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© 1990 Oxford University Press

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Long-Term Alteration of Adult Bone Marrow Colony Formation by Prenatal Chlordane Exposure

JOHN B. BARNETT*, BENNY L. BLAYLOCK*, JAY GANDY{dagger}, JAY H. MENNA*, RICHARD DENTON* and LEE S. F. SODERBERG*

*Department of Microbiology and Immunology, University of Arkansas for Medical Sciences Little RocK Arkansas 72205 {dagger}Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences Little RocK Arkansas 72205

Received May 19, 1989; accepted December 1, 1989

Long-Term Alteration of Adult Bone Marrow Colony Formation by Prenatal Chlordane Exposure. BARNETT, J. B., BLAYLOCK, B. L., GANDY, J., MENNA, J. H., DENTON, R., AND SODERBERG, L. S. F. (1990). Fundam. Appl. Toxicol. 14, 688–695. Female mice were treated with either 0, 4, or 8 mg of chlordane per kilogram body weight daily for 18 days during pregnancy. The offspring of these mice were assayed for bone marrow hematopoietic activity at 100 and 200 days of age. Hematopoietic activity was evaluated for in vitro granulocyte-macrophage colony-forming units (GM-CFU) and m vivo spleen CFU (CFU-S). The consistent finding was a significant depression both of the numbers of bone marrow GM-CFU and of the CFU-S in offspring exposed to either 4 or 8 mg/kg chlordane even at 100 and 200 days after cessation of treatment. Prenatal treatment with chlordane did not affect the number of recoverable viable bone marrow cells at either of these time points. Ontological development was selectively affected by chlordane exposure, since subchronic (18 day) treatment of adult mice did not significantly alter bone marrow GM-CFU or CFU-S levels. These data suggest that the decreased delayed-type hypersensitivity reactions noted previously in mice exposed to chlordane prenatally may be due to a change in the functional capacity of myeloid lineage cells rather than altered T cell function.


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