PMID- 14514952
OWN - NLM
STAT- MEDLINE
DCOM- 20040806
LR  - 20131121
IS  - 1096-6080 (Print)
IS  - 1096-0929 (Linking)
VI  - 76
IP  - 2
DP  - 2003 Dec
TI  - Developmental atrazine exposure suppresses immune function in male, but not 
      female Sprague-Dawley rats.
PG  - 366-75
AB  - Each year, 75 million pounds of the broadleaf herbicide atrazine (ATR) are 
      applied to crops in the United States. 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 
      postnatal 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 the 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 the suppression of PRL or THs.
FAU - Rooney, Andrew A
AU  - Rooney AA
AD  - College of Veterinary Medicine, Anatomy, Physiological Sciences and Radiology, 
      North Carolina State University, Raleigh, North Carolina 27695, USA. 
      rooney.andrew@epa.gov
FAU - Matulka, Raymond A
AU  - Matulka RA
FAU - Luebke, Robert W
AU  - Luebke RW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20030926
PL  - United States
TA  - Toxicol Sci
JT  - Toxicological sciences : an official journal of the Society of Toxicology
JID - 9805461
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Herbicides)
RN  - 3A64E3G5ZO (Bromocriptine)
RN  - 721M9407IY (Propylthiouracil)
RN  - QJA9M5H4IM (Atrazine)
SB  - IM
MH  - *Abnormalities, Drug-Induced
MH  - Adjuvants, Immunologic/administration & dosage/*toxicity
MH  - Administration, Oral
MH  - Animals
MH  - Animals, Suckling
MH  - Atrazine/administration & dosage/*toxicity
MH  - Body Weight/drug effects
MH  - Bromocriptine/toxicity
MH  - Congenital Hypothyroidism
MH  - Female
MH  - Herbicides/administration & dosage/*toxicity
MH  - Hypoproteinemia/blood/chemically induced/congenital
MH  - Hypothyroidism/blood/chemically induced
MH  - Immune System/abnormalities/*drug effects/growth & development
MH  - Immunity/*drug effects
MH  - Lactation/*drug effects
MH  - Longevity/drug effects
MH  - Organ Size/drug effects
MH  - Pregnancy
MH  - Propylthiouracil/toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sex Factors
EDAT- 2003/09/30 05:00
MHDA- 2004/08/07 05:00
CRDT- 2003/09/30 05:00
PHST- 2003/09/30 05:00 [pubmed]
PHST- 2004/08/07 05:00 [medline]
PHST- 2003/09/30 05:00 [entrez]
AID - kfg250 [pii]
AID - 10.1093/toxsci/kfg250 [doi]
PST - ppublish
SO  - Toxicol Sci. 2003 Dec;76(2):366-75. doi: 10.1093/toxsci/kfg250. Epub 2003 Sep 26.