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At least 19 recordsLinked to original sources
PubMed1993

Age-related changes in hepatic and splenic insulin receptors and serum insulin and glucose levels in inbred mice.

Inbred mice of strains A/J, DBA/1J, and SJL/J were housed and aged in our animal colony, and parameters of carbohydrate metabolism were assessed at various ages. The patterns of age-related change were both organ- and strain-specific. Age-related changes in two of the strains were associated with relative carbohydrate intolerance. Common to all three strains was a biphasic pattern of change in hepatic insulin receptor number, with a decrease in early life and a return to earlier levels late in life. In both A/J and DBA/1J mice, there was a sharp increase in serum insulin level (twofold to 9.7-fold) that corresponded to the decrease in hepatic insulin receptors and was associated with hyperglycemia; no significant change in serum insulin or glucose levels was seen in SJL/J mice, despite a similar biphasic pattern in hepatic insulin receptor concentration. Age-related changes in splenic insulin receptors resembled changes in the liver in A/J and SJL/J mice, ie, there were synchronous biphasic age-related patterns. This was not the case in the spleens of DBA/1J mice, in which we did not observe age-related changes. There was no change in insulin receptor affinity with age, nor was there any difference in affinity between tissues or mouse strains. The pattern of change in hepatic insulin receptors and serum insulin levels was more complex than has been previously recognized. We do not know the mechanisms responsible for this complex pattern, but it must involve at least two discrete age-related events.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1998

Initial levels of azoxymethane-induced DNA methyl adducts are not predictive of tumor susceptibility in inbred mice.

Inbred mice vary in susceptibility to colon carcinogens such as 1,2-dimethylhydrazine (DMH). Differential susceptibility may depend, in part, on formation of promutagenic DNA methyl adducts within target colonic mucosa. The present study was undertaken to evaluate the extent of DNA adduct formation in susceptible (SWR) and resistant (AKR) mice acutely exposed to the colon carcinogen azoxymethane (AOM), a direct metabolite of DMH. In the first experiment, 8-week-old SWR and AKR mice were treated i.p. with 20 mg/kg AOM and sacrificed 6 h later. DNA was isolated from distal colon and liver, and O6-methylguanine (O6-MeGua) adduct levels were assessed by immunoslot blot (ISB) analysis, using a monospecific antibody raised against O6-methyldeoxyguanosine. HPLC-fluorescence detection was also used to quantitate 06-MeGua and 7-methylguanine (7-MeGua), and to generate standard curves. At 6 h, both O6-MeGua and 7-MeGua were significantly higher (2- to 3-fold, p < 0.05) in AKR colon, while an opposite pattern was found in liver. In Experiment 2, mice were injected with AOM (20 mg/kg) and euthanized 12 and 48 h later. At 12 h, O6-MeGua levels were higher in colons (1.4-fold) of SWR mice. Forty-eight hours after treatment, however, adduct levels in colon were markedly (5-fold) reduced in SWR but were unchanged from 12 h in AKR. To further compare activation of AOM in both strains, colon microsomes were incubated with AOM and calf thymus DNA. Comparable levels of O6-MeGua were detected by ISB, demonstrating equivalent metabolic capacity in both SWR and AKR mice. These studies suggest that differential susceptibility to AOM-induced colon carcinogenesis is not based on initial target tissue DNA alkylation and unlikely to depend on differential metabolic capacity.

Animals↗
PubMed1991

The genetic basis of host resistance to Bacillus anthracis in inbred mice.

Inbred mice of the C3H/He (resistant) and C57BL/6 (susceptible) strains and their hybrids were used in experiments to investigate the genetic regulation of host resistance to B. anthracis. The susceptibility of F1 mice to a standard spore suspension was similar to that of the resistant parent and not intermediate between values for the parent strains. There were no differences in mortality rate between F1 and reciprocal cross mice. Analysis of the results indicated that resistance of mice to B. anthracis is regulated by a single dominant gene.

Animals↗
PubMed1975

Effects of cigarette smoking on aryl hydrocarbon hydroxylase activity in lungs and tissues of inbred mice.

Inbred strains of mice have been classified as aromatic hydrocarbon responsive or nonresponsive depending upon whether the parenteral administration of these substances increases hepatic aryl hydrocarbon hydroxylase (AHH) activity. Aromatic hydrocarbon responsiveness is controlled by genes at a small number of loci. Using 3-methylcholanthrene as inducing agent, strains A/J, C3H/HeJ, and C57BL/6J have been classified as responsive, whereas strains AKR/J, DBA/2J, and SWR/J are nonresponsive. Inhalation of cigarette smoke by both hepatic responsive and nonresponsive mice induces AHH activity in lung, but not in liver, stomach, small intestine, or kidney. The responsive strains have significantly higher levels of basal and induced AHH in the lung than do the hepatic nonresponsive strains. However, because of the especially low basal activity of AHH in lungs of hepatic nonresponsive strains, the ratio of AHH activity in animals treated with cigarette smoke to that in untreated animals is higher in nonresponsive than in responsive strains. AHH activity in lungs is fully induced within 6 to 12 hr after smoke inhalation and remains at the same level whether animals are treated 1 day or daily for 4 week;. AHH in lung returns to basal levels within 5 days after cessation of smoking.

Animals↗
PubMed1998

Differential metabolite accumulation may be the cause of strain differences in sensitivity to streptozotocin-induced beta cell death in inbred mice.

Inbred strains of mice vary in their sensitivity to the diabetogenic effects of streptozotocin (STZ). To investigate the basis for this strain difference we exposed islet cells from two strains of mice that differ in sensitivity to the drug. We examined them morphologically and measured islet NAD + NADH content, streptozotocin metabolite accumulation, glucose transport capacity, Glut2 levels and medium nitrite accumulation. C57bl/6J mice were more sensitive to STZ than Balb/c mice as judged by the extent of pancreatic insulin depletion and beta cell death, in vivo and in vitro. The mode of cell death was necrosis. After a 30-min in vitro exposure to the drug the more sensitive C57bl/6J islets contained higher levels of streptozotocin metabolites and less NAD + NADH than the more resistant Balb/c islets. The lack of any strain differences in 3-O-methyl glucose transport, Glut2 levels and medium nitrite accumulation suggested that STZ transport and nitric oxide metabolism were not responsible for differences in STZ sensitivity and metabolite accumulation. Thus the strain differences in STZ sensitivity appears to be due to intracellular events within the beta cell occurring after STZ transport and before NAD + NADH depletion. STZ metabolite accumulation appears to be associated with STZ sensitivity. Further studies are warranted to determine if differential STZ metabolite accumulation is responsible for STZ sensitivity.

Animals↗
PubMed1977

Genetic differences inthe te of histidase synthesis in inbred mice.

Inbred strains of mice fall into two groups with respect to their liver histidase activity levels, high strains having approximately twice as much activity as low strains. Analysis of the F1, F2, and backcross progeny of the mating of a high activity strain (C57BL/6J) and a low activity strain (C3H/HeJ) indicates that the difference between the strains is determined by a single genetic locus with two alleles exhibiting additive inheritance. No differences with respect to various physical and kinetic parameters were found in studies of partially purified histidase from both strains. Quantitation of the amount of enzyme present by immunotitration showed that the amount of enzyme antigen is proportional to the level of enzyme activity in the two strains. Measurements of the relative rates of histidase synthesis by combined radiochemical and immunological techniques showed that the relative rate of synthesis was closely correlated with the amount of enzyme present. Rates of enzyme degradation in the two strains, measured by recovery of activity after irreversible inhibition with nitromethane, were the same.

Ammonia-Lyases↗
PubMed1978

Lithium chloride toxicity and pharmacodynamics in inbred mice.

Inbred strains of male mice (C3H, DBA, BALB, C57) were used to determine whether genetic factors play a role in lithium toxicity. Significant differences in the LD50 for LiCl were observed between the mouse strains after a subcutaneous injection of 37 degrees isotonic LiCl. The LD50 values in the C3H, DBA, BALB and C57 strains were 17.4, 17.6, 18.2, and 19.4 mmol/kg, respectively. Significant differences were also observed between the mouse strains in the concentrations of lithium in plasma, heart, liver, kidney and brain 2 hrs. after a subcutaneous injection of 15.1 or 18.2 mmol/kg LiCl, but the lithium concentrations were not related in an obvious manner to LiCl toxicity. The results show that genetic factors can influence the toxicity and pharmacodynamics of lithium.

Animals↗
PubMed1999

Maternal behavior in female C57BL/6J and DBA/2J inbred mice.

Inbred strains of mice exhibit different patterns of maternal behavior, providing material for studies of genetic influences on the expression of maternal behavior. Beginning 1 day after birth, maternal behavior was recorded daily for 14 days in the first and second litters of C57BL/6J (B6) and DBA/2J (D2) mothers. D2 mice had higher pup survival than B6 mice, and pup survival was higher in both strains in second litters than in first litters. D2 mothers spent more time engaged in maternal behavior, especially resting with, crouching over, and nursing pups than B6 mothers with first litters, but not with second litters. Not all measures of maternal behavior were correlated with pup survival; with both litters, B6 mothers retrieved pups faster than D2 mothers.

Analysis of Variance↗
PubMed1992

Auditory brainstem function of the F1 offspring of the cross of CBA/CaJ and AU/SsJ inbred mice.

Inbred strains of laboratory mice have several distinct advantages as models for examining conditions that influence the human auditory system, but the CBA/J mouse which has most often been used as a normal model has recently been found to have several disadvantages. This paper is the first report of the auditory brainstem responses (ABRs) of the F1 offspring of CBA/CaJ and AU/SsJ parents. At midlife, high-frequency ABR thresholds are lower in the F1 than in either parental genotype. Tuning curves obtained by forward masking of the ABR also display heterosis, i.e. they are narrower in the F1 than in either parental strain.

Animals↗
PubMed1980

Post-ictal resistance to audiogenic seizures in inbred mice.

Inbred audiosensitive mice exposed to a prolonged auditory signal recovered and remained refractory to further audiogenic seizures as long as the signal was continued. Susceptibility to audiogenic seizures returned upon cessation of sound. The rate of return was the same whether the sound stimulus was brief or prolonged. In a small proportion of test animals, which failed to become fully refractory, the continuing auditory stimulus proved lethal. Mice maintained in the post-seizure refractory state were fully susceptible to Metrazol-induced seizures.

Acoustic Stimulation↗
PubMed1985

A single gene difference determines relative susceptibility to caffeine-induced lethality in SWR and CBA inbred mice.

Inbred mouse strains SWR and CBA differ markedly in their relatively susceptibility to the acute toxic effects of intraperitoneally administered caffeine. At a dose of 187 mg/kg, SWR mice survive a stress-potentiated lethality test apparently related to the generation of tonic seizures; in contrast, CBA mice usually die in less than 30 seconds after this dose. Progeny from several different genetic crosses were characterized to determine the genetic basis underlying this phenotypic difference in caffeine sensitivity. F1 progeny from reciprocal crosses of the parental strains were uniformly sensitive to caffeine-induced lethality, i.e., caffeine responsiveness behaves like an autosomal dominant trait. Self-crossing of F1 individuals produced both progeny which were resistant to caffeine-induced lethality (26% of the total) and those which were susceptible (74%). Backcrosses of the F1 animals to the CBA parent produced no (0/19) resistant progeny. In contrast, backcrosses of F1 animals to SWR produced 54% resistant progeny. These data indicate that the difference in susceptibility to caffeine-induced lethality between these strains is determined by a single pair of autosomal alleles in which susceptibility (responsiveness) to this methylxanthine is dominant to resistance (nonresponsiveness).

Animals↗
PubMed1981

Differences in resistance to Trypanosoma musculi infection among strains of inbred mice.

Inbred strains of mice were inoculated with Trypanosoma musculi, and the course of the ensuing parasitemia was followed. The mouse strains fell into three groups: those displaying high and moderate (fivefold less) parasitemia and C57BL/6 (B/6) mice which had exceptionally low infections. To gain insight concerning the mechanisms responsible for interstrain variations in infections, several types of experiments were performed. Comparison of the ability of spleen cells from the various strains to provide the growth-promoting substances required by T. musculi for growth in culture revealed that B/6 cells were deficient; this suggested one mechanism for regulating parasite infections. Exposure of C3H (high parasitemia) and B/6 mice to graded levels of ionizing radiation revealed that B/6 mice have much greater innate resistance to infection than do C3H mice. The effects of treating mice with silica dust or mercaptoethanol indicated that relative resistance to infection is not primarily associated with macrophage activity or limited growth-promoting substances. We conclude that variations in immune responsiveness to parasite antigens (probably not associated with the H-2 complex), possibly in concert with variations in a non-immunological mechanism, account for interstrain variation in resistance to T. musculi infections.

Animals↗
PubMed1990

Strain-dependent effects of phenobarbital on liver tumor promotion in inbred mice.

Inbred strains of mice were found to differ significantly in their susceptibility to liver tumor promotion by PB. The susceptibility to promotion of hepatocarcinogenesis by this drug was a dominant trait in crosses between the sensitive DBA and resistant C57 mice. The reciprocal F1 hybrids responded similarly to tumor promotion by PB. PB promoted the development of hepatoblastomas in D2B6F1 males but not in B6D2F1 mice. Female mice of the D2B6F1 cross, similarly exposed to PB, failed to develop hepatoblastomas. These results suggested a sex-linked differential response to the development of hepatoblastomas in reciprocal F1 hybrids that are genetically identical except for the reverse origin of their X and Y chromosomes. Differences in the promoting effects of PB between C57 and DBA mice appeared to correlate with differences in the metabolism/detoxification of this drug. In conclusion, mouse strains that differ in susceptibility to two-stage liver carcinogenesis provide excellent opportunities to investigate the genetic and/or biochemical mechanisms responsible for these differences. Understanding these mechanisms may lead to the identification of factors that affect liver tumor development not only in mice but in other species as well.

Adenoma↗
PubMed1988

Genetic complementation of defects in vaccine-induced immunity against Schistosoma mansoni in P- and A-strain inbred mice.

Inbred P- and A-strain mice are deficient in their capacity to develop resistance to challenge infection in response to vaccination with irradiated cercariae of Schistosoma mansoni and are also defective in their cell-mediated response as assessed by the activity of antigen-elicited macrophages in killing schistosome larvae in vitro. In contrast, vaccinated (P x A)F1 mice displayed high levels of both immunity to challenge and macrophage larvicidal activity, indicating that the P- and A-strain defects in the vaccine-induced response are controlled by distinct genetic loci.

Animals↗
PubMed1979

Genetic regulation of mup production in recombinant inbred mice.

Inbred strains of mice excrete all three major urinary proteins (mups) when induced by testosterone, but differ as to the relative proportions and total levels of each mup present. We have now determined the urinary mup phenotypes before and after testosterone treatment of seven recombinant inbred strains derived from progenitor strains exhibiting different mup phenotypes. The results confirm previous observations indicating that total control of mup protein production is a multigenic process. One locus, Mup-a on chromosome 4, determines the relative mup protein proportions after induction by testosterone. Mup-a, together with other genetic sites, determines the basal mup proportions. Genes other than Mup-a determine the kinetics of mup induction and total mup excretion.

Alleles↗
PubMed1982

Experimental infection of inbred mice with herpes simplex virus. IV. Comparison of interferon production and natural killer cell activity in susceptible and resistant adult mice.

Inbred mouse strains differ in susceptibility to infection with herpes simplex virus type 1 or type 2 (HSV-1, HSV-2). In this study interferon production was tested in the peritoneal exudate of mice after intraperitoneal (i.p.) injection of HSV-1 or HSV-2. In HSV-resistant mice (C57 BL/6, C3 H/HeJ) high titers of interferon were already present 2 to 4 hours after injection. In comparison, less resistant mice (DBA/2, AKR) lacked this early response. There was no correlation between interferon titers and resistance at post-infection times later than twelve hours. At twelve hours, however, high titers of HSV were detected in the peritoneum of DBA/2 mice and significantly lower titers in C57 BL/6 mice. In a comparative analysis of eight different inbred mouse strains, again early (2 to 4 hours) interferon production was correlated to resistance. In assays of HSV-stimulated early (24 hours) NK cell responses not only the good interferon producer strains but also one of the less resistant low interferon producers (BALB/c) showed significant cytotoxic activities. Conversely, SJL mice that are very low in HSV-induced NK cell activity are resistant and show high early interferon responses at the local site.

Animals↗
PubMed1993

Effect of dietary cholesterol and taurocholate on cholesterol 7 alpha-hydroxylase and hepatic LDL receptors in inbred mice.

Compared to BALB/c mice, inbred C57BL/6 mice are more susceptible to developing fatty streak atherosclerotic lesions when fed a cholesterol-rich diet containing taurocholate. We examined the metabolic basis for the taurocholate requirement. In contrast to widely accepted assumptions, taurocholate did not increase cholesterol absorption in either strain of mouse. However, in susceptible C57BL/6 mice, taurocholate was required to increase plasma concentrations of apoB. In both strains, the cholesterol-rich diet increased both the activity and mRNA for 7 alpha-hydroxylase, a compensatory response to maintain cholesterol homeostasis. In both strains, adding taurocholate to the diet suppressed both the activity and mRNA for 7 alpha-hydroxylase, thus blocking this important compensatory response. The cholesterol-rich diet (without taurocholate) significantly increased hepatic cholesterol content in both strains of mice, but repressed low density lipoprotein (LDL) receptor mRNA only in BALB/c mice (not in C57BL/6 mice). However, adding taurocholate to the cholesterol-rich diet did decrease LDL receptor mRNA in C57BL/6 mice. In C57BL/6, but not in BALB/c mice, there was a linear parallel relationship between 7 alpha-hydroxylase mRNA and LDL receptor mRNA. These data show the existence of strain-specific differences in the effects of dietary cholesterol and taurocholate on 7 alpha-hydroxylase and LDL receptor expression. The combined data suggest that genetic factors determine how the expression of hepatic LDL receptors responds to dietary cholesterol and taurocholate.

Animals↗
PubMed1982

Synaptosomal uptake studies on recombinant inbred mice; neurotransmitter interaction and behavioral correlates.

The uptake of noradrenaline, choline and GABA into whole brain synaptosomes from the mice inbred strains C57BL/6By, BALB/cBy, their reciprocal crosses and seven recombinant inbred strains derived from the F2 crosses was measured in order to study the relation between different neurotransmitter systems and their possible correlations with behavioral parameters. Analysis of variance demonstrated significant differences in both Vmax and Km for each substrate between the inbred strains studied. Only the Km for GABA uptake did not reach significance although a strong trend (P = 0.07) was apparent. For none of the uptake parameters clear strain distribution patterns were found. A positive phenotypic as well as genotypic correlation was found between the Vmax and Km for noradrenaline, choline and GABA uptake. A genetic analysis showed a positive correlation between the Vmax for noradrenaline and choline uptake. Since prior to these neurochemical studies, all subjects were tested in a variety of behavioral paradigms, phenotypic and genotypic correlations between behavioral and neurochemical parameters could be calculated. The most consistent correlations were found between noradrenaline and choline uptake and water consumption and the preference ratio as measured in a conditioned taste aversion test.

Animals↗