Maternal exposure causes mitochondrial dysfunction in brain, liver, and heart of mouse fetus: An explanation for perfluorooctanoic acid induced abortion and developmental toxicity

被引：50
|
作者：
Salimi, Ahmad [1 ]
Jahromi, Mahnia Nikoosiar [2 ]
Pourahmad, Jalal [2 ]
机构：
[1] Ardabil Univ Med Sci, Sch Pharm, Dept Pharmacol & Toxicol, Ardebil, Iran
[2] Shahid Beheshti Univ Med Sci, Dept Pharmacol & Toxicol, Fac Pharm, POB 14155-6153, Tehran, Iran
来源：
ENVIRONMENTAL TOXICOLOGY | 2019年 / 34卷 / 07期
关键词：
developmental toxicity; embryo-fetal toxicity; mitochondria; perfluorooctanoic acid (PFOA); SULFONATE PFOS; JUSTIFICATION; DISORDER; PPAR;
D O I：
10.1002/tox.22760
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
Perfluorooctanoic acid (PFOA) is an octanoic acid and is found in wildlife and humans. We have investigated mitochondrial toxicity in isolated mitochondria from, placenta, brain, liver, and heart after oral exposure with PFOA in mice during gestational days (7-15). Histopathological examination and mitochondrial toxicity parameters were assayed. Results indicated that PFOA decreased the weight of the fetus and placenta, the length of the fetus and the diameter of the placenta, dead fetuses and dead macerated fetuses in treated mice with 25 mg/kg. Histopathological examination showed that PFOA induced pathological abnormalities in liver, brain, heart, and placenta. Also, PFOA induced mitochondria toxicity in brain, liver, heart of mouse fetus. Our results indicate that PFOA up to 20 mg/kg exposure adversely affect embryofetal/developmental because for mitochondria dysfunction. These results suggested that mitochondrial dysfunction induced by PFOA in liver, heart, and brain lead to developmental toxicity and abnormality in tissues.
引用
收藏
页码：878 / 885
页数：8
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