Khanna V K, Husain R, Seth P K
Industrial Toxicology Research Centre, Lucknow, India.
J Toxicol Environ Health. 1992 Aug;36(4):293-305. doi: 10.1080/15287399209531640.
Exposure to acrylamide (3-10 mg/kg body weight) was found to be lethal for protein-deficient pregnant rats as evidenced by their increased mortality. It had no such effect on the normal protein diet fed pregnant and nonpregnant rats and the protein-malnourished nonpregnant rats. Protein deficiency during pregnancy caused a significant decrease in the activity of brain monoamine oxidase and acetylcholinesterase and striatal [3H]spiperone binding, known to label dopamine receptors; had no significant effect on the binding of 3H-QNB (quinuclidinyl benzilate) to cerebellar and [3H]diazepam to frontocortical membranes, known to label muscarinic and benzodiazepine receptors, respectively; and had no significant effect on brain glutathione (GSH) levels in comparison with pregnant rats fed normal protein diet. Exposure to acrylamide (2 mg/kg body weight) in protein-malnourished pregnant rats caused a marked decrease in the activity of monoamine oxidase and acetylcholinesterase and also in the binding of [3H]spiperone, [3H]QNB, and [3H]diazepam to striatal, cerebellar, and frontocortical membranes, respectively. Kinetic studies revealed that decreased binding of these ligands in the specific brain regions were due to decreased receptor sites (Bmax). A reduction in the brain glutathione content was also observed in these animals in comparison with those fed a low-protein diet during pregnancy. Pregnant rats fed a normal-protein diet on acrylamide exposure, however, showed no such biochemical changes in comparison with the pregnant rats fed normal protein diet. Also, no effect on any of the parameters studied was observed in the adult nonpregnant rats fed a low-protein diet (for 18 d) and those exposed to the monomer (d 6-17) fed either a normal- or low-protein diet in comparison with respective controls. The results indicate that pregnancy under conditions of malnutrition modifies the susceptibility of pregnant rats toward acrylamide.
研究发现，丙烯酰胺（3 - 10毫克/千克体重）对蛋白质缺乏的怀孕大鼠具有致死性，其死亡率增加即证明了这一点。而对于喂食正常蛋白质饮食的怀孕和未怀孕大鼠以及蛋白质营养不良的未怀孕大鼠，丙烯酰胺并无此作用。孕期蛋白质缺乏导致脑单胺氧化酶和乙酰胆碱酯酶活性显著降低，以及纹状体[3H]司哌罗宁结合显著降低，后者可标记多巴胺受体；对3H - QNB（东莨菪碱）与小脑膜的结合以及[3H]地西泮与前额皮质膜的结合并无显著影响，前者可标记毒蕈碱受体，后者可标记苯二氮䓬受体；与喂食正常蛋白质饮食的怀孕大鼠相比，对脑谷胱甘肽（GSH）水平也无显著影响。蛋白质营养不良的怀孕大鼠接触丙烯酰胺（2毫克/千克体重）会导致单胺氧化酶和乙酰胆碱酯酶活性显著降低，同时[3H]司哌罗宁、[3H]QNB和[3H]地西泮分别与纹状体、小脑和前额皮质膜的结合也显著降低。动力学研究表明，这些配体在特定脑区结合减少是由于受体位点（Bmax）减少。与孕期喂食低蛋白饮食的大鼠相比，这些动物的脑谷胱甘肽含量也有所降低。然而，喂食正常蛋白质饮食的怀孕大鼠接触丙烯酰胺后，与喂食正常蛋白质饮食的怀孕大鼠相比，并未出现此类生化变化。此外，与各自的对照组相比，喂食低蛋白饮食18天的成年未怀孕大鼠以及在第6 - 17天接触单体且喂食正常或低蛋白饮食的成年未怀孕大鼠，在所研究的任何参数上均未观察到影响。结果表明，营养不良条件下的怀孕会改变怀孕大鼠对丙烯酰胺的易感性。
