Sodium selenite protects from 3-nitropropionic acid-induced oxidative stress in cultured primary cortical neurons

Colle, Dirleise; Santos, Danúbia Bonfanti; Souza, Viviane de Oliveira Nogueira; Lopes, Mark William; Leal, Rodrigo Bainy; Brocardo, Patricia de Souza; Farina, Marcelo

doi:10.1007/s11033-018-4531-y

Cited by 17 publications

(6 citation statements)

References 82 publications

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“…It has been observed that oxidative and inflammatory cell damage induced by glutamate in mouse hippocampal neuronal cell culture was reversed by the overexpression of selenoprotein H in these cells [ 158 ]. Similar results were obtained when pretreating mouse cortical neurons exposed to 3-nitropropionic (inducer of oxidative damage) acid with sodium selenite, where the latter protected these cells against free radical damage and stimulated glutathione peroxidase activity [ 159 ]. It has also been observed that selenoproteins prevent or suppress the activation of NLRP3 inflammasomes by removing multiple free radicals [ 160 ].…”

Section: Contribution Of Micronutrients To the Therapy Of Oxidative/inflammatory Diseases Through Their Mitochondrial Actionssupporting

confidence: 61%

Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases

et al. 2021

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Exaggerated oxidative stress and hyper-inflammation are essential features of oxidative/inflammatory diseases. Simultaneously, both processes may be the cause or consequence of mitochondrial dysfunction, thus establishing a vicious cycle among these three factors. However, several natural substances, including melatonin and micronutrients, may prevent or attenuate mitochondrial damage and may preserve an optimal state of health by managing the general oxidative and inflammatory status. This review aims to describe the crucial role of mitochondria in the development and progression of multiple diseases as well as the close relationship among mitochondrial dysfunction, oxidative stress, and cytokine storm. Likewise, it attempts to summarize the main findings related to the powerful effects of melatonin and some micronutrients (vitamins and minerals), which may be useful (alone or in combination) as therapeutic agents in the treatment of several examples of oxidative/inflammatory pathologies, including sepsis, as well as cardiovascular, renal, neurodegenerative, and metabolic disorders.

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Section: Contribution Of Micronutrients To the Therapy Of Oxidative/inflammatory Diseases Through Their Mitochondrial Actionssupporting

confidence: 61%

Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases

et al. 2021

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“…Oxidative stress and mitochondrial dysfunction are characteristic features of some neurodegenerative pathologies, such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). It is worth mentioning that over the past years the potential application of antioxidants in the treatment of these diseases has been explored [96,97]. In this context, the role of Na 2 SeO 3 in the oxidative stress events of the neurotoxicity caused by paraquat (PQ) has been investigated due to its known antioxidant properties.…”

Section: Sodium Selenite and Neurodegenerative Diseasesmentioning

confidence: 99%

Seleno-Metabolites and Their Precursors: A New Dawn for Several Illnesses?

et al. 2022

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Selenium (Se) is an essential element for human health as it is involved in different physiological functions. Moreover, a great number of Se compounds can be considered potential agents in the prevention and treatment of some diseases. It is widely recognized that Se activity is related to multiple factors, such as its chemical form, dose, and its metabolism. The understanding of its complex biochemistry is necessary as it has been demonstrated that the metabolites of the Se molecules used to be the ones that exert the biological activity. Therefore, the aim of this review is to summarize the recent information about its most remarkable metabolites of acknowledged biological effects: hydrogen selenide (HSe−/H2Se) and methylselenol (CH3SeH). In addition, special attention is paid to the main seleno-containing precursors of these derivatives and their role in different pathologies.

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“…3-nitropropionic acid (3-NPA), a mitochondrial complex II inhibitor, is mainly used in neurological research. Its effect on ovarian function has not been reported and requires further exploration [ 4 ]. SIRT1 was reported to have a strong correlation with ovarian reserve and could be a marker of ovarian aging [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Decrease in ovarian reserve through the inhibition of SIRT1-mediated oxidative phosphorylation

Liu

Chen

Wang

et al. 2022

Aging

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Objective: To establish an oxidative stress-induced model of premature ovarian insufficiency (POI) and to explore the effect of SIRT1 and mitochondrial oxidative phosphorylation on the ovarian reserve. Methods: Mice were treated with intraperitoneal injections of 3-nitropropionic acid (3-NPA) at different doses and for different time periods to induce a model of POI. Subsequently, the efficiency of each regimen was evaluated. The expression of SIRT1 in ovarian tissue was examined. Then, SIRT1 was knocked down in human luteinized granulosa cells (GCs), and its function and related receptor and gene expression were examined. Finally, a SIRT1 antagonist and agonist were used to explore the effects of SIRT1 on ovarian function in vivo and on the change in mitochondrial oxidative phosphorylation complexes (OXPHOS). Results: Decreases in ovarian reserve were successfully induced through the intraperitoneal injection of 40 mg/kg 3-NPA for 3 weeks, and SIRT1 was down-regulated in the model group. The knockdown of SIRT1 impaired the estrogen synthesis capacity of human GCs and decreased the expression of related genes. 3-NPA and SIRT1 antagonist Ex-527 decreased ovarian function and inhibited OXPHOS. In contrast, the SIRT1 agonist resveratrol promoted the recovery of ovarian function in the model group and improved OXPHOS. Additionally, P53, CASPASE 3, and BAX were down-regulated and BCL2 was up-regulated in the 3-NPA and Ex-527 groups; opposite trends were observed after resveratrol treatment. Conclusions: The intraperitoneal injection of 40 mg/kg 3-NPA for 3 weeks could effectively induce POI. The increase in oxidative stress inhibited SRIT1 and mitochondrial oxidative phosphorylation, inducing follicular apoptosis.

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Sodium selenite protects from 3-nitropropionic acid-induced oxidative stress in cultured primary cortical neurons

Cited by 17 publications

References 82 publications

Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases

Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases

Seleno-Metabolites and Their Precursors: A New Dawn for Several Illnesses?

Decrease in ovarian reserve through the inhibition of SIRT1-mediated oxidative phosphorylation

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