DDD

Inbr: F 50 +. Albino. Genet: c. Origin: According to Tanaka Matsuzawa (1990) "Inbreeding of dd mice maintained at Denken was commenced in 1957 and the resulting inbred strain was named DDD after dd at Denken. The ancestors of dd mice had come from Germany. The process of introduction to Japan and the history of these mice were surveyed in the literatures, since the description concerning them had been confused. As a result, the following history was confirmed: the original colony of mice of an unknown size was introduced from the Hoechst Company, Frankfurt a.m. Main, Germany into the Kitasato Institute, Tokyo, Japan by Dr. Tsuneo Komatsu under the direction of Dr. Sahachiro Hata in autumn, 1928. Dr. Hata and his colleagues bred these mice to use for medical researches and called them "deutsche Maus". Their descendants (one male and one female) were shipped to the Health Institute of Manchuria Railway, Talien (currently called Dalian), China on demand of Dr. Koji Ando in 1934. Two males and eight females from the Talien colony were shipped back to Dr. Saburo Kojima, the Institute for Infectious Diseases, Tokyo, Japan in 1943. They had been maintained without crossing with another colony at the Institute, from which mice were distributed to many institutes throughout Japan between 1944 and 1960, and served as the starting nuclei of many inbred or outbred strains. The "deutsche Maus" was named dd mice after "deutsche Maus at Denken" in 1952. Thus, the mouse strains connected with dd mice usually have D, DD or dd at the head in their names."

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Characteristics

Mammary tumours 8% at 14 months in virgin and 14% at 14 months in force-bred females. Mammary tumour virus carried by the strain is probably of plaque-inducing group found in DD, RIII and BR6 but not in C3H (Matsuzawa et al., 1974., 1974). Develop a high incidence of heritable hydronephrosis, with a higher incidence observed in males and females. This appears to be caused by an abnormally high internal pressure in the renal pelvis leading to incomplete protection against the vesico-urethral reflex (Mannen et al 1991). Host of a very stable, transplantable pregnancy-dependent mammary tumour TPDMT-4 (Matsuzawa and Yamamoto, 1975). Resistant to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). High incidence of lethality among F1 Dh/+ male mice resulting from a cross between DDD females and DH-Dh/+ males, however, this is not observed in the reciprocal cross (Suto et al, 1996).

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Mannen H., Tsuji S., and Goto N. (1991) Incomplete protection mechanism against vesico-urethral reflex and hydronephrosis in the inbred mouse strain DDD. Lab. Anim. 25, 156-161.

Matsuzawa A., Yamamoto T., and Suzuki K. (1974) Pregnancy dependence of mammary tumors in strain DDD mice. J. Natl. Cancer Inst. 52, 449-453.

Matsuzawa A. and Yamamoto T. (1975) Response of a pregnancy-dependent mammary tumour to hormones. J. Natl. Cancer Inst. 55, 447-456.

Suto J., Wakayama T., Imamura K., Goto S., and Fukuta K. (1996) High lethality of F1 (dh/+) male-mice from the cross between DDD female and Dh (Dh/+) male. Exp. Anim. 45, 99-101.

Tsubura A., Senzaki H., Oyaizu T., Fujita Y., and Morii S. (1993) Strain differences in neoplastic response to DMBA-induced uterine vascular tumors in mice. International Journal of Oncology 2, 927-930.

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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK