Vitamin C prevents hypothyroidism associated neuronal damage in the hippocampus of neonatal and juvenile rats: A stereological study

Khordad, Elnaz; Alipour, Fatemeh; Beheshti, Farimah; Hosseini, Mahmoud; Rajabzadeh, Aliakbar; Asiaei, Farimah; Seghatoleslam, Masoumeh

doi:10.1016/j.jchemneu.2017.11.011

Cited by 16 publications

(11 citation statements)

References 49 publications

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“…These alterations are attributed to hippocampal damage, for hypothyroidism is associated with cell damage of the pyramidal neurons of the hippocampus in both rats (Alva-Sánchez et al, 2009a) and humans (Cooke et al, 2014). Hypothyroid rats show reductions in the total weight of the hippocampus and in the volume on the Ammon's horn (Madeira et al, 1992), which is consistent with an increase in the proportion of atrophic neurons in this region (Alva-Sánchez et al, 2009b;Khordad et al, 2018) and a reduction of the number of pyramidal cells particularly in CA1 (Madeira et al, 1992). Along with this, dendritic arborization and dendritic spine density are also reduced in the pyramidal cells of CA1 and CA3 (Sala-Roca et al, 2008).…”

Section: Introductionmentioning

confidence: 73%

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

Martínez-Salazar¹,

Villanueva²,

Pacheco-Rosado³

et al. 2020

Acta Neurobiologiae Experimentalis

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Adult-onset hypothyroidism is associated with an increase in cell atrophy of the hippocampal pyramidal neurons. Physical exercise implies diverse actions on the neural tissue that promote neuron proliferation and survival. The beneficial effects of exercise seem to be inversely linked to its intensity, so that strenuous exercise has reduced protective effects. In this study we evaluated the capacity of a moderate forced-exercise routine to counteract the neurodegenerative effects of a hypothyroid condition induced during adulthood.Simultaneously with a chronic anti-thyroid chemical treatment, a group of rats was forced to walk in a motorized wheel for 30 min daily five times a week. In four weeks of treatment the rats developed a plain hypothyroid condition that in non-exercised rats was accompanied by a marked increase in the number of atrophic cells in all CA regions of the hippocampus. The forced-exercise treatment did not counter the development of hypothyroidism and its signs, but it did prevent almost completely the associated neuronal damage in all CA regions. The forced exercise also improved the cognitive function in a spatial-learning test. These results indicate that moderate exercise has the potential to prevent the structural and functional deficits associated with a hypothyroid condition.

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Section: Introductionmentioning

confidence: 73%

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

Martínez-Salazar¹,

Villanueva²,

Pacheco-Rosado³

et al. 2020

Acta Neurobiologiae Experimentalis

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“…The administration of vitamin C by intracerebroventricular microinjection before lipopolysaccharide exposure has protected the male C57BL/6 mice from cognitive impairments as the antioxidant prevented the activation of microglia and the release of pro-inflammatory cytokines, decreased the malondialdehyde levels, and increased the activity of superoxide dismutase [114]. Moreover, vitamin C has also proved to protect male rat pups against hippocampal neuronal induced by neonatal hypothyroidism [115] and protected cells against methamphetamine toxicity by attenuating ROS production, apoptosis, and autophagy [116].…”

Section: Antioxidants For Neuroprotectionmentioning

confidence: 99%

Antioxidant Therapies for Neuroprotection—A Review

Teleanu

Chircov

Grumezescu

et al. 2019

JCM

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Although moderate concentrations of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are crucial for various physiological processes within the human body, their overproduction leads to oxidative stress, defined as the imbalance between the production and accumulation of ROS and the ability of the body to neutralize and eliminate them. In the brain, oxidative stress exhibits significant effects, due to its increased metabolical activity and limited cellular regeneration. Thus, oxidative stress is a major factor in the progressive loss of neurons structures and functions, leading to the development of severe neurodegenerative disorders. In this context, recent years have witnessed tremendous advancements in the field of antioxidant therapies, with a special emphasis for neuroprotection. The aim of this paper is to provide an overview of the oxidative stress and antioxidant defense mechanisms and to present the most recent studies on antioxidant therapies for neuroprotection.

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“…Clinical and experimental reports suggest that THs replacement therapy can partially reverse negative effects of hypothyroidism on learning and memory, but a full recovery of T3 content in target Loading [MathJax]/jax/output/CommonHTML/jax.js tissues, especially in the brain, is far from reach and therefore, more appropriate treatments are required (Chaalal et al 2019). It has been reported that antioxidant agents are able to decrease the side effects of hypothyroidism on learning and memory (Asiaei et al 2017;Beheshti et al 2017;Baghcheghi et al 2018a; Khordad et al 2018;Baghcheghi et al 2020). In addition, some of the vitamins have been shown…”

Section: Introductionmentioning

confidence: 99%

Folic acid attenuated learning and memory impairment via inhibition of oxidative damage and acetylcholinesterase activity in hypothyroid rats

et al. 2021

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Hypothyroidism has been associated with cognitive decline. Considering the role that has been suggested for folic acid (FA) in cognitive performance, the present study was designed to investigate the effects of FA against hypothyroidism-induced cognitive impairment, oxidative damage and acetylcholinesterase (AChE) activity alterations in propylthiouracil (PTU)-induced hypothyroid rats.In this study, PTU (0.05% in drinking water) and FA (5, 10, and 15 mg/kg, oral gavage) were administered to the rats for a period of 7 weeks. Then, behavioral performance was tested using Morris water maze (MWM) and passive avoidance (PA) tasks. Finally, oxidative stress indicators and AChE activity were assayed in the brain tissues.The impairing effect of hypothyroidism on cognitive performance was markedly alleviated by FA especially at the higher doses. In the MWM test, FA reduced escape latency and travelled distance, compared to the non-treated hypothyroid group. In the PA test, the latency to enter the dark chamber was signi cantly enhanced by FA as compared to the non-treated hypothyroid group (p < 0.05-p < 0.001).Besides, FA attenuated AChE activity and malondialdehyde level but increased superoxidase dismutase enzyme activity and total thiol content (p < 0.05-p < 0.001).In conclusion, FA could improve learning and memory ability in hypothyroid rats. The observed protective effects may be mediated through regulation of oxidative stress and AChE activity.

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Vitamin C prevents hypothyroidism associated neuronal damage in the hippocampus of neonatal and juvenile rats: A stereological study

Cited by 16 publications

References 49 publications

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

Antioxidant Therapies for Neuroprotection—A Review

Folic acid attenuated learning and memory impairment via inhibition of oxidative damage and acetylcholinesterase activity in hypothyroid rats

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