Transplacental and direct action of orthoaminoazotoluene of organ cultures of embryonic mouse liver

1976 ◽  
Vol 82 (3) ◽  
pp. 1399-1402
Author(s):  
T. S. Kolesnichenko ◽  
N. V. Popova
1993 ◽  
Vol 14 (7) ◽  
pp. 1457-1463 ◽  
Author(s):  
Yi Sun ◽  
Larry W. Oberley ◽  
Terry D. Oberley ◽  
James H. Elwell ◽  
Elaine Sierra-Rivera

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Dionysios Chartoumpekis ◽  
Athanasios Niarchos ◽  
Christina Petropoulou ◽  
Panagiota Batzali ◽  
Venetsana Kyriazopoulou ◽  
...  

2003 ◽  
Vol 176 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C Menendez ◽  
R Baldelli ◽  
JP Camina ◽  
B Escudero ◽  
R Peino ◽  
...  

Leptin is a circulating hormone secreted by adipose tIssue which acts as a signal to the central nervous system where it regulates energy homeostasis and neuroendocrine processes. Although leptin modulates the secretion of several pituitary hormones, no information is available regarding a direct action of pituitary products on leptin release. However, it has been pointed out that leptin and TSH have a coordinated pulsatility in plasma. In order to test a direct action of TSH on in vitro leptin secretion, a systematic study of organ cultures of human omental adipose tIssue was performed in samples obtained at surgery from 34 patients of both sexes during elective abdominal surgery. TSH powerfully stimulated leptin secretion by human adipose tIssue in vitro. In contrast, prolactin, ACTH, FSH and LH were devoid of action. These results suggest that leptin and the thyroid axis maintain a complex and dual relationship and open the possibility that plasmatic changes in TSH may contribute to the regulation of leptin pulses.


1985 ◽  
Vol 1 (4) ◽  
pp. 311-333 ◽  
Author(s):  
Michael A. Pereira

Significant numbers of chemicals have been shown to be carcinogenic in mouse liver although they do not exhibit carcinogenic activity in other organs or tissues of mice or rats. This review focuses on the reasons for the unique susceptibility of the mouse liver to these carcinogens and the extent to which the carcinogenic activity of a chemical in mouse liver can be used to predict carcinogenicity in humans. Many of these mouse liver carcinogens lack genotoxic activity and, as such, have been proposed to be tumor promoters. Two mechanisms that may explain the action of nongenotoxic carcinogens in mouse liver are reviewed. These are: (1) direct action on precursor cancer cells, either to accelerate their growth or to prevent their death and (2) the selective growth advantage, resulting from regenerative hyperplasia of precursor cancer cells in response to the necrosis of normal cells produced by hepatotoxins. Estimating human health risks on the basis of mouse liver tumor data is believed to differ for nongenotoxic and genotoxic carcinogens in two fundamental ways. The first involves intraspecies extrapolation and the second involves low-dose extrapolation. In conclusion, although mouse liver tumor data are seen to be of value in estimating human health hazard, it is important to distinguish between genotoxic and nongenotoxic mechanisms in applying such data. Further study of the biochemical and molecular mechanisms of chemical carcinogens is necessary to determine the relationship between their activity in mouse liver and their activity in humans.


1973 ◽  
Vol 241 (107) ◽  
pp. 66-68 ◽  
Author(s):  
R. WILLIAMSON ◽  
CHRISTINE E. DREWIENKIEWICZ ◽  
J. PAUL

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