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ToxSci Advance Access published online on September 26, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg250
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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Received August 8, 2003; accepted September 12, 2003
© 2003 Society of Toxicology

Immunotoxicology

Developmental Atrazine Exposure Suppresses Immune Function in Male, but not Female Sprague-Dawley Rats

Andrew A. Rooney 1*, Raymond A. Matulka 2, and Robert Luebke 3

1 College of Veterinary Medicine, Anatomy, Physiological Sciences and Radiology, NCSU, Raleigh, North Carolina 27695
2 Curriculum in Toxicology, UNC, Research Triangle Park, North Carolina 27710
3 Immunotoxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, U. S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711

* To whom correspondence should be addressed. E-mail: rooney.andrew{at}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 .


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