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Publication : Alterations in growth, haematopoiesis and serum chemistry profiles in fitness 1(4226SB) mutant mice.

First Author  Schultze AE Year  1997
Journal  Comp Haematol Int Volume  7
Issue  3 Pages  143-151
Mgi Jnum  J:43923 Mgi Id  MGI:1099145
Doi  10.1007/BF02652592 Citation  Schultze AE, et al. (1997) Alterations in growth, haematopoiesis and serum chemistry profiles in fitness 1(4226SB) mutant mice. Comp Haematol Int 7(3):143-151
abstractText  We investigated patterns of growth, haematopoiesis and alterations in serum chemistry profiles that were associated with an N-ethyl-N-nitrosourea-induced mutation in the fitness I locus in chromosome 7 in mice. Mice hemizygous for the fit 1 mutation [c fit 1(4226SB)/Df(c Mod2 sh1)(26DVT)] had growth retardation characterised by decreased body weights, shorter body lengths and tail lengths at 40 and 60 days of age compared to normal homozygous control, mice [c(ch)+/c(ch)+]. Haemograms revealed that mice hemizygous for the fit 1(4226SB) mutation that were killed 40 days had microcytic, hypochromic anaemia that was mildly regenerative in nature. No significant differences were detected in total leucocyte counts, differential leucocyte counts and platelets counts between hemizygous mutant mice and control mice. Haemograms from the surviving mice hemizygous for the fit 1(4226SB) mutation that were killed at 60 days indicated that the haemoglobin concentrations, mean corpuscular volumes and mean corpuscular haemoglobin concentrations were significantly decreased compared to normal controls. The reticulocyte counts and the platelet counts from the mice hemizygous for the fit 1(4226SB) mutation were mildly increased were compared to normal controls killed at 60 days. Serum chemistry analyses at 40 days of age indicated that the hemizygous fit I mutant mice had hypoproteinaemia characterised by hypoalbuminaemia and hypoglobulinaemia. They also developed hypoglycaemia, mild hyperphosphataemia and moderate elevation in the activity of alkaline phosphatase in serum. Quantitative isozyme analysis indicated that the increase in total serum alkaline phosphatase activity in the hemizygous mutant mice was due to an increase in the bone isozyme. In addition to those alterations in the serum chemistry profile noted above, hemizygous mutant mice killed at 60 days had an extremely mild increase in urea nitrogen concentration and mildly increased activities of alanine aminotransferase and aspartate aminotransferase in serum. From these data, it was concluded that the fit 1(4226SB) mutation in mice causes growth retardation, microcytic, hypochromic anaemia, and alterations in serum chemistry profiles that suggest lesions in one or more organ systems. The exact mechanism(s) by which the fit 1(4226SB) mutation mediates these lesions remains to be elucidated.
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