| Literature DB >> 29179976 |
Elnaz Khordad1, Fatemeh Alipour1, Farimah Beheshti2, Mahmoud Hosseini3, Ali Akbar Rajabzadeh4, Farimah Asiaei1, Masoumeh Seghatoleslam5.
Abstract
Hypothyroidism causes an imbalance in antioxidant and pro-oxidants criteria in the brain and enhances the concentration of reactive oxygen species (ROS), and neuronal damage has been observed following an excessive ROS. The main purpose of this study was to examine the preventive effect of vitamin C on hypothyroidism associated neuronal damage in the hippocampus of neonatal and juvenile rats. Pregnant rats after delivery of their pups were randomly divided into four groups and treated with (1) normal drinking water as a control group, (2) Propylthiouracil (PTU) 0.005% added to drinking water, (3-, 4) PTU + Vit C 10 mg/ kg and PTU + Vit C 100 mg/ kg to drinking water. Treatment was carried out during rat's lactation period until to the postnatal day (PND) 60. To assess the histological and stereological changes that occur in this study, brains of 5 male pups were extracted. The number of dark neurons and apoptotic cells in the hippocampal sub-regions of PTU group was significantly greater than the control group's hippocampal sub-regions. In addition, hypothyroidism induced a reduction in the hippocampal volume and increased the numerical density and the total amount of dark neurons. The vitamin C only dose of 100 mg/kg significantly reduced the number of dark neurons and apoptotic cells (P < 0.01) and considerably weakened the influence of hypothyroidism on the volume reduction of the hippocampus (P < 0.05). The current study suggested that vitamin C administration has a possibility to prevent hippocampal neuronal damage caused by neonatal and juvenile hypothyroidism in rats.Entities:
Keywords: Antioxidant; Apoptosis; Dark neuron; Hypothyroidism; Neuroprotection
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Year: 2017 PMID: 29179976 DOI: 10.1016/j.jchemneu.2017.11.011
Source DB: PubMed Journal: J Chem Neuroanat ISSN: 0891-0618 Impact factor: 3.052