanisms. The occurrence of liver hemangiosarcomas in male mice has been linked to oxidative damage subsequent to RBC hemolysis and iron deposition and activation of macrophages (Kupffer cells) in the liver, events that exhibit a threshold in both animals and humans. 2-Butoxyethanol is metabolized to 2-butoxyacetaldehyde and 2butoxyacetic acid, and although the aldehyde metabolite is short lived, the potential exists for this metabolite to cause DNA damage. The present study examined whether 2-Butoxyethanol and its metabolites, 2-butoxyacetaldehyde and 2-butoxyacetic acid, damaged mouse endothelial cell DNA using the comet assay. No increase in DNA damage was observed following 2-Butoxyethanol (1–10mM), 2-butoxyacetaldehyde (0.1–1.0mM), or 2-butoxyacetic acid (1–10mM) in endothelial cells after 2, 4, or 24 h of exposure. Additional studies examined the involvement of hemolysis and macrophage activation in 2-Butoxyethanol carcinogenesis. DNA damage was produced by hemolyzed RBCs (10 3 10 6 , 4 h), ferrous sulfate (0.1–1.0mM; 2–24 h), and hydrogen peroxide (50–100mM; 1–4 h) in endothelial cells. Hemolyzed RBCs also activated macrophages, as evidenced by increased tumor necrosis factor (TNF) a, while neither 2-Butoxyethanol nor butoxyacetic acid increased TNF-a from macrophages. The effect of activated macrophages on endothelial cell DNA damage and DNA synthesis was also studied. Coculture of endothelial cells with activated macrophages increased endothelial cell DNA damage after 4 or 24 h and increased endothelial cell DNA synthesis after 24 h. These data demonstrate that 2-Butoxyethanol and related metabolites do not directly cause DNA damage. Supportive evidence also demonstrated that damaged RBCs, iron, and/or products from macrophage activation (possibly reactive oxygen species) produce DNA damage in endothelial cells and that activated macrophages stimulate endothelial cell proliferation. These events coupled together provide the events necessary for the induction of hemangiosarco

Yoshikata Koga – 3rd expert on this subject based on the ideXlab platform

  • Intermolecular Interactions in 2-Butoxyethanol−DMSO−H2O†
    The Journal of Physical Chemistry, 1996
    Co-Authors: Peter Westh‡ And, Yoshikata Koga

    Abstract:

    Excess partial molar enthalpy, HBE, and chemical potential, μBE, of 2-Butoxyethanol (B) were determined in ternary mixtures of B, dimethyl sulfoxide (D), and H2O. The data were obtained in small enough mole fraction increments to evaluate the so-called interaction functions, ∂HBE/∂xB, ∂HBE/∂xD, ∂μBE/∂xB, and ∂μBE/∂xD. These interaction functions previously proved useful in elucidating the “mixing schemes” in binary aqueous solutions of B and D. For the binary mixtures, it was found that both B and D influenced H2O in the following manner:  in the water-rich composition range (region I) within a certain threshold (xB < 0.0175 and xD < 0.28 at 25 °C), both solutes enhance the hydrogen-bonded network of water in their vicinity, and the mixtures retain the percolated nature of the network. At higher B or D concentrations (region II) a qualitatively different mixing scheme becomes operative. The results from this work suggest that, in the ternary mixtures, solute B and D influences the percolated hydrogen bond...

  • Ionic conductivity in the water-rich region of aqueous 2-Butoxyethanol
    Canadian Journal of Chemistry, 1995
    Co-Authors: Yoshikata Koga, Kataryna T. Puhacz

    Abstract:

    Ionic conductivities of HCl, KOH, and KCl were measured in aqueous solutions of 2-Butoxyethanol (BE) at 25 °C. The quantity, Λj′ = σ/xj, which is almost proportional to the molar conductivity, was extrapolated to the infinite dilution xj → 0. σ is the conductivity and xj is the mole fraction of j(= HCl, KOH, or KCl). The plots of 0Λj′, the value of Λj′ extrapolated to infinite dilution, against xBE showed a change in slope at xBE = 0.0175. The previous work from this laboratory indicated that the mixing scheme changes qualitatively at the same locus, xBE = 0.0175. By mixing scheme we simply mean the way in which BE and H2O molecules mix with each other. Assuming additivity in 0Λj′ in terms of constituent ions, those values for H+OH− were calculated. Plots of thus calculated as a function of xBE in the water-rich region, 0 < xBE < 0.0175, suggest that the hydrogen bond probability decreases in the bulk of solution, as xBE increases. Keywords: aqueous 2-Butoxyethanol, ionic conductivities, mixing schemes, h…

  • Anomalous X-ray scattering from aqueous 2-Butoxyethanol at XBE = 0.06 near freezing
    Chemical Physics Letters, 1994
    Co-Authors: Yoshikata Koga, Keiko Nishikawa, Kasumi Yoshino, Ibuki Tanaka, Yingnian Xu, Yoshiyuki Amemiya

    Abstract:

    Abstract Small angle X-ray scattering was measured from aqueous 2-Butoxyethanol of mole fraction X BE = 0.06 at 273, 278 and 298 K. Anomalously strong scattering was observed at 273 and 278 K. The scattering intensity I is proportional to s −3 in the range s −1 , where s is the momentum transfer of scattering, s =4π sin θ/λ. This dependence is in contrast to the Ornstein—Zernicke regime, or more generally Fisher’s dependence, I ∼ s −2+η , commonly observed near the critical demixing of a binary mixture.