Effects of selenium treatment on 6-n-propyl-2-thiouracil-induced impairment of long-term potentiation

Bitiktas, S.; Tan, Burak; Batakci, Melek; Kavraal, S.; Dursun, Nurcan; Süer, Cem

doi:10.1016/j.neures.2016.02.001

Cited by 12 publications

(5 citation statements)

References 39 publications

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“…Earlier reports also suggest that early signs of cellular degeneration of germ cells might lead to disturbance of its plasmalemma structure causing shedding [41,42]. Our results on the Se treatment of AgNP-exposed rats showed alleviation of the histopathological changes in testes tissue which is consistent with previous studies that Se can interact in the body of mammals reducing toxicity of some compounds [43][44][45]. It could be that Se administration prevents free radical formation by increasing antioxidant activity of tissue as evident in our studies and prevent AgNP toxicity.…”

Section: Discussionsupporting

confidence: 92%

Sodium Selenite Protects Against Silver Nanoparticle-Induced Testicular Toxicity and Inflammation

Ansar

Abudawood

Hamed

et al. 2016

Biol Trace Elem Res

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Metal nanomaterials hold great potential and play an important role in consumer products. However, the increasing use of nanomaterials has raised concern over inadvertent exposure and potential risks for human health and the environment. Henceforth, in vivo testing of nanoparticles and protection against its toxicity is required. Using rat as an animal model, effect of sodium selenite (Se), an essential trace element, on rat testes exposed to silver nanoparticles (AgNPs) was evaluated. Male rats were treated with AgNPs (5 mg/kg/b.w) i/p or Se (0.2 mg/kg/b.w) by gavage. AgNP administration decreased Glutathione (GSH) levels and activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and increased levels of malondialdehyde (MDA) and expression of interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α). However, treatment with Se increased GSH levels and activities of SOD, CAT, and GPx compared with AgNP-treated group and decreased the level of MDA and inflammatory biomarkers significantly (p < 0.05) as compared with AgNP-treated group. Light microscopic analyses also revealed that AgNP induced histopathological changes in testes tissue. Further, protection by Se on biochemical results was confirmed by alleviation of the histopathological changes in the tissue. Results show the adverse effects of AgNPs on the male reproductive tract, particularly spermatogenesis, and suggest that Se possesses significant potential in reducing AgNP-induced testicular toxicity.

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Section: Discussionsupporting

confidence: 92%

Sodium Selenite Protects Against Silver Nanoparticle-Induced Testicular Toxicity and Inflammation

Ansar

Abudawood

Hamed

et al. 2016

Biol Trace Elem Res

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“…Recently, Se has been shown to interact in the body of mammals, reducing toxicity of certain compounds. [65][66][67] It could be that Se administration prevents free radical formation by increasing antioxidant activity of tissue, as evident in our studies, and prevent AgNPs' toxicity.…”

Section: Discussionsupporting

confidence: 53%

Antioxidant and hepatoprotective role of selenium against silver nanoparticles

Ansar

Alshehri

Abudawood

et al. 2017

IJN

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Silver nanoparticles (AgNPs) have attracted the most interest in terms of their potential biomedical and industrial applications. However, these nanoparticles have shown their toxic behavior toward environment, living tissues, and organisms. Selenium (Se), an essential trace element, is necessary for various metabolic processes, including protection against oxidative stress and immune function. The present study was undertaken to evaluate the effect of Se against AgNP-induced hepatic oxidative stress. AgNPs were synthesized and then prepared nanoparticles were characterized using various analytical techniques such as UV-visible spectroscopy, X-ray diffraction, and transmission electron microscopy. Rats were administered AgNPs intraperitoneally (5 mg/kg/day) and Se (0.2 mg/kg) was given by gavage. AgNP administration induced hepatic damage as indicated by the serum marker enzymes with reduction in levels of glutathione, and decrease in activities of SOD, CAT, and GSH-peroxidase ( P <0.05). Decrease in levels of total antioxidant capacity (TAC) and increase in level of C-reactive protein (CRP) was also observed in AgNP-treated group compared to control group. However, Se markedly attenuated AgNP-induced biochemical alterations, levels of TAC, CRP, and serum transaminases (AST, ALT) ( P <0.05). Taken together, these findings suggest that administration of AgNPs produces hepatotoxicity in rats, whereas Se supplementation attenuates these effects.

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“…In our study, which was carried out to understand the potential effects of hypothyroidism on gene expression, plasma-free T4 levels in propylthiouracil (PTU)treated rats decreased compared to the control group after the administration for 21 days (20 mg/kg/day dose), in accordance with both the literature and referencing doses previously administered in our laboratory. 15 , 16 This situation supported the hypothesis that hypothyroidism was induced.…”

Section: Discussionsupporting

confidence: 82%

The Expression of Neurodegeneration-Related Genes in the Hippocampus of Hypothyroid Rats Following Long-Term Potentiation

Altunkaya,

Babur,

Barutcu

et al. 2024

The Eurasian Journal of Medicine

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Background: In our research, we examined how the induction of long-term potentiation (LTP) in the hippocampus of hypothyroid rats affects the mRNA levels of several proteins involved with neurodegeneration, including Gsk3, Cdk5, Akt1, Mapt, P35 (Anxa), Capn1, Bace1, and Psen2. Methods: Wistar-albino rats, consisting of 12 males, were used in the research, and they were separated into 2 groups: control (n = 6) and hypothyroidism (n = 6). To induce hypothyroidism, propylthiouracil was added to drinking water at a dosage of 20 mg/kg/day. The test stimulus intensity was calculated, basal recordings were acquired, and LTP was induced by administering 100 Hz high-frequency stimulation (HFS) for 1 second with a 5-minute delay when the rats were aged 60 days. The population spike (PS) amplitude and excitatory postsynaptic potential (EPSP) slope were measured in the granule cell layer of the dentate gyrus. Using reverse transcription polymerase chain reaction, the mRNA levels of neurodegenerative genes were assessed in induced hippocampal tissues after the LTP protocol. The free T4 levels in plasma were measured using a plate reader with the commercial ELISA kit. Results: Following HFS, LTP was solely induced in the EPSP slope and PS amplitude in the control group. The impaired LTP response of the hypothyroidism group was accompanied by an increase in Akt1-mRNA expression and a decrease in Gsk3ß expression, whereas the value genes’ mRNA expression levels did not differ significantly from those of the control group. Conclusion: The hypothyroidism-related LTP impairment could be caused by a reduction in PI3K/AKT signaling . Further investigation of this path is required to elucidate the pathophysiology of impaired synaptic plasticity in hypothyroidism.

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Effects of selenium treatment on 6-n-propyl-2-thiouracil-induced impairment of long-term potentiation

Cited by 12 publications

References 39 publications

Sodium Selenite Protects Against Silver Nanoparticle-Induced Testicular Toxicity and Inflammation

Sodium Selenite Protects Against Silver Nanoparticle-Induced Testicular Toxicity and Inflammation

Antioxidant and hepatoprotective role of selenium against silver nanoparticles

The Expression of Neurodegeneration-Related Genes in the Hippocampus of Hypothyroid Rats Following Long-Term Potentiation

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