Crépeaux Guillemette, Grova Nathalie, Bouillaud-Kremarik Pascaline, Sikhayeva Nurgul, Salquèbre Guillaume, Rychen Guido, Soulimani Rachid, Appenzeller Brice, Schroeder Henri
Unité de Recherche Animal et Fonctionnalités des Produits Animaux, INRA UC340, Université de Lorraine, Vandoeuvre-lès-Nancy, France.
Laboratory of Analytical Human Biomonitoring-CRP-Santé, Université du Luxembourg, Campus Limpertsberg, 162A, Avenue de la Faiencerie, L-1511 Luxembourg, Luxembourg.
Neurotoxicology. 2014 Jul;43:90-101. doi: 10.1016/j.neuro.2014.03.012. Epub 2014 Apr 4.
Humans are exposed to polycyclic aromatic hydrocarbons (PAHs), a family of ubiquitous neurotoxic pollutants, mainly through ingestion of contaminated food. Developing organisms can be exposed also to PAHs due to the ability of these compounds to pass through the placental barrier as well as through the breast milk. Previous animal studies have reported that the exposure of rats to a 16 PAH mixture at environmental doses strictly limited to gestation did not induce any long-lasting consequences, whereas gestational and lactational PAH exposure induced long-term behavioral and cerebral metabolic effects. In the present study, short-term effects of exposures to the same PAH mixture during gestation, or during gestation and lactation, were assessed by evaluating motor and sensory development of rat pups, and by measuring cerebral cytochrome oxidase activity (a marker of energetic metabolism) in different brain areas. Brain levels of PAHs and some monohydroxylated metabolites were also evaluated in pups at birth and at 21 days of postnatal life. No significant short-term modifications of behavioral development and of cerebral metabolism were observed following an early PAH exposure whatever the dose and the period of exposure. Surprisingly, the same brain levels of concentration of PAHs and metabolites were observed in control and exposed pups in both studies. These analytical results raise the difficulty in overcoming environmental contamination of control animals and the choice of such controls in experimental studies which focus on neurotoxicity of exposure to low levels of pollutants.
人类主要通过摄入受污染的食物接触多环芳烃(PAHs),这是一类普遍存在的神经毒性污染物。发育中的生物体也可能接触到PAHs,因为这些化合物能够穿过胎盘屏障以及通过母乳传递。先前的动物研究报告称,大鼠在严格限于妊娠期的环境剂量下接触16种PAH混合物不会产生任何长期后果,而妊娠期和哺乳期接触PAHs会导致长期的行为和脑代谢影响。在本研究中,通过评估幼鼠的运动和感觉发育,以及测量不同脑区的脑细胞色素氧化酶活性(能量代谢的标志物),来评估在妊娠期或妊娠期和哺乳期接触相同PAH混合物的短期影响。还评估了幼鼠出生时和出生后21天的脑PAHs水平和一些单羟基化代谢物。无论剂量和暴露时期如何,早期PAH暴露后均未观察到行为发育和脑代谢的显著短期变化。令人惊讶的是,在两项研究中,对照幼鼠和暴露幼鼠的脑PAHs和代谢物浓度水平相同。这些分析结果增加了克服对照动物环境污染的难度,以及在关注低水平污染物暴露神经毒性的实验研究中选择此类对照的难度。