Lassiter T Leon, Brimijoin Stephen
Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
Neurotoxicol Teratol. 2008 Mar-Apr;30(2):125-30. doi: 10.1016/j.ntt.2007.10.004. Epub 2007 Nov 6.
Pesticides that target molecules with critical roles in brain function deserve careful scrutiny for potential developmental neurotoxicity. In this study, time-pregnant rats were dosed daily by gavage with chlorpyrifos (2.5 mg/kg) from gestational day 7 through the end of lactation on postnatal day 21 (PND 21), and offspring were weighed regularly from birth until brain harvest at PND 22 or young adulthood (PND 95-101). The chlorpyrifos exposure caused excess weight gain in males beginning at PND 45 and reaching levels 10.5% above control by PND 72, while volumetric measurements showed that the exposed males were also 12% larger than controls. The body weight response showed an inverted U-shaped relation to chlorpyrifos dose. These data suggest delayed disturbances in body weight and density as previously unsuspected adverse consequences of developmental exposure to an environmental pesticide. Although we do not regard our findings as definitive evidence that chlorpyrifos exposure is a risk factor for obesity, the potential implications nonetheless deserve serious consideration.
针对在脑功能中起关键作用的分子的农药，因其潜在的发育神经毒性值得仔细审查。在本研究中，从妊娠第7天到产后第21天（出生后第21天，PND 21）哺乳期结束，对怀孕的大鼠每天经口灌胃给予毒死蜱（2.5毫克/千克），并从出生起定期称重大鼠后代，直到在出生后第22天或成年早期（PND 95 - 101）进行脑采集。毒死蜱暴露导致雄性大鼠从出生后第45天开始体重过度增加，到出生后第72天比对照组高出10.5%，而体积测量显示，暴露的雄性大鼠也比对照组大12%。体重反应与毒死蜱剂量呈倒U形关系。这些数据表明，体重和密度出现延迟紊乱，这是发育过程中接触环境农药以前未被怀疑的不良后果。尽管我们不认为我们的发现是毒死蜱暴露是肥胖风险因素的确凿证据，但潜在影响仍值得认真考虑。
