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Inbred Strains of Mice: C3H


Inbr: F130 to F170 depending on substrain. Agouti. Genet: +, rd. Developed by Strong 1920 from a cross of Bagg albino with DBA male (see CBA) with selection for a high incidence of mammary tumours. Now among the most widely used of all mouse strains. Most substrains have a good reproductive performance. Unfostered substrains (which are now relatively rare since 'SPF' animals have become popular) have a high incidence of mammary tumours (usually > 90% at one year) caused by a virus which is passed from mother to offspring through the milk. Fostering of the young or transfer of fertilised ova to a mammary tumour virus-free strain eliminates the virus, and substantially reduces the incidence of mammary tumours. Note that all `SPF' stock will be free of this virus. \par

The unfostered substrains are widely used in cancer research for the sake of their mammary tumours. Fostered stock are widely used as a general-purpose strain which is readily available and well known. The strain should be used with care in behavioural studies, since it carries the rd (retinal degeneration) gene and is blind after about 6 weeks. \par

Some substrain differences are large, and can not be accounted for solely on the basis of mutation, and must be ascribed either to substantial residual heterozygosity or genetic contamination (McLaren and Tait, 1969), though C3H/HeJ is known to differ from C3H/He as a result of a mutation at the lps (lipopolysaccharide) locus. \par

The following major substrains are recognised: \par


Strong to Bittner 1931, to Kirschbaum 1952. Has 83% mammary tumours in unfostered breeders. Low leukaemia. \par


Origin not known, but has a very high incidence of lymphatic leukaemia (over 90%) (Fuchs, 1962). \par


This substrain was passed to Heston in 1941,and is now the most widely distributed of all. Non-fostered substrains have more than 90% mammary tumours by about 11 months. Fostered substrains have a high incidence of hepatomas (Festing and Blackmore, 1971). \par


Heston, to Jackson Laboratory in 1947, and now widely distributed. Has poor immune response to endotoxic lipopolysaccharide due to a B-cell deficit (Rosenstreich and Glode, 1975; Coutinho, 1976). \par


A substrain developed by transfer of fertilised ova to strain C57BL by Deringer. This substrain lacks the mammary tumour virus and therefore has a lower incidence of mammary tumours (4% in virgin females and 55% in breeding females and 74% in force-bred females) (Deringer, 1959a). \par


Inbr. N10F12 (1993). The a allele transferred from C57BL/6J. Now used to create a B6C3Fe-a/a non-agouti hybrid as a coat colour marker for stocks maintained by ovarian transfer.

C3HeB/Fe (syn: TC3H)

Developed by Fekete in 1948 by transfer of fertilized ova of C3H/HeJ to C57BL/6. Lacks mammary tumour virus. \par


`Mahogany' coat colour mutation occurred spontaneously in C3H/He stock held at Laboratory Animals Centre, Carshalton, in 1967. The strain has been propagated because authenticity can be guaranteed by the colour of the coat. \par


Congenic line developed by backcrossing the Avy to the C3H background. Has an exceptionally high mammary tumour incidence, virtually 100% at 7-8 months. The fostered substrain C3H-Avy fB has a 90% incidence of mammary tumours transmitted by either parent (Vlahakis et al., 1970., 1970). \par

C3H.PRI-Flvr (formerly C3H.RV ) and C3H.M.Dom-Flvr

Congenic line resistant to flavivirus (arbovirus) infection, developed by Groschel and Koprowski (1965) by backcrossing the resistance gene from PRI to C3H, and by Shallam by backcrossing the resistance gene from wild M.m. domesticus to C3H.


Low intrastrain aggression (10/14) (Southwick and Clark, 1966). Long latency to emerge from home-cage (6/7), low rearing (7/7), long latency to cross barrier in open-field (6/7), low hole-in-the-wall entries (6/7) and low Y-maze exploration (7/7) (McClearn et al., 1970., 1970). Low open-field activity (13/13) (Bruell, 1964). Low open-field defaecation (5/5) (Bruell, 1969). High food drive (3/15) (Thompson, 1953), but poor performance in food-seeking task (5/6) (Henderson, 1970). Short time of immobility in a forced swimming test (9/9) (Nikulina et al 1991).

Low shock-avoidance learning (8/9) (Bovet et al., 1966., 1966, 1969). Good short- term but poor long-term memory in contrast with DBA/2 (Bovet et al., 1969., 1969). Good T-maze learning (1/6) (Stasik, 1970). Poor water-escape learning (6/6) (Festing, 1973b). Low radial-arm maze learning (3/3) (Ammassari-Teule et al, 1993). High social grooming score during aggressive encounters (3/14) (Southwick and Clark, 1968). \par

Carries the retinal degeneration gene and is capable of pattern discrimination up to 40 days, and brightness discrimination to at least 100 days (Nagy and Misanin, 1970).

Life-span and spontaneous disease

Almost 100% of mammary tumours in females of unfostered substrains (Heston, 1963). Mammary adenocarcinomas in unfostered substrains less than 1% in males, 95% in breeding and 88% in virgin females. Lymphatic leukaemia zero incidence (Hoag, 1963). Mammary tumours 100% at 6.8 months in C3H-Avy , 90% in C3H- Avy fC57BL at 15.3 months. Mammary tumours 40% at 18.8 months in C3HfC57BL, but 99% at 7.2 months in unfostered C3H (Heston and Vlahakis, 1971). Mammary tumours 37% at 2 years in fostered substrain (Bentvelzen et al., 1970., 1970). Median latent period to develop mammary tumours in unfostered substrains ranged from 276 to 566 days, depending on breeding status and environmental stress (Riley, 1975). A high proportion of the mammary tumours are of the acinar type (2/7) (Tengbergen, 1970). Incidence of mammary tumours reduced by bromocriptine and interferon Stravoravdi et al, 1993).

Hepatomas 72-91% in males at 14 months, 59% in virgin females, 30-38% in breeding females (Heston, 1963). Hepatomas have eosinophilic cytoplasmic inclusion bodies (Liebelt et al., 1971., 1971). Good model of genetic predisposition to hepatocellular tumours, susceptibility being associated with six chromosomal regions (Dragani et al, 1995). Point mutations in H-ras do not generally play a major or initiating role in spontaneous hepatocarcinogenesis in this strain (Enomoto et al, 1993).

Lung adenomas 2-10% in fostered A substrain, leukaemia 6-30% (Muhlbock and Tengbergen, 1971). Occasional Harderian gland tumours (Heston, 1963). Rare "lipomatous" hamartomas or choristomas have been noted (Adkison et al 1991).

Life-span in SPF fostered conditions intermediate in both sexes (11/17 = 590 days in males, 12/17 = 676 days in females). Liver tumours 9-23%, lung tumours 2-10% and mammary tumours 21-36%. Heart defects 13-26% and cystic ovaries 13-26% (Festing and Blackmore, 1971). Tail lesions similar in appearance to bit wounds were found in grouped C3H/HeJ by Les (1972). Develop dystrophic cardiac calcification which may be related to disturbed myocyte calcium metabolism (Brunnert, 1997).

Can be made obese by a suitable diet (Fenton and Dowling, 1953). Resistant to the development of aortic cartilaginous metaplasia (contrast C57BL/6) (Qiao et al, 1995). Resistant to diet-induced aortic fatty streak lesions which correlates with a high level of paroxinase mRNA (contrast C57BL/6) (Shih et al, 1996).


Primary lung tumours 8% in males, 4% in breeding females and 10% in Virgin females. Lymphatic leukaemia zero. Mammary adenocarcinomas zero in males, 12% in breeding females, 2% in virgin females (Hoag, 1963). Ovarian tumours 47% in Virgin and 37% in breeding females, 29% in force-bred females (Heston, 1963). Hepatomas 91% in breeding males, 58% in Virgin and 30% in breeding females (Murphy, 1966). Life-span above average in both sexes (16/22 = 652 days in males, 17/22 = 657 days in females). High gross tumour incidence in males (5/22) (Storer, 1966).

Normal physiology and biochemistry

Low blood pressure (15/17) (Mullink et al., 1975). Low serum calcium in Fg substrain (5/6) but He substrain has high level at 4 months (1/6) (Barrett et al., 1975., 1975). High serum cholesterol (1/5) (Bruell et al., 1962., 1962). High plasma cholesterol (11/11) and triglycerides (10/11). High erythrocyte catalase (5/18) (Hoffman and Rechcigl, 1971). Low serum haptoglobin level (10/11) (Peacock et al, 1967 , 1967). Low peripheral nerve conduction velocity (6/6) (Hegmann, 1972). Low percentage of time spent sleeping (5/6) with low percentage of slow-wave sleep (5/6) and small diurnal variation (5/6) (Valatx and Bugat, 1974). High brain glutamic acid decarboxylase (GABA) in He-mg substrain (2/10) (Gaitonde and Festing, 1976). High brain aromatic L-amino acid decarboxylase (1/5) in C3H/2 substrain (Pryor et al., 1966., 1966). Low metabolic rate (5/6) (Pennycuik, 1967). High liver tyrosine aminotransferase level in fasted mice (1/10) (Blake, 1970). Low adrenal corticosteroid production (4/4) (Nandi et al., 1967., 1967). High peptidyl proline hydroxylase activity in tumour tissue and mammary gland fat pad (1/5) (Cutroneo et al., 1973., 1973). Slow cell turnover as judged by rate of clearance of DNA- bound radioactivity (14/17) (Heiniger et al., 1972., 1972). Harderian gland has a high porphyrin content (2/16) (Margolis, 1971). Low hepatic ammonia-lyase activity (5/6 and 6/6 in two substrains) (Hanford et al., 1974., 1974). Low spermatozoal beta-glucuronidase activity (9/9) (Erickson, 1976). Low basal level of renal glutathione S-transferase (4/4) but high basal level of renal glutathione reductase (1/4) (Misra et al 1991). Low hepatic nicotinamide N-methyltransferase levels (10/10) (Scheller et al, 1996). Maintain normal auditory sensitivity beyond one year of age in both HeJ and HeSnJ substrains, but by 30 months there was little hearing function due to sensorineural degeneration (Trune et al, 1996).

High level of alpha-fetoprotein in plasma at 7 days (2/6) (Adinolfi et al 1990). Resistant to the development of atherosclerosis on a semi-synthetic high fat diet (cf 5/9) (Nishina et al, 1993). Loci on chromosomes 1, 3, 5 and 11 are associated with variation in high density lipoprotein levels with coordinate expression of cholesterol-7-alpha hydroxylase in a cross involving atherosclerosis susceptible C57BL/6 mice (Machleder et al, 1997).

Hepatic iodothyonine deiodinase activity was only 18% of that found in C57BL/6 mice (Schoenmakers et al, 1993). Decreased levels of deiodinase mRNA and hyperthyroxinemia associated with a 21-base pair insert in the promoter region of the type 1 deiodinase gene (Maia et al, 1995). Resistant to severe hypercapnia with hypoxia assessed by elevated minute ventilation rate (8/8) (Tankersley et al, 1994). Has a slow and deep breathing pattern phenotype (contrast C57BL/6) (Tankersley et al, 1997). High intra-ocular pressure (1/4) (John et al, 1997).


Low systolic blood pressure (19/19) (Schlager and Weibust, 1967). Low plasma cholinesterase activity in females (18/22) (Angel et al, 1967). High N'- methylnicotinamide oxidase activity (1/7) (Huff and Chaykin, 1967).


Low total leukocyte count (18/18), low erythrocyte count (16/18), low haematocrit (18/18), low haemoglobin (17/18) (Russell et al., 1951., 1951). Small thymus/body weight ratio (5/6) (Belyaev et al., 1970., 1970), small thymus/body weight ratio (6/8 to 8/8, depending on age) (Albert et al., 1965., 1965). Large pituitary (1/6) (Sinha et al., 1975., 1975). Adrenal gland X zone large (1/8), with high incidence of vacuolisation (2/6) (Delost and Chirvan-Nia, 1958). Low percentage of mice have accessory spleens (9/9) (Hummel et al., 1966., 1966). Many Peyer's patches (2/7) (Hummel et al., 1966., 1966). Plasma volume low (4/4) at 5.97 ml/100 g and red cell volume low (4/4) at 4.64ml/100g body weight in He substrain (Kano and Mizuma, 197.4). Intermediate proportion of sperm-head abnormalities (2/5, 13%) in C3H/HeJ (Styrna et al 1991). High retinal ganglion cell number (24/24) in HeJ (Williams et al, 1996). High bone density of femur (1/11) (Beamer et al, 1996).

Megakaryocytes have a higher average ploidy than all other mouse strains tested. This is due to multiple additive alleles (McDonald and Jackson, 1994).


Large brain weight (15/18 male, 17/18 female) (Storer, 1967). Small brain/body weight ratio (19/20) (Roderick et al., 1973., 1973).


Susceptible to skin ulceration to DMBA (cf. 13/22) (Thomas et al., 1973., 1973). Sensitive to the development of uterine tumours following treatment with DMBA at 4-weeks of age (cf 3/6) (Tsubura et al, 1993). Susceptible to induction of subcutaneous tumours by 3-methylcholanthrene (1/14 to 4/14, depending on substrain) (Kouri et al., 1973., 1973). Susceptible to tumour induction by 3-methylcholanthrene in fostered and unfostered substrains (1/8 to 2/8) (Whitmire and Salerno, 1972), (2/12) (Whitmire et al., 1971., 1971). Susceptible to induction of liver (1/6) but resistant to pulmonary (5/6) tumours by neonatally administered DMBA (Flaks, 1968). High susceptibility to tumour induction by 3,4-benzpyrene (1/6) (Liebelt et al., 1970., 1970). High susceptibility to induction of mammary tumours by urethane (2/7) (Bentvelzen et al., 1970., 1970). High incidence of gastric tumours after administration of methylcholanthrene by gavage (2/5) (Akamatsu and Barton, 1974). Susceptible to fibrosarcoma induction by methylcholanthrene (2/15 male, 1/15 female) (Strong, 1952). Highly susceptible to the induction of hepatocellular tumours by various carcinogens, with the volume of hepatic lesions being >100-fold greater than in more resistant strains. Susceptibility is linked to at least six chromosomal regions (Dragani et al, 1995). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-ras and p53, respectively (Masui et al, 1997).

Phenobarbitone in the diet to give an intake of 85mg/kg per day resulted in 70% of animals developing basophilic nodules by 91 weeks of age (contrast 4% in C57BL/6), but no increase in liver carcinomas (Evans et al, 1992). However, there was a two-fold greater level of DNA synthesis in C3H mice relative to C57BL/6 mice after partial hepatactomy, though partial hepatectomy is a tumour promoter in C57BL/6 but not in C3H mice (Bennett et al, 1995).

Insensitive to histamine (9/9) (Brown, 1965). Airways of C3H/HeJ hyporeactive to acetylcholine (c.f. 3/7) (Zhang et al, 1995). Resistant to teratogenic effect of acetazolamide (5/6) (Green et al., 1973., 1973). Pentobarbital i.p. induces hepatic epoxide hydrase (cf. 4/7) (Oesch et al., 1973., 1973). Sensitive to X-irradiation (25/27) (Roderick, 1963). Long survival on Warfarin (12/12) (Lush and Arnold, 1975). Sensitive to hyperbaric oxygen (2/18) (Hill et al., 1968., 1968). Sensitive uterine response to oestrogens (5/5) (Chai and Dickie, 1966). Short hexobarbital sleeping time (3/9) (Vesell, 1968). Long survival in 90% oxygen (1/10) and highly susceptible to pulmonary hyaline-membrane formation (1/10) (Lieberman and Kellog, 1967). Resistant to the induction of pulmonary fibrosis by bleomycin (contrast C57BL/6) (Haston et al, 1996), and irradiation though the sensitivity of lung fibroblasts to irradiation in-vitro does not correlate with in-vivo sensitivity (Dileto and Travis, 1996). Sensitive to chloroform toxicity (cf. 4/9) (Deringer et al., 1953., 1953). Susceptible to toxic effects of isoniazid (10/10) (Taylor, 1976b). High ED50 to behavioural effects of nicotine (17/19) (Marks et al 1989). Low self-selection of nicotine (5/6) which is inversely correlated with sensitivity to nicotine-induced seizures (Robinson et al, 1996).

Low bronchial reactivity (5/6) to methacholine and serotonin (Konno et al 1993). No increase in renal lipid peroxidation following treatment with nickel (4/4) (Misra et al 1991). Susceptible to biliary tract injury following oral dosing with 500 micrograms of the fungal toxin sporidesmin (2/4) (Bhathal et al 1990). Low histamine release from peritoneal mast cells induced by compound 48/80, a calcium dependent histamine releaser ( c.f. 5/8) (Toda et al 1989). High histamine release from peritoneal mast cells induced by Ca2+ ionophore A23187 ( c.f. 7/8, contrast C57BL/6) (Toda et al 1989). Cadmium highly hepatotoxic (1/5) (Shaikh et al, 1993). Resistant (cf 3/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995, Kleeberger et al, 1993). Susceptible to weight loss induced by cocaine, but this is attenuated by anisomycin (cf SJL, CBA) (Shimosato et al, 1994). Estrogen does not induce an increase in VLDL and LDL-cholesterol (like BALB/c, contrast C57BL/6 and C57L)) (Srivastava, 1995).


Susceptible to skin ulceration by DMBA (cf. 13/22) (Thomas et al., 1973., 1973). Sensitive to X-irradiation (23/27) (Roderick, 1963). Good ovulatory response (94%) to 3 I.U. PMS (1/6), but poor response (33%) to 7 I.U. PMS. Response facilitated by exposure to males (Zarrow et al., 1971., 1971). Susceptible (cf 5/8) to ozone-induced decreases of tracheal potential (Takahashi et al, 1995).


Sensitive to amyloid induction (2/10) but low level of spontaneous amyloid formation (Ram et al., 1969., 1969). Low lymphocyte phytohaemagglutinin response (38/43) (Heiniger et al., 1975., 1975). Good immune response to small doses of bovine gamma globulin (cf. 4/8) (Levine and Vaz, 1970). Poor immune response to Cholera A and B antigens (8/8) (Cerny et al., 1971., 1971). Good splenic PFC immune response to pneumococcal polysaccharide (2/9) (Amsbaugh et al., 1972., 1972). Females fail to reject male skin grafts after 100 days (contrast nine strains) (Gasser and Silvers, 1971). Poor immune response to ovomucoid and ovalbumin (cf. 2/12) (Vaz et al., 1971., 1971). Poor primary immune response to bovine serum albumin (5/6) (James and Milne, 1972). Good immune response to Salmonella anatum (1/5) and S. senftenberg (2/5) lipopolysaccharide (Di Pauli, 1972). Responder to synthetic polypeptide Glu57, Lys38, Ala5 (cf. 3/7) (Pinchuk and Maurer, 1965). Good immune response to Vi antigen (2/5) (Gaines et al., 1965., 1965). Precipitating and skin-sensitising antibodies have slow electrophoretic mobility (2/6) (Fahey, 1965). High antibody affinity to HSA (3/9) (Petty et al., 1972., 1972). Erythrocytes have high agglutinability (cf. 14/25) (Rubinstein et al., 1974., 1974). Low immune response to ferritin in He substrain (15/16) (Young et al., 1976., 1976). Non- discriminator between `H' and `L' sheep erythrocytes (cf. 6/18) (McCarthy and Dutton, 1975). High anti-DNP antibody concentration (2/7) (Paul et al., 1970., 1970). Antibodies to lipoid A antigen do not cross-react with sheep red blood cells (contrast eight strains). Strain also resistant to toxic effect of Salmonella lipopolysaccharide (1/8) (Rank et al., 1969., 1969). Refractory to sensitising effects of HSF from Bordetella pertussis to histamine (contrast sixteen strains) (Bergman and Munoz, 1968).

Low level of "leakiness" when the scid mutation is maintained on this genetic background (contrast CB17) (Nonoyama et al, 1993).

Good immune response to Pro-Gly-Pro-ovalbumin (1/7) and (Pro-Gly- Pro)n (2/7) (Fuchs et al., 1974., 1974). High susceptibility (3/12) to IgE-mediated passive cutaneous anaphylaxis (De Souza et al., 1974., 1974). Good immune response to Salmonella strasbourg lipopolysaccharide (1/7) (Di Pauli, 1972). Low PHA- stimulated lymphocyte blastogenic response in Ent substrain (6/6) (Hellman and Fowler, 1972). Erythrocytes of C3HeB/FeJ have a high agglutinability (cf. 14/25) (Rubinstein et al., 1974., 1974). He substrain resistant to induction of anaphylactic shock by ovalbumin (cf. 6/13) (Tanioka and Esaki, 1971). He and HeN substrains are susceptible (2/12) to experimental autoimmune orchitis induced by two or three sc injections with viable syngeneic testicular germ cells without any adjuvants, but C3H/BiKi is resistant (12/12) (Tokunaga et al 1993). High immune response to ganglio-series gangliosides in C3H/HeN (c.f. 2/10), but low response in C3H/HeJ (c.f. 4/10) (Kawashima et al 1992). Anti-BPO IgE monoclonal antibody did not produce potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) mice (c.f. 5/8) (Harada et al 1991). Carries a strain-specific allele at the alpha globin locus (Sato et al, 1996).

High natural killer cell response to the immunostimulent 7-allyl-8-oxoguanosine (1/6) (Pope et al, 1994).


Resistant to infection by Salmonella typhimurium strain C5 (5/7) (Plant and Glynn, 1974), Susceptible to Mycoplasma fermentens (1/6) (Gabridge et al., 1972., 1972). Experimental Mycoplasma pulmonis infection results in acute pneumonia with severe hemorrhage, edema and often death (Faulkner et al, 1995). Susceptible to mammary tumour virus, which is carried in an active form in unfostered substrains (Murray and Little, 1967). Susceptible to oncogenic effect of polyoma virus given at birth (Law, 1966a). Susceptible to measles virus induced encephalitis, which correlates with a high cytotoxic T-lymphocyte response (like C57BL/6, contrast BALB/c) (Niewiesk et al, 1993).

Susceptible to Mycobacterium marinum (2/9)(Shepard and Habas, 1967). Susceptible to infection by Mycobacterium marinum (1/6) (Yamamoto et al 1991). Susceptible to infection by Entamoeba histolytica (1/4) (Neal and Harris, 1975). Resistant to mouse hepatitis virus (Bang and Warwick, 1960). 100% transmission of murine leukaemia virus (Scripps) through three successive generations (cf. 2/5) (Jenson et al., 1976., 1976). Highly susceptible to measles virus (cf. 3/6) (Rager-Zisman et al., 1976., 1976). The BiDa substrain is susceptible (9/9) to tumorigenesis following infection with polyoma virus in contrast with C57BL/6 (Freund et al 1992) and C57BR/cd due to a single dominant gene Pyvs for susceptibility, which may be identical to Mtv-7 (Lukacher et al, 1995). Highly susceptible to tumour induction by polyoma virus (1/9) (Freund et al, 1992). Following administration of murine cytomegalovirus, C3H mice exhibited minimal carditis after neonatal or adult infection. However neonatal infection appears to accelerate age-related cardiopathy, which is severe in retired breeders of this strain. (contrast BALB/c and C57BL/10) (Price et al 1991). Highly susceptible to Lyme borreliosis (Borrelia burgdorferi) when inoculated at 3 weeks of age (1/5) and as adults. Mice inoculated at age 3 weeks also developed polyarthritis, but severity was reduced when inoculated as adults. Carditis was also common (Barthold et al 1990), and mice were susceptible to the development of arthritis (contrast BALB/c) (Matyniak and Reiner, 1995). Resistant to intra-vaginally innoculated Neisseria gonorrhoeae (c.f. 5/5) (Johnson et al 1989). Resistant (3/10) to infection with Ehrlichia risticii (Williams and Timoney, 1994). Susceptibile to infection by Helicobacter felis with moderate to severe chronic active gastritis in the body of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). \par


Substrain (which carries the lps mutation) resistant to LCM virus (76% survival) prior to 1970, but has now become susceptible (3% survival) (Oldstone and Dixon, 1973). Resistant to LCM virus infection (1/5) (Oldstone and Dixon, 1968). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher et al., 1975., 1975). Susceptible to lethal infection with Rickettsia akari strain Kaplan, in contrast with seven other substrains of C3H and 24 other strains (Anderson and Osterman 1980a,b). Mouse mammary tumor proviral loci have been identified by Lee and Eicher (1990). High immunological response to Salmonella typhi porins (1/4) (Gonzales et al, 1995). Resistant to infection with Mycobacterium paratuberculosis (contrast BALB/c) (Tanaka et al, 1994).

Susceptible, with high amylase response to the fungus Paracoccidioides brasiliensis (cf 6/12) (Xidieh et al, 1994). Resistant to Leishmania major (contrast BALB/c) (Laskay et al, 1995, Scott et al, 1996). Lipopolysaccharide mutant (lps) and non-mutant mice are equally susceptible to Escherichia coli (Hopkins et al, 1996). \par


Highly susceptible to mammary tumour virus, but believed to be free of the virus (Murray and Little, 1967). Low susceptibility to BALB/Tennant leukaemia virus (11/12) (Tennant, 1965). Resistant to induction of diabetes mellitus by encephalomyocarditis virus (cf. 7/14) (Boucher et al., 1975., 1975).


Breeding performance intermediate/good (5/25 He substrain, 10/25 He-mg sub-line). Colony output 1.1 to 1.4 young/female/week. Litter size at weaning 5.9 (8/25) (Festing, 1976a). Good reproductive performance (2/8), litter size 6.4, sterility 10% (Nagasawa et al., 1973., 1973). Large litter size (1/6 to 3/6), high proportion of females produce four or more litters (1/6) and high proportion of fertile matings (1/6) (Fernandes et al., 1973., 1973). Good breeding performance, 2.0 to 2.2 young per female per month (9/24 to 7/24) in fostered and unfostered substrains, respectively (Hansen et al., 1973., 1973). C3H/HeJ has shorter and less regular oestrus cycles than C57BL/6J (Nelson et al 1992). Early opening of vagina and first cornification (1/3 compared with C57BL/6 and DBA/2), but late onset of cyclicity (3/3) (Nelson et al 1990) \par \par


High reproductive performance (1/8). Litter size 6.4 + 0.2, sterility 4% (Nagasawa et al., 1973., 1973).


Recommended host for the following transplantable tumours: lymphosarcoma 6C3HED and mammary adenocarcinomas C3HBA and H2712 (Kaliss, 1972). Recommended host for sarcoma BP8 used as a model for screening potential anticancer drugs (E.O.R.T.C. Screening Group, 1972). High mortality after neonatal thymectomy (6/6) (Law, 1966a). \par

High rate of spontaneous mutations (1/21) and total deviants (4/21) (Schlager and Dickie, 1967). \par


Recommended host for transplantable hepatoma H4 (Kaliss, 1972). High incidence of spontaneous `deviants' (5/21) (Schlager and Dickie, 1967).

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

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