Selenium protects cerebral cells by cisplatin induced neurotoxicity

Karavelioğlu, Ergün; Boyacı, Mehmet Gazi; Şimşek, Nejdet; Sonmez, Mehmet Akif; Koç, Rabia; Karademir, Mustafa; Güven, Mustafa; Eser, Olcay

doi:10.1590/s0102-865020150060000004

Cited by 23 publications

(13 citation statements)

References 31 publications

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“…CP binds to the nuclear and mitochondrial DNA of the neurons, which may trigger the activation of RhoA GTPase enzyme and induction of the inflammatory pathways 38,39 . Nuclear DNA damage leads to p53 activation and triggers apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of thymoquinone against cisplatin-induced cardiac injury in rats

et al. 2016

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PURPOSE: To investigate the possible protective effect of thymoquinone (TQ) in cisplatin (CP) induced myocardial injury. METHODS:A total of 28 adult male Wistar-Albino rats were randomly and equally divided into four groups as follows: Group 1 (control), Group 2 (CP at 15 mg/kg dose), Group 3 (TQ 40 mg/kg/day for two days prior to CP injection and on third day, CP at 15 mg/kg dose was intraperitoneally administered and TQ treatment continued until fifth day) and Group 4 (TQ at 40mg/kg/day dose for five days). RESULTS:There was a significant increment in CP group in terms of congestion, edema and pycnotic nuclei in myocardial fibers, comparing with other groups. TQ group exhibited significant increase in expression of antiapoptotic protein Bcl-2, comparing with CP group (p<0.05). In only CP administered group, expression of antiapoptotic protein Bcl-2 was lowest comparing with other groups. CONCLUSION:Established data indicate that cisplatin is cardiotoxic and thymoquinone may be useful in treating CP-induced cardiac injury.

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Section: Discussionmentioning

confidence: 99%

Effects of thymoquinone against cisplatin-induced cardiac injury in rats

et al. 2016

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“…With prolonged treatment, they gradually lead to disturbance of proprioception, which may result in ataxic gait [ 23 ]. The clinical manifestations of encephalopathy accompanying platinum-based therapy usually appear with an increase in cumulative dose [ 24 ]. Sensory manifestations of platinum compounds-induced neuropathy are often accompanied by ototoxicity [ 25 ].…”

Section: Side Effects Of Platinum-based Compounds In Clinical Pracmentioning

confidence: 99%

Antioxidant Supplementation in the Treatment of Neurotoxicity Induced by Platinum-Based Chemotherapeutics—A Review

Stanković

Selaković

Mihailović

et al. 2020

IJMS

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Cancer represents one of the most pernicious public health problems with a high mortality rate among patients worldwide. Chemotherapy is one of the major therapeutic approaches for the treatment of various malignancies. Platinum-based drugs (cisplatin, oxaliplatin, carboplatin, etc.) are highly effective chemotherapeutic drugs used for the treatment of several types of malignancies, but their application and dosage are limited by their toxic effects on various systems, including neurotoxicity. Simultaneously, researchers have tried to improve the survival rate and quality of life of cancer patients and decrease the toxicity of platinum-containing drugs by combining them with non-chemotherapy-based drugs, dietary supplements and/or antioxidants. Additionally, recent studies have shown that the root cause for the many side effects of platinum chemotherapeutics involves the production of reactive oxygen species (ROS) in naive cells. Therefore, suppression of ROS generation and their inactivation with antioxidants represents an appropriate approach for platinum drug-induced toxicities. The aim of this paper is to present an updated review of the protective effects of different antioxidant agents (vitamins, dietary antioxidants and supplements, medicaments, medicinal plants and their bioactive compounds) against the neurotoxicity induced by platinum-based chemotherapeutics. This review highlights the high potential of plant antioxidants as adjuvant strategies in chemotherapy with platinum drugs.

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“…Selenium has been demonstrated to reduce ROS production [15, 16], protect cells against glutamate toxicity [17], oxidative stress [18] and inflammatory cytokines [19, 20]. Animal experiments have showed that selenium supplementation reduces ROS production, ameliorates cisplatin induced neurotoxicity and ischemia-induced brain damage [21, 22]. However, the mechanisms by which selenium exerts its protective effect against glutamate insult in neuronal cells remains ambiguous.…”

Section: Introductionmentioning

confidence: 99%

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

Ibeanu

Wang

et al. 2017

BMC Neurosci

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BackgroundPrevious studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.ResultsWe find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.ConclusionThese findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.

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Selenium protects cerebral cells by cisplatin induced neurotoxicity

Cited by 23 publications

References 31 publications

Effects of thymoquinone against cisplatin-induced cardiac injury in rats

Effects of thymoquinone against cisplatin-induced cardiac injury in rats

Antioxidant Supplementation in the Treatment of Neurotoxicity Induced by Platinum-Based Chemotherapeutics—A Review

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

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