Department of Obstetrics, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China (mainland).
Med Sci Monit. 2017 Aug 12;23:3890-3896. doi: 10.12659/msm.903006.
BACKGROUND The aim of this study was to investigate the cardiotoxicity and mechanism of particulate matter 2.5 (PM2.5) exposure on offspring rats during pregnancy. MATERIAL AND METHODS Wistar rats were used to establish a PM2.5 exposure animal model during pregnancy, and they were divided into a control group, a low-dose group, a middle-dose group, and a high-dose group according to PM2.5 exposure dose. The pathological changes of heart tissue, the rate of myocardial cell apoptosis, the levels of LDH, AST, and CM-KB in serum, and the difference in mitochondrial fusion genes (OPA1 and Mfn1) and mitochondrial genes (Drp1 and Fis1) were compared among groups. RESULTS The arrangement of myocardial fibers in offspring mice of PM2.5 exposure groups became disordered, the shape of some cardiomyocytes became irregular, and some staining darker nuclei appeared. The apoptotic rates of myocardium in offspring rats exposed to PM2.5 were (12.61±0.93)% in the low-dose group, (25.14±1.53)% in the middle-dose group, and (30.13±1.50)% in the high-dose group, which were all significantly higher than in the control group (9.12±0.80)% (P<0.05). The levels of LDH, AST, and CM-KB and the expression of OPA1, Mfn1, Drp1, and Fis1 in offspring mice of PM2.5 exposure groups increased with the increase of PM2.5 exposure dose, and were significantly higher than that of the control group (P<0.05). CONCLUSIONS The mitochondria of the offspring mice were damaged due to the abnormal expression of mitochondrial fusion/splicing gene by PM2.5 exposure during pregnancy, and the hearts of offspring mice were damaged due to damaged mitochondria.
本研究旨在探讨孕期暴露于细颗粒物 2.5（PM2.5）对仔鼠的心脏毒性及其机制。
采用 Wistar 大鼠建立 PM2.5 孕期暴露动物模型，根据 PM2.5 暴露剂量将其分为对照组、低剂量组、中剂量组和高剂量组。比较各组仔鼠心脏组织病理学变化、心肌细胞凋亡率、血清中 LDH、AST、CM-KB 水平，以及线粒体融合基因（OPA1、Mfn1）和线粒体基因（Drp1、Fis1）的差异。
PM2.5 暴露组仔鼠心肌纤维排列紊乱，部分心肌细胞形态不规则，出现染色较深的核。PM2.5 暴露组仔鼠心肌细胞凋亡率分别为低剂量组（12.61±0.93）%、中剂量组（25.14±1.53）%和高剂量组（30.13±1.50）%，均显著高于对照组（9.12±0.80）%（P<0.05）。PM2.5 暴露组仔鼠血清中 LDH、AST、CM-KB 水平及 OPA1、Mfn1、Drp1、Fis1 表达均随 PM2.5 暴露剂量的增加而升高，且均显著高于对照组（P<0.05）。
孕期 PM2.5 暴露可通过异常表达线粒体融合/剪接基因导致仔鼠线粒体损伤，进而导致仔鼠心脏损伤。
