Molecular role of catalase on oxidative stress-induced Ca<sup>2+</sup>signaling and TRP cation channel activation in nervous system

Nazıroğlu, Mustafa

doi:10.3109/10799893.2012.672994

Cited by 165 publications

(91 citation statements)

References 52 publications

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“…20) TRPV1 channel is a non-selective cation channel, which serves as a pain receptor, and is activated by capsaicin, increased temperature (>43°C), oxidative stress, or hypertonicity. 21,22) However, the role of TRPV1 channel in radiation-induced cellular responses has not been clarified. Therefore, in this study, we investigated the radio-sensitizing effect of TRPV1 channel inhibitors in cancer cells.…”

Section: Abstract γ-Ray; Radiosensitizer; Transient Receptor Potentimentioning

confidence: 99%

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Nishino

Tanamachi

Nakanishi

et al. 2016

Biological & Pharmaceutical Bulletin

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Radiosensitizers are used in cancer therapy to increase the γ-irradiation susceptibility of cancer cells, including radioresistant hypoxic cancer cells within solid tumors, so that radiotherapy can be applied at doses sufficiently low to minimize damage to adjacent normal tissues. Radiation-induced DNA damage is repaired by multiple repair systems, and therefore these systems are potential targets for radiosensitizers. We recently reported that the transient receptor potential vanilloid type 1 (TRPV1) channel is involved in early responses to DNA damage after γ-irradiation of human lung adenocarcinoma A549 cells. Therefore, we hypothesized that TRPV1 channel inhibitors would have a radiosensitizing effect by blocking repair of radiation-induced cell damage. Here, we show that pretreatment of A549 cells with the TRPV1 channel inhibitors capsazepine, AMG9810, SB366791 and BCTC suppressed the γ-ray-induced activation of early DNA damage responses, i.e., activation of the protein kinase ataxia-telangiectasia mutated (ATM) and accumulation of p53-binding protein 1 (53BP1). Further, the decrease of survival fraction at one week after γ-irradiation (2.0 Gy) was enhanced by pretreatment of cells with these inhibitors. On the other hand, inhibitor pretreatment did not affect cell viability, the number of apoptotic or necrotic cells, or DNA synthesis at 24 h after irradiation. These results suggest that inhibition of DNA repair by TRPV1 channel inhibitors in irradiated A549 cells caused gradual loss of proliferative ability, rather than acute facilitation of apoptosis or necrosis. TRPV1 channel inhibitors could be novel candidates for radiosensitizers to improve the efficacy of radiation therapy, either alone or in combination with other types of radiosensitizers. Key words γ-ray; radiosensitizer; transient receptor potential vanilloid type 1 channelRadiation therapy plays an important role in treatment of numerous cancers, 1) because ionizing radiation induces potentially lethal DNA damage, such as DNA double-strand breaks (DSBs). Although DSBs cause cell death or genomic instability, 2,3) they can be repaired by mechanisms such as non-homologous end joining (NHEJ) or homologous recombination (HR). NHEJ rejoins the DNA ends without requiring sequence homologies, and is mediated by a DNA-dependent protein kinase holoenzyme. On the other hand, HR processes use undamaged homologous DNA sequences (sister chromatid or the homologous chromosome) to ensure the fidelity of the repair process. [4][5][6] The DNA damage response pathways protect genomic integrity and act as a barrier against cancer, 7) and are important for recovery of irradiated normal cells. However, overexpression of DNA repair proteins is involved in radioresistance of cancer cells, [8][9][10] and therefore these mechanisms also decrease the efficiency of radiation therapy.Since ionizing radiation does not discriminate between cancer cells and normal cells, damage to normal tissues is usually a dose-limiting factor in radiation therapy. In addition, many solid ...

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Section: Abstract γ-Ray; Radiosensitizer; Transient Receptor Potentimentioning

confidence: 99%

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Nishino

Tanamachi

Nakanishi

et al. 2016

Biological & Pharmaceutical Bulletin

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“…The intracellular Ca 2+ concentration has an important influence on numerous physiological functions such as generation of action potentials, synaptic transmission, plasticity, and cell survival in neurons (Nazıroğlu, 2012;Kumar et al, 2014). Cation channels play a significant role in modulating intracellular Ca 2+ concentrations in all cells, including neurons, because Ca 2+ passes the cell membranes to enter the cytosol by way of these channels (Nazıroğlu, 2012;Kumar et al, 2014).…”

Section: +mentioning

confidence: 99%

“…Cation channels play a significant role in modulating intracellular Ca 2+ concentrations in all cells, including neurons, because Ca 2+ passes the cell membranes to enter the cytosol by way of these channels (Nazıroğlu, 2012;Kumar et al, 2014).…”

Section: +mentioning

confidence: 99%

“…The hippocampus is protected from oxidative damage by antioxidants Övey and Nazıroğlu, 2015). Enzymatic antioxidants such as glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) and nonenzymatic antioxidant defense systems such as vitamin E and glutathione exist in the hippocampus in order to scavenge ROS (Nazıroğlu, 2011(Nazıroğlu, , 2012. One of the main nonenzymatic antioxidants in the hippocampus is melatonin (N-acetyl-5-methoxytryptamine), which is a hormone produced and released by the pineal gland ) accumulation and excessive oxidative stress in the hippocampus and brain cortex have long been known as major contributors to the etiology of epilepsy.…”

Section: Introductionmentioning

confidence: 99%

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Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

Nazıroğlu¹

2015

Turk J Biol

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Calcium ion (Ca 2+ ) accumulation and excessive oxidative stress in the hippocampus and brain cortex have long been known as major contributors to the etiology of epilepsy. I have reviewed the role of Ca 2+ signaling through cation channels and mitochondriamediated oxidative stress on epilepsy in human and animals. A review of the relevant papers and results from recent studies were obtained from PubMed and the Science Citation Index. Current literature findings indicate that melatonin and agomelatine reduce activation of hippocampal transient receptor potential (TRP), glutamate receptors, and voltage-gated calcium channels that are critical for the development of abnormal Ca 2+ homeostasis and oxidative stress and associated mitochondrial dysfunction. In addition, low doses of melatonin induce anticonvulsant action through increase of GABA levels in the hippocampus and brain cortex. The accumulating evidence implicates a modulator role of melatonin on excessive oxidative stress products, plus mitochondrial and Ca 2+ dysregulations in epilepsy. The evidence indicates that modulation of oxidative stress and neuronal Ca 2+ handling occurs through effects on TRP channels, suggesting an increasingly viable approach for therapeutic interventions against epilepsy.

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“…The antioxidant enzyme system is the most important defense mechanism against membrane damage induced by lipid peroxidation in mammalian cells. CAT is another enzyme that catalyzes the dissociation of hydrogen peroxide and other lipid peroxides, thereby protecting the cell membranes and hemoglobins against oxidation (Bleecker et al, 1994;Nazıroğlu, 2012). CAT is present in virtually all cells in the body and it is especially effective in the case of high hydrogen peroxide concentrations (Bushnell et al, 1994;Nazıroğlu, 2012).…”

Section: Discussionmentioning

confidence: 99%

The effects of midazolam and etomidate on the antioxidant system in the rat liver

Bayram¹,

Öncü²,

Uz³

et al. 2015

Turk J Biol

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This study was conducted to investigate the histopathological and biochemical effects of midazolam and etomidate, which are intravenous anesthetics used in surgical operations, on rat liver. There were 3 study groups each consisting of 9 animals: the control, midazolam, and etomidate groups. Midazolam and etomidate were administered 10 times with 1-day intervals. At the end of the study, tissues were taken for histological examination and biochemical analysis. We determined superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) levels in the liver. There was a slight increase in MDA level in the midazolam-exposed group when compared with the controls, and this was not statistically significant. However, SOD and CAT activities were significantly increased in the midazolam group. We found slight damage in histological sections in parallel to biological findings. MDA levels were significantly increased in the etomidate group and SOD and CAT activities were also prominent in this group. More histological changes like hepatocyte degeneration, vascular congestion, and mononuclear cell infiltration were observed in the etomidate group and this was statistically significant. We can say that these intravenous anesthetic agents may cause dose-dependent damage in tissue. Therefore, we think that one must be cautious of the administration duration and dose levels of anesthetics during surgical operations.

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Molecular role of catalase on oxidative stress-induced Ca²⁺signaling and TRP cation channel activation in nervous system

Cited by 165 publications

References 52 publications

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

The effects of midazolam and etomidate on the antioxidant system in the rat liver

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Molecular role of catalase on oxidative stress-induced Ca2+signaling and TRP cation channel activation in nervous system

Cited by 165 publications

References 52 publications

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Radiosensitizing Effect of TRPV1 Channel Inhibitors in Cancer Cells

Role of melatonin on calcium signaling and mitochondrial oxidativestress in epilepsy: focus on TRP channels

The effects of midazolam and etomidate on the antioxidant system in the rat liver

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Molecular role of catalase on oxidative stress-induced Ca²⁺signaling and TRP cation channel activation in nervous system