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Marc B Hershenson – One of the best experts on this subject based on the ideXlab platform.

  • Rhinovirus 16 3C Protease Induces Interleukin-8 and Granulocyte-Macrophage Colony-Stimulating Factor Expression in Human Bronchial Epithelial Cells
    Pediatric Research, 2004
    Co-Authors: Ann W Funkhouser, Jeong-ah Kang, Jing Li, Limei Zhou, Julian Solway, Marc B Hershenson
    Abstract:

    Rhinovirus (RV), a member of the Picornaviridae family, accounts for many virus-induced asthma exacerbations. RV induces Airway Cell chemokine expression both in vivo and in vitro . Because of the known interactions of proteases with Cellular functions, we hypothesized that RV 3C protease is sufficient for cytokine up-regulation. A cDNA encoding RV16 3C protease was constructed by PCR amplification and transfected into 16HBE14o− human bronchial epithelial Cells. 3C protease induced expression of both IL-8 and GM-CSF, as well as transcription from both the IL-8 and GM-CSF promoters. 3C expression also induced activator protein 1 and NF-κB transcriptional activation. Finally, mutation of IL-8 promoter AP-1 and NF-κB promoter sequences significantly reduced 3C-induced responses. Together, these data suggest expression of RV16 3C protease is sufficient to induce chemokine expression in human bronchial epithelial Cells, and does so in an AP-1- and NF-κB–dependent manner.

  • rhinovirus 16 3c protease induces interleukin 8 and granulocyte macrophage colony stimulating factor expression in human bronchial epithelial Cells
    Pediatric Research, 2004
    Co-Authors: Ann W Funkhouser, Jeong-ah Kang, Limei Zhou, Julian Solway, Alan Tan, Mark K Abe, Marc B Hershenson
    Abstract:

    Rhinovirus (RV), a member of the Picornaviridae family, accounts for many virus-induced asthma exacerbations. RV induces Airway Cell chemokine expression both in vivo and in vitro. Because of the known interactions of proteases with Cellular functions, we hypothesized that RV 3C protease is sufficient for cytokine up-regulation. A cDNA encoding RV16 3C protease was constructed by PCR amplification and transfected into 16HBE14o− human bronchial epithelial Cells. 3C protease induced expression of both IL-8 and GM-CSF, as well as transcription from both the IL-8 and GM-CSF promoters. 3C expression also induced activator protein 1 and NF-κB transcriptional activation. Finally, mutation of IL-8 promoter AP-1 and NF-κB promoter sequences significantly reduced 3C-induced responses. Together, these data suggest expression of RV16 3C protease is sufficient to induce chemokine expression in human bronchial epithelial Cells, and does so in an AP-1- and NF-κB–dependent manner.

D E Devor – One of the best experts on this subject based on the ideXlab platform.

  • Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in Syrian hamsters or C3H/HeNCr mice.
    Journal of cancer research and clinical oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induce P-450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40-110 mg IPO/kg i.p. and necropsied 15-48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2-3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24-48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors.(ABSTRACT TRUNCATED AT 400 WORDS)

  • Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in Syrian hamsters or C3H/HeNCr mice
    Journal of Cancer Research and Clinical Oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induce P -450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N -nitrosomethyl- n -heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40–110 mg IPO/kg i.p. and necropsied 15–48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N -nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2–3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24–48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors. In conclusion, these experiments show, in original tumor settings of the lung, that it is possible to achieve Cell-specific cytotoxic effects based on Cellular composition and functional maturity, i.e., toxicity in carcinomas of predominantly nonciliated bronchiolar Cells but not in tumors of alveolar type II Cell lineage.

  • acute effects of 4 ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in syrian hamsters or c3h hencr mice
    Journal of Cancer Research and Clinical Oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induceP-450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mgN-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40–110 mg IPO/kg i.p. and necropsied 15–48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmolN-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2–3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24–48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors. In conclusion, these experiments show, in original tumor settings of the lung, that it is possible to achieve Cell-specific cytotoxic effects based on Cellular composition and functional maturity, i.e., toxicity in carcinomas of predominantly nonciliated bronchiolar Cells but not in tumors of alveolar type II Cell lineage.

Ann W Funkhouser – One of the best experts on this subject based on the ideXlab platform.

  • Rhinovirus 16 3C Protease Induces Interleukin-8 and Granulocyte-Macrophage Colony-Stimulating Factor Expression in Human Bronchial Epithelial Cells
    Pediatric Research, 2004
    Co-Authors: Ann W Funkhouser, Jeong-ah Kang, Jing Li, Limei Zhou, Julian Solway, Marc B Hershenson
    Abstract:

    Rhinovirus (RV), a member of the Picornaviridae family, accounts for many virus-induced asthma exacerbations. RV induces Airway Cell chemokine expression both in vivo and in vitro . Because of the known interactions of proteases with Cellular functions, we hypothesized that RV 3C protease is sufficient for cytokine up-regulation. A cDNA encoding RV16 3C protease was constructed by PCR amplification and transfected into 16HBE14o− human bronchial epithelial Cells. 3C protease induced expression of both IL-8 and GM-CSF, as well as transcription from both the IL-8 and GM-CSF promoters. 3C expression also induced activator protein 1 and NF-κB transcriptional activation. Finally, mutation of IL-8 promoter AP-1 and NF-κB promoter sequences significantly reduced 3C-induced responses. Together, these data suggest expression of RV16 3C protease is sufficient to induce chemokine expression in human bronchial epithelial Cells, and does so in an AP-1- and NF-κB–dependent manner.

  • rhinovirus 16 3c protease induces interleukin 8 and granulocyte macrophage colony stimulating factor expression in human bronchial epithelial Cells
    Pediatric Research, 2004
    Co-Authors: Ann W Funkhouser, Jeong-ah Kang, Limei Zhou, Julian Solway, Alan Tan, Mark K Abe, Marc B Hershenson
    Abstract:

    Rhinovirus (RV), a member of the Picornaviridae family, accounts for many virus-induced asthma exacerbations. RV induces Airway Cell chemokine expression both in vivo and in vitro. Because of the known interactions of proteases with Cellular functions, we hypothesized that RV 3C protease is sufficient for cytokine up-regulation. A cDNA encoding RV16 3C protease was constructed by PCR amplification and transfected into 16HBE14o− human bronchial epithelial Cells. 3C protease induced expression of both IL-8 and GM-CSF, as well as transcription from both the IL-8 and GM-CSF promoters. 3C expression also induced activator protein 1 and NF-κB transcriptional activation. Finally, mutation of IL-8 promoter AP-1 and NF-κB promoter sequences significantly reduced 3C-induced responses. Together, these data suggest expression of RV16 3C protease is sufficient to induce chemokine expression in human bronchial epithelial Cells, and does so in an AP-1- and NF-κB–dependent manner.

William W. Busse – One of the best experts on this subject based on the ideXlab platform.

  • Host immune responses to rhinovirus: Mechanisms in asthma
    The Journal of allergy and clinical immunology, 2008
    Co-Authors: J.t. Kelly, William W. Busse
    Abstract:

    Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many Airway Cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial Cells and possibly macrophages. Infection of epithelial Cells generates a variety of proinflammatory mediators to attract inflammatory Cells to the Airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial Airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment.

  • The relationship of sputum eosinophilia and sputum Cell generation of IL-5.
    The Journal of Allergy and Clinical Immunology, 2000
    Co-Authors: Cheri A. Swensen, Elizabeth A. B. Kelly, Hirohito Kita, William W. Busse
    Abstract:

    Abstract Background: Eosinophil recruitment to the Airway after antigen challenge is regulated by many factors, including Airway Cell generation of cytokines. Objectives: The purpose of this study was to determine the relationship between sputum Cell generation of IL-5 and the appearance of eosinophils in the sputum after antigen challenge. Methods: Sputum samples from 11 allergic subjects were collected before and again 4 and 24 hours after antigen challenge. In 6 of these subjects, induced sputum samples were also obtained 48 hours and 7 days after challenge. Sputum leukocyte differential and Cell counts and eosinophil-derived neurotoxin levels were determined. Sputum Cells were then cultured with PHA (10 μg/mL) to stimulate IL-5 and IFN-γ, which were measured in culture supernatants. Results: An increase in sputum eosinophils and eosinophil-derived neurotoxin levels was detected at 4 hours after antigen challenge, with peak values at 24 hours. In contrast, significant increases in ex vivo generation of IL-5 by sputum Cells was not seen until 24 hours after challenge. At 24 hours, PHA-induced IL-5 correlated with airspace eosinophil values ( r s = 0.78, P P r s = –0.68, P Conclusion: Although eosinophils are increased in the Airway lumen as early as 4 hours, the ex vivo generation of IL-5 by sputum Cells is first noted in samples obtained 24 hours after antigen challenge. This suggests that the early (4 hours) recruitment of eosinophils to the Airway lumen may be regulated by factors other than IL-5 or that mucosal Cells (rather than airspace Cells) contribute to the IL-5 generation at this time point. Furthermore, IL-5 generation by airspace Cells may be more responsible for either eosinophil recruitment or retention at later time points. (J Allergy Clin Immunol 2000;106:1063-9.)

S Rehm – One of the best experts on this subject based on the ideXlab platform.

  • Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in Syrian hamsters or C3H/HeNCr mice.
    Journal of cancer research and clinical oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induce P-450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40-110 mg IPO/kg i.p. and necropsied 15-48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2-3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24-48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors.(ABSTRACT TRUNCATED AT 400 WORDS)

  • Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in Syrian hamsters or C3H/HeNCr mice
    Journal of Cancer Research and Clinical Oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induce P -450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N -nitrosomethyl- n -heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40–110 mg IPO/kg i.p. and necropsied 15–48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N -nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2–3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24–48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors. In conclusion, these experiments show, in original tumor settings of the lung, that it is possible to achieve Cell-specific cytotoxic effects based on Cellular composition and functional maturity, i.e., toxicity in carcinomas of predominantly nonciliated bronchiolar Cells but not in tumors of alveolar type II Cell lineage.

  • acute effects of 4 ipomeanol on experimental lung tumors with bronchiolar or alveolar Cell features in syrian hamsters or c3h hencr mice
    Journal of Cancer Research and Clinical Oncology, 1993
    Co-Authors: S Rehm, D E Devor
    Abstract:

    4-Ipomenaol (IPO) has been shown to induceP-450-mediated necrosis of Clara Cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-Cell-derived adenocarcinomas and mouse alveolar type II Cell tumors. Clara Cells serve as stem Cells for Airway Cell renewal and, therefore, tumors derived from Clara Cells may likewise differentiate into various bronchiolar Cell types, or undergo squamous Cell metaplasia. Bronchiolar Cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mgN-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-Cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40–110 mg IPO/kg i.p. and necropsied 15–48 h later. Solid and papillary tumors with alveolar Cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmolN-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2–3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24–48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining Cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous Cell carcinomas. Susceptible Cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar Cells. Undifferentiated and squamous tumor Cells were resistant to IPO, as were resident normal alveolar type II Cells. However, some adenocarcinomas composed primarily of ciliated and mucous Cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar Cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar Cell tumors. In conclusion, these experiments show, in original tumor settings of the lung, that it is possible to achieve Cell-specific cytotoxic effects based on Cellular composition and functional maturity, i.e., toxicity in carcinomas of predominantly nonciliated bronchiolar Cells but not in tumors of alveolar type II Cell lineage.