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  • 1
    Electronic Resource
    Electronic Resource
    Theophylline-induced mesenteric periarteritis in F344/N rats (1998)
    Springer
    Archives of toxicology 72 (1998), S. 731-737 
    Details
    ISSN: 1432-0738
    Keywords: Key words Theophylline ; Alkaloid ; Pharmaceutical ; Bronchodilator ; Arteritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The toxicity and carcinogenic potential of theophylline (an alkaloid bronchodilator drug) was investigated in male and female F344/N rats in 16-day, 14-week, and 2-year gavage and feeding studies. In 16-day studies, rats were fed diets containing 0, 500, 1000, 2000, 4000, and 8000 ppm of theophylline or given 0, 12.5 (twice daily), 25 (once daily), 50 (once daily), 50 (twice daily), 100 (once daily), 200 (once daily), 200 (twice daily), and 400 (once daily) mg theophylline/kg body weight in corn oil by gavage. In 14-week studies, rats were fed diets containing 0, 1000, 2000, and 4000 ppm theophylline or given 0, 37.5, 75, and 150 mg/kg body weight theophylline in corn oil by gavage. In 2-year gavage studies, rats were given 0, 7.5, 25, and 75 mg/kg body weight in corn oil. In 16-day gavage studies, treatment-related periarteritis occurred in arteries of the pancreas and adjacent to the mesenteric lymph nodes of early death male and female rats given 400 mg/kg once daily. In the 14-week studies, treatment-related periarteritis occurred at similar sites and in male rats exposed to 75 and 150 mg/kg, and in all exposed female rats (gavage studies), in females exposed to 1000 ppm, and in both sexes exposed to 2000 and 4000 ppm (feeding studies). In the 2-year study, chronic periarteritis was significantly increased only in the males receiving 75 mg/kg of theophylline. The adventitia, media and intima of medium- and large-sized mesenteric arteries were involved. Similar to other vasodilator chemicals, the pathogenesis of theophylline-induced vascular lesions may be a consequence of hemodynamic changes induced in the vascular wall.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050567
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of Melatonin and Linolenic Acid on Mammary Cancer in Transgenic Mice with c-neu Breast Cancer Oncogene (2000)
    Springer
    Breast cancer research and treatment 64 (2000), S. 287-296 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; c-neu transgenic mice ; melatonin ; linolenic acid ; flaxseed oil ; IGF-1 concentrations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer is one of the most common cancers and is a leading cause of mortality in women. The TG.NK transgenic mouse line expresses the c-neu breast cancer oncogene under the control of a MMTV promoter and appears to be a useful animal model for evaluation of intervention strategies to delay/prevent breast cancer. Fiber-rich nonpurified diet (NTP-2000) and some retinoid analogues have been shown to significantly delay the development of mammary cancer in the TG.NK model. Four-week-old hemizygous TG.NK female mice with MMTV/c-neu oncogene fed NTP-2000 diet were gavaged with 0.05–0.2 ml of flaxseed oil as the source of ω-3 rich PUFA, or melatonin at 50–200 mg/kg or a combination of 0.10 ml flaxseed oil and 50 mg/kg melatonin in a gavage volume of 0.2 ml per mouse with corn oil as the vehicle for 30 weeks. The time course of the mammary tumor incidence pattern was advanced by flaxseed oil compared to the control. At the high dose (0.2 ml) of flaxseed oil, when the ω-6: ω-3 PUFA ratio was closer to 1, there was some delay in the growth of mammary tumors. Melatonin delayed the appearance of palpable tumors and the growth of the tumors with a dose-related statistically significant negative trend for the incidence of tumors. The combination of flaxseed oil and melatonin caused a significant decrease in the number of tumors and tumor weight per mouse compared to the control and to flaxseed oil but not to melatonin alone. Flaxseed oil may delay the growth of mammary tumors if the ω-6:ω-3 PUFA ratio of fat consumed is closer to 1. Melatonin has the potential to markedly delay the appearance of palpable mammary tumors. Studies are in progress with the TG.NK mouse model to understand the histological and molecular changes associated with the dose-response pattern of mammary tumor incidence and growth after treatment with a broad range of doses of melatonin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026552405042
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  • 3
    Electronic Resource
    Electronic Resource
    Influence of diet on mammary cancer in transgenic mice bearing an oncogene expressed in mammary tissue (1997)
    Springer
    Breast cancer research and treatment 45 (1997), S. 149-158 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; c-neu/erbB2 oncogene ; diet ; dietary fiber ; transgenic mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer is one of the most commoncancers in women. The laboratory rat treated withstrong carcinogen is the most commonly used animalmodel for study of breast cancer. Transgenic mouselines with homologues of human breast cancer oncogeneshave been developed. The transgenic mouse line TG.NKwith c-neu, the human breast cancer oncogene homologueof erbB2, was evaluated to determine its suitabilityfor study of intervention strategies to delay/prevent thedevelopment of breast cancer. There were no palpablemammary tumor masses up to 22-weeks of age,and almost all mice fed a purified dietdeveloped palpable mammary tumors by 28-weeks of age.Nonpurified diets decreased the incidence and multiplicity, anddelayed the development of mammary tumors as comparedto a purified diet. Increasing the fiber contentof nonpurified diet decreased the tumor incidence further.There is approximately a 19-week interval between weaningand development of palpable mammary masses to evaluateintervention strategies to delay or prevent the developmentof mammary cancer in the TG.NK mouse model.Fiber from nonpurified cereal ingredients appears to behighly beneficial in delaying the development of mammarycancer in TG.NK mice, and this observation isin agreement with human epidemiological findings. Therefore, theTG.NK transgenic mouse with oncogene c-neu (erbB2), appearsto be a useful animal model for evaluationof dietary intervention strategies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005822318256
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of retinoid analogues on mammary cancer in transgenic mice with c-neu breast cancer oncogene (1998)
    Springer
    Breast cancer research and treatment 48 (1998), S. 265-271 
    Details
    ISSN: 1573-7217
    Keywords: breast cancer ; c-neu transgenic mice ; N-(4-hydroxyphenyl) retinamide ; arotinoid Ro 40-8757 ; retinoid analogues
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer is one of the most common cancers and is a leading cause of mortality in women. The TG.NK transgenic mouse line expresses the c-neu breast cancer oncogene under the control of an MMTV promoter and appears to be a useful animal model for evaluation of intervention strategies to delay/prevent breast cancer. Fiber-rich nonpurified diet (NTP-2000), as compared to a purified diet (AIN-76A), has previously been shown to significantly delay the development of mammary cancer in the TG.NK model. Four-week old hemizygous TG.NK female mice with MMTV/c-neu oncogene were fed NTP-2000 diet containing the retinoid analogue 4-hydroxyphenyl retinamide (4-HPR) at 5 mM/kg or an arotinoid Ro 40-8757 at 2 and 3 mmol/kg for 26 weeks. The 4-HPR at 5 mmol/kg diet delayed the development of palpable tumors up to 24 weeks, but by 26 weeks, the incidence was not significantly different from the NTP-2000 diet control group. However, the 4-HPR diet markedly decreased the average weight of the tumors at 26 weeks. The 4-HPR diet also caused a significant increase in body weight without an increase in food consumption. Arotinoid Ro-40-8757 at both doses inhibited the development of mammary tumors for the duration of the study. However, the Ro 40-8757 at 3 mmol/kg appeared to be toxic as indicated by a significant depression of the average body weight with alopecia and skin scaling in some mice. Our observations with TG.NK transgenic mouse and fiber-rich diet (NTP-2000) indicate that the arotinoid Ro 40-8757 has a markedly higher inhibitory effect on the development of mammary cancer than 4-HPR. Studies to evaluate genetic changes and expression of hormonal receptors and growth factors associated with the inhibition of mammary cancer development by the retinoid analogues are in progress.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005957620881
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  • 5
    Electronic Resource
    Electronic Resource
    Changes associated with delay of mammary cancer by retinoid analogues in transgenic mice bearing c-neu oncogene (1999)
    Springer
    Breast cancer research and treatment 58 (1999), S. 239-252 
    Details
    ISSN: 1573-7217
    Keywords: N-(4-hydroxyphenyl) retinamide ; arotinoid Ro 40-8757 ; breast cancer ; erbB2 expression ; IGF-1 levels ; toxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Breast cancer is one of the common cancers and is a leading cause of cancer mortality in women. The TG.NK transgenic mouse line on FVB strain background expresses the c-neu oncogene under the control of a MMTV promoter in mammary tissue and appears to be a useful animal model for evaluation of strategies to delay or prevent mammary cancer. Fiber-rich nonpurified diet (NTP-2000) and some retinoid analogues have delayed mammary cancer in the TG.NK model. Four week old hemizygous TG.NK female mice with MMTV/c-neu (erbB2) activated oncogene were fed NTP-2000 diet containing the retinoid analogue 4-hydroxyphenylretinamide (4-HPR) at 7 mmol/kg or the arotinoid Ro 40-8757 at 1.5 and 2.5 mmol/kg for 26 weeks. The 4-HPR at 7 mmol/kg diet delayed the development of palpable tumors up to 24 weeks, but by 26 weeks, the incidence markedly increased and was closer to the NTP-2000 diet control group. However, the 4-HPR diet markedly decreased the average weight of the tumors at 26 weeks with no decrease in multiplicity. The 4-HPR also caused significant increase in liver weights without an effect on body weight. Arotinoid Ro 40-8757 caused marked decrease in the number and branching of mammary ducts, and inhibited mammary tumor development with significant decrease in the incidence, multiplicity, and tumor weights compared to the NTP-2000 diet control. Arotinoid also caused a significant dose-related increase in liver weights without a significant effect on body weights. At the doses tested, the arotinoid but not 4-HPR decreased the circulating levels of IGF-1. However, there was no association between the IGF-1 levels and the size, incidence, or absence of tumors when evaluated for any treatment group or for all mice in the study irrespective of treatment. The oncogene erbB2 (c-neu) and the growth factor EGF expression were more prominent in the small tumors of the mice treated with arotinoid than in the larger tumors of the control group. PCNA staining was observed in areas where there was high erbB2 and EGF staining. The delay in onset of mammary tumors by the above retinoid analogues may be related to the delay in development of mammary glands.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006315716713
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    Paper (German National Licenses)
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