Vitamin E effects on developmental disorders in fetuses and cognitive dysfunction in adults following acrylamide treatment during pregnancy.


Erdemli Z., ERDEMLİ M. E., TÜRKÖZ Y., Yigitcan B., ALADAĞ M. A., ÇİĞREMİŞ Y., ...More

Biotechnic & histochemistry : official publication of the Biological Stain Commission, vol.96, pp.11-19, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 96
  • Publication Date: 2021
  • Doi Number: 10.1080/10520295.2020.1751880
  • Journal Name: Biotechnic & histochemistry : official publication of the Biological Stain Commission
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, Biotechnology Research Abstracts, CAB Abstracts, EMBASE, Food Science & Technology Abstracts, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.11-19
  • Keywords: acrylamide, brain derived neurotrophic factor, cognitive functions, neurotoxicity, postnatal development, pregnancy, vitamin E, EXPOSURE, GENOTOXICITY, METABOLISM, CELLS, ACID, RATS
  • Inonu University Affiliated: Yes

Abstract

We investigated the effects of acrylamide (AA) and vitamin E treatment during pregnancy on brain tissues of fetuses and on adult rats. Pregnant rats were divided into five groups: control, corn oil, vitamin E, AA, vitamin E +AA. The rats administered AA received10 mg/kg/day and those administered vitamin E received 100 mg/kg/day both by via oral gavage for 20 days. On day 20 of pregnancy, half of the pregnant rats were removed by cesarean section in each group. Morphological development parameters were measured in each fetus and histopathological, biochemical and genetic analyses were conducted on the fetuses. The remaining pregnant rats in each group gave birth to the fetuses vaginally and biochemical, histopathological, genetic and cognitive function tests were conducted when the pups were 8 weeks old. AA administration caused adverse effects on fetus number, fetal weight, crown-rump length, placenta and brain weight. AA negatively affected malondialdehyde, reduced glutathione, total oxidant and antioxidant status, brain derived neurotrophic factor (BDNF) levels, brain tissue morphology, histopathology error score and gene expression (BDNF/beta-actin mRNA ratio) in fetuses. AA administration caused disruption of biochemical, histopathological and cognitive functions in adult rats. Vitamin E provided protection against neurotoxicity in both fetuses and adult rats. We conclude that exposure to AA during pregnancy should be avoided and adequate amounts of antioxidants, such as vitamin E, should be consumed.