Gestational exposure to acrylamide suppresses luteal endocrine function through dysregulation of ovarian angiogenesis, oxidative stress and apoptosis in mice

被引:14
作者
Yu, Dainan [1 ]
Jiang, Xun [1 ,2 ]
Ge, Wenjing [1 ,3 ]
Qiao, Bo [1 ]
Zhang, Dalei [1 ]
Liu, Hui [1 ]
Kuang, Haibin [1 ,4 ]
机构
[1] Nanchang Univ, Dept Physiol, Basic Med Coll, Nanchang 330006, Jiangxi, Peoples R China
[2] Nanchang Univ, Dept Clin Med, Clin Med Coll 1, Nanchang 330006, Jiangxi, Peoples R China
[3] Nanchang Univ, Sch Queen Mary, Dept Clin Med, Nanchang 330006, Jiangxi, Peoples R China
[4] Nanchang Univ, Med Expt Teaching Ctr, Jiangxi Prov Key Lab Reprod Physiol & Pathol, Nanchang 330006, Jiangxi, Peoples R China
关键词
Acrylamide; Corpus luteum; Endocrine; Ovary; Pregnancy; GENE-EXPRESSION; HISTOPATHOLOGY; PARAMETERS; HORMONES;
D O I
10.1016/j.fct.2021.112766
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The discovery of acrylamide in various carbohydrate-rich foods cooked at high temperatures has attracted public health concerns. This study aimed to elucidate the effects and mechanisms additional with acrylamide exposure on the luteal function in vivo during early- and mid-pregnancy. Mice were fed with different dosages of acrylamide (0, 10 and 50 mg/kg/day) by gavage from gestational days (GD) 3 to GD 8 or GD 13. The results indicated that acrylamide exposure significantly decreased levels of serum progesterone and estradiol, and the numbers and relative areas of ovarian corpora lutea. The expression levels of Hsd3b1, Cyp11a1 and Star mRNA markedly reduced in acrylamide-treated ovaries. Furthermore, acrylamide exposure obviously suppressed the activities of catalase and superoxide dismutase, but increased the levels of H2O2 and malondialdehyde. Additionally, acrylamide treatment significantly inhibited luteal angiogenesis and induced the apoptosis of ovarian cells by upregulation of P53 and Bax protein and down-regulation of Bcl-2 protein. Thus, our results showed that gestational exposure to acrylamide significantly inhibited luteal endocrine function via dysregulation of ovarian angiogenesis, oxidative stress and apoptosis in vivo.
引用
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页数:8
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