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DEVELOPMENTAL ATRAZINE EXPOSURE SUPPRESSES IMMUNE FUNCTION IN MALE, BUT NOT FEMALE SPRAGUE-DAWLEY RATS
Citation:
Rooney, A A., R. A. Matulka, AND R W. Luebke. DEVELOPMENTAL ATRAZINE EXPOSURE SUPPRESSES IMMUNE FUNCTION IN MALE, BUT NOT FEMALE SPRAGUE-DAWLEY RATS. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 76(2):366-375, (2003).
Description:
Developmental Atrazine Exposure Suppresses Immune Function in Male, but not Female Sprague-Dawley Rats
Andrew A. Rooney,*,1 Raymond A. Matulka,? and Robert Luebke?
*College of Veterinary Medicine, Anatomy, Physiological Sciences and Radiology, NCSU, Raleigh, North Carolina 27695, rooney.andrew@epa.gov; ?Curriculum in Toxicology, UNC, Research Triangle Park, North Carolina 27710,matulka.ray@epa.gov; ?Immunotoxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, U. S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711, luebke.robert@epa.gov
Running Head: Developmental Immunotoxicity of Atrazine
Section: Immunotoxicology
Disclaimer
This report has been reviewed by the Environmental Protection Agency's Office of Research and Development, and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
Address for Correspondence:
Andrew A. Rooney
US Environmental Protection Agency
Division of Experimental Toxicology
Immunotoxicology Branch, B 143-01
Research Triangle Park, NC 27711
Tel: (919) 541-1492
Fax: (919) 541-3538
e-mail: rooney.andrew@epa.gov
Abstract
Each year 75 million pounds of the broadleaf herbicide atrazine (ATR) are applied to crops in the US. Despite limited solubility, ATR is common in ground and surface water, making it of regulatory concern. ATR suppresses the immunomodulatory hormones prolactin (PRL) and the thyroid hormones (THs), with developmental exposure to ATR permanently disrupting PRL regulation. We hypothesized that ATR may cause developmental immunotoxicity through its disruption of PRL or THs. To test this hypothesis, pregnant Sprague-Dawley (SD) rats were exposed to 35 mg ATR/kg/d from gestational day (GD) 10 through post-natal day (PND) 23. Separate groups were exposed to bromocryptine (BCR at 0.2 mg/kg/2x/day) to induce hypoprolactinemia or to propylthiouracil (PTU at 2 mg/kg/day) to induce hypothyroidism. After offspring reached immunologic maturity (at least 7-weeks-old), the following immune functions were evaluated: natural killer (NK) cell function, delayed-type hypersensitivity (DTH) responses, phagocytic activity of peritoneal macrophages and antibody response to sheep erythrocytes (SRBC). ATR decreased the primary antibody and DTH responses in male offspring only. Neither PTU, nor BCR, caused immunosuppression in any measured variable, although PTU increased phagocytosis by peritoneal macrophages. These results demonstrate that developmental exposure to ATR produced gender-specific changes in immune function in adult rats, and suggest that immune changes associated with ATR are not mediated through suppression of PRL or THs.
Key Words: atrazine; developmental immunotoxicity; prolactin; thyroid hormones; rats; pesticides