Neonatal mouse hip joint and hindlimb anomalies induced by prenatal exposure to Ara-C.
To induce hip joint anomalies and assess their relationship with hindlimb anomalies, pregnant mice (Jcl;ICR) were injected intraperitoneally with a single dose of 5.0 or 7.5 mg/kg of cytosine arabinoside (Ara-C) on dg 8, 9.5, or 11. On the 24th postnatal day, surviving offspring were stained by alizarin red S and anomalies were observed. Hip joint anomalies were observed only in one group exposed to 7.5 mg/kg on dg 9.5; the incidence of the hip joint anomalies in this group was about 30%. The types of hip anomalies observed were femoral shaft dysplasia, pseudoarthrosis of the femur, femoral head dysplasia, acetabular dysplasia, fusion between the femoral head and acetabulum, and pseudoarthrosis of the coxal bone. All of these anomalies were associated with preaxial hyperplasia of the hind paws and lower leg anomalies. Strangely, while newborns with no hip joint anomalies had a fairly high rate of oligodactyly, no newborn with hip joint anomalies had oligodactyly.[1]References
- Neonatal mouse hip joint and hindlimb anomalies induced by prenatal exposure to Ara-C. Chiba, K., Ishikawa, H., Rahman, M.E., Endo, A. Reprod. Toxicol. (1996) [Pubmed]
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