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Comparative Susceptibility of a Wild‐Derived Strain of Mus musculus molossinus and Laboratory Mice to Teratogenesis by Ethylnitrosourea
Author(s) -
NAGAO Tetsuji,
TAKASHIMA Hiromasa,
MIYASHITA Nobumoto,
FUJIKAWA Kazuo,
MORIWAKI Kazuo
Publication year - 1995
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.1995.tb00959.x
Subject(s) - ethylnitrosourea , teratology , biology , gestation , strain (injury) , laboratory mouse , mouse strain , embryo , ratón , andrology , fetus , phenotype , physiology , genetics , endocrinology , pregnancy , anatomy , medicine , gene , mutant
A wild‐derived strain of Japanese house mice, Mus musculus molossinus (MSM), was compared with laboratory mice (DBA/2N, C57BL/6, C3H/He, BDF 1 , and ICR) for the susceptibility to teratogenic effect of ethylnitrosourea (ENU). ENU was applied i.p. to mice in each strain on day 7 of gestation. On day 18 of gestation, uterine contents were examined and viable fetuses were inspected for external and skeletal malformations. The dose (mg/kg) required to induce 25% embryonic lethality (LD 25 ) was 46 in MSM and 28–54 in the laboratory mice. The frequencies of external and of skeletal malformations at LD 25 were, respectively, 8 and 47% in MSM, 29–97% and 65–95% in the laboratory mice. Thus, MSM was less susceptible to ENU teratogenesis compared to any of the laboratory mice used and the difference in the susceptibility between MSM and the laboratory mice was more marked for external malformations than for skeletal malformations. These results are compatible with the hypothesis that laboratory mice may have genetic traits that facilitate teratological assays of drugs.