Heat-induced inhibition of superoxide dismutase and accumulation of reactive oxygen species leads to HT-22 neuronal cell death

El-Orabi, Naglaa F.; Rogers, Colin B.; Edwards, Heather Gray; Schwartz, Dean D.

doi:10.1016/j.jtherbio.2010.11.002

Cited by 28 publications

(20 citation statements)

References 65 publications

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“…Heat stress was also shown to decrease superoxide dismutase 1 (SOD-1) mRNA levels, cytoplasmic SOD protein and enzyme activity, leading to the increase of ROS generation [18]. Furthermore, heat stress leads to an overproduction of transition metal ions (TMI), which can make electron donations to oxygen, forming superoxide anions [19,20].…”

Section: Superoxide Anionmentioning

confidence: 99%

“…MnSOD plays an important role in thermotolerance. Lowering SOD enzyme levels results in a significant reduction in thermal resistance [49], whereas overexpression of MnSOD by stable transfection provides cellular resistance against the cytotoxic effects of hyperthermia [18,50,51]. These results suggest that superoxide free radicals, or their reaction products, are responsible for much of the cytotoxicity of hyperthermia.…”

Section: Mitochondrial Antioxidant System and Thermal Sensitivitymentioning

confidence: 99%

See 1 more Smart Citation

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Slimen¹,

Najar

Ghram

et al. 2014

International Journal of Hyperthermia

546

246

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In recent years there has been enormous interest in researching oxidative stress. Reactive oxygen species (ROS) are derived from the metabolism of oxygen as by-products of cell respiration, and are continuously produced in all aerobic organisms. Oxidative stress occurs as a consequence of an imbalance between ROS production and the available antioxidant defence against them. Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer's and autoimmune diseases are mediated by oxidative stress. Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress. This manuscript describes the main mitochondrial sources of ROS and the antioxidant defences involved to prevent oxidative damage in all the mitochondrial compartments. It also deals with discussions concerning the cytotoxic effect of heat stress, mitochondrial heat-induced alterations, as well as heat shock protein (HSP) expression as a defence mechanism.

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Section: Superoxide Anionmentioning

confidence: 99%

Section: Mitochondrial Antioxidant System and Thermal Sensitivitymentioning

confidence: 99%

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Slimen¹,

Najar

Ghram

et al. 2014

International Journal of Hyperthermia

546

246

View full text Add to dashboard Cite

show abstract

“…Reactive oxygen species (ROS), containing hydrogen peroxide, hydroxyl radical and free radicals play an important role in normal physiology, but their overproduction may be a cause of some pathological states. On the other hand, scavenging enzyme systems, including catalase and superoxide dismutase (SOD), are available to protect cells against damage caused by ROS 6 . The balance between oxidation and reduction reactions regulates the homeostasis of the cell.…”

Section: Introductionmentioning

confidence: 99%

Metabonomics Approach to Assessing the Modulatory Effects of Kisspeptin-10 on Liver Injury Induced by Heat Stress in Rats

Hou

Wang

Ping

et al. 2017

Sci Rep

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The protective effects of Kisspeptin on heat-induced oxidative stress in rats were investigated by using a combination of biochemical parameters and metabonomics. Metabonomic analyses were performed using gas chromatography/mass spectrometry in conjunction with multivariate and univariate statistical analyses. At the end point of the heat stress experiment, histological observation, ultrastructural analysis and biochemical parameters were measured. Metabonomic analysis of liver tissue revealed that Kisspeptin mainly attenuated the alteration of purine metabolism and fatty acid metabolism pathways. Futhermore, Kisspeptin also increased the levels of GSH, T-AOC as well as SOD activities, and upregulated MDA levels. These results provide important mechanistic insights into the protective effects of Kisspeptin against heat-induced oxidative stress.

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“…The HT-induced elevation of O 2 À is thought to be due to the activation of xanthine oxidase and/or mitochondria respiratory reaction chain [7]. In addition, HT has been shown to decrease the expression level of SOD1 (CuZnSOD) and its enzyme activity, leading to an increase in ROS production [9]. Wan et al [10] recently reported that a decrease in SOD2 (MnSOD) activity accounted for the enhanced ROS levels in heat-treated platelets.…”

Section: Induction Of Oxidative Stress By Htmentioning

confidence: 99%

Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification

Tabuchi

Ahmed

Kondo

2016

Hyperthermic Oncology From Bench to Bedside

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Hyperthermia (HT) is considered to be a possible treatment modality for various cancers, and its pleiotropic effects support its combined use with radiotherapy and/or chemotherapy. However, clinical results by HT alone have not always been satisfactory. In mammalian cells, HT elicits a wide spectrum of alterations in cellular morphology, biochemistry and function. One of these HT-induced alterations, oxidative stress, has been attributed to the increased production of reactive oxygen spaces (ROS), and is known to play an important role as an intracellular mediator of HT-induced cell death, including apoptosis. Indeed, it has been well established that increases in intracellular oxidative stress significantly enhance HT-induced apoptosis. Attention has therefore been focused on the development of heat sensitizers to modulate the intracellular ROS. Interestingly, the modification of oxidative stress via addition of ROS-generating compounds significantly enhanced the apoptosis elicited by HT. In this chapter, we describe the induction of oxidative stress by HT and enhancement of HT-induced apoptosis by oxidative stress modification, and we discuss the possible mechanisms underlying this enhancement.

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Heat-induced inhibition of superoxide dismutase and accumulation of reactive oxygen species leads to HT-22 neuronal cell death

Cited by 28 publications

References 65 publications

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Metabonomics Approach to Assessing the Modulatory Effects of Kisspeptin-10 on Liver Injury Induced by Heat Stress in Rats

Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification

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