Toxicology and carcinogenicity studies of diuretics in F344 rats and B6C3F1 mice 2. Furosemide

1990 ◽  
Vol 10 (5) ◽  
pp. 369-378 ◽  
Author(s):  
John R. Bucher ◽  
James Huff ◽  
Joseph K. Haseman ◽  
Scot L. Eustis ◽  
William E. Davis ◽  
...  
Keyword(s):  
B6c3f1 Mice ◽  
F344 Rats

Correlation of DNA adduct formation and riddelliine-induced liver tumorigenesis in F344 rats and B6C3F1 mice[Cancer Lett. 193 (2003) 119–125]

2004 ◽  
Vol 207 (1) ◽  
pp. 119-125 ◽  
Author(s):  
Ming W Chou ◽  
Jian Yan ◽  
Jasyl Nichols ◽  
Qingsu Xia ◽  
Frederick A Beland ◽  
...  
Keyword(s):  
Adduct Formation ◽  
Dna Adduct ◽  
B6c3f1 Mice ◽  
F344 Rats

scholarly journals Metabolism and Disposition of Phenolphthalein in Male and Female F344 Rats and B6C3F1 Mice

1998 ◽  
Vol 42 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Robert J. Griffin ◽  
Veronica B. Godfrey ◽  
Leo T. Burka
Keyword(s):  
Male And Female ◽  
B6c3f1 Mice ◽  
F344 Rats

scholarly journals Eight-Week Toxicity Study of 60 Hz Magnetic Fields in F344 Rats and B6C3F1 Mice

1997 ◽  
Vol 35 (1) ◽  
pp. 55-63 ◽  
Author(s):  
G. A. BOORMAN ◽  
J. R. GAUGER ◽  
T. R. JOHNSON ◽  
M. J. TOMLINSON ◽  
J. C. FINDLAY ◽  
...  
Keyword(s):  
Magnetic Fields ◽  
Toxicity Study ◽  
B6c3f1 Mice ◽  
F344 Rats

Toxicology and carcinogenesis studies of isophorone in F344 rats and B6C3F1 mice

Toxicology ◽  
1986 ◽  
Vol 39 (2) ◽  
pp. 207-219 ◽  
Author(s):  
John R. Bucher ◽  
James Huff ◽  
William M. Kluwe
Keyword(s):  
B6c3f1 Mice ◽  
F344 Rats

scholarly journals Subchronic Toxicity of Triethylenetetramine Dihydrochloride in B6C3F1 Mice and F344 Rats

1996 ◽  
Vol 29 (2) ◽  
pp. 185-193
Author(s):  
DAVID L. GREENMAN ◽  
ROBERT L. MORRISSEY ◽  
WILLIAM BLAKEMORE ◽  
JAMES CROWELL ◽  
PAUL SIITONEN ◽  
...  
Keyword(s):  
Subchronic Toxicity ◽  
B6c3f1 Mice ◽  
F344 Rats

Analysis of chloroethane toxicity and carcinogenicity including a comparison with bromoethane

2008 ◽  
Vol 24 (10) ◽  
pp. 655-675 ◽  
Author(s):  
JW Holder
Keyword(s):  
Adrenal Glands ◽  
Structural Analogue ◽  
Endometrial Cells ◽  
Female Mice ◽  
Carcinogenic Potential ◽  
B6c3f1 Mice ◽  
Hypothalamic Pituitary Axis ◽  
Endometrial Cancers ◽  
F344 Rats ◽  
Excessive Stress

Chloroethane (CE) gas carcinogenicity is analyzed and determined from a National Toxicology Program (NTP) bioassay where an inhalation concentration of 15,000 ppm CE gas in air produced the highest incidence of an uncommon-to-rare tumor ever observed by the NTP. Persistently inhaled CE produces endometrial cancers in female mice. The first-tumor-corrected uterine endometrial incidence (I) in B6C3F1 mice is 90%, but no significant tumors occurred in F344 rats. The endometrial cancers dispersed by 1) migrating locally to the adjacent myometrium, 2) then migrating to the bloodstream by intravasation, 3) entering 17 distal organs by extravasation and adapting to the new tissue environment. Distal cancers retained sufficient endometrial cell features to be recognized at each metastatic site. CE produced one of the highest metastasis rates ever observed by NTP of 79%. Comparing CE with bromoethane (BE), a structural analogue, it was found that BE too produced rare murine endometrial cancers yielding the second highest NTP incidence rate of I = 58% with a similar high malignancy rate of 56%. Because of the historical rarity of endometrial tumors in the B6C3F1 mouse, both of these SAR haloethanes seem to be evoking a strong, related carcinogenic potential in B6C3F1 mice, but not in F344 rats. The question of whether humans are similar to mice or to rats is addressed here and in Gargas, et al., 2008. The powerful carcinogenesis caused by these halohydrocarbons may have been caused by excessive and metabolically unresolved acetaldehyde (AC) which is directly generated by Cyp2E1 in the oxidative elimination of CE. With >95% AC metabolic production, as predicted from pharmacokinetic (PK) studies depending on CE exposure, AC is the main elimination intermediate. AC is a known animal carcinogen and a strongly suspected human carcinogen. Also, CE causes incipient decreases of tissue essential glutathione pools [GSH] by Phase II conjugation metabolic elimination of CE (and BE), by glutantione transferase (GST), in most organs (except brain) exposed to high circulating CE and it metabolites. In three laboratories, an excessive stress reaction of hyperkinesis was observed only during 15,000 ppm gas exposure but not when the exposure ceased or when exposure was presented at 150 ppm. Test rodents other than the female mice did not exhibit a pattern of visible stress nor did they have a carcinogenic response to CE gas. Unremitting stress has been documented to contribute a feedback to the hypothalamus which stimulates the hypothalamic-pituitary-axis (HPA), which in turn, induces the adrenal glands. Because estrus and estrogen and progesterone levels were unaltered by CE gas, the adrenal over stimulation, causing high steroid output, may be the penultimate step in this extraordinary carcinogenic response. High adrenal production of corticosteroids could adversely promote endometrial cells to cancers in mice − a mechanism that has already been observed in humans.

Toxicity and carcinogenicity studies of Caramel Colour IV in F344 rats and B6C3F1 mice

1992 ◽  
Vol 30 (5) ◽  
pp. 431-443 ◽  
Author(s):  
K.M. MacKenzie ◽  
B.G. Boysen ◽  
W.E. Field ◽  
S.R.W. Petsel ◽  
C.I. Chappel ◽  
...  
Keyword(s):  
B6c3f1 Mice ◽  
F344 Rats

Carcinogenicity of catechol in F344 rats and B6C3F1 mice

1993 ◽  
Vol 14 (3) ◽  
pp. 525-529 ◽  
Author(s):  
Masao Hirose ◽  
Shoji Fukushima ◽  
Hikaru Tanaka ◽  
Emiko Asakawa ◽  
Satoru Takahashi ◽  
...  
Keyword(s):  
B6c3f1 Mice ◽  
F344 Rats
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