Attenuation of Cerebral Oxygen Toxicity by Sound Conditioning

Shupak, Avi; Tal, Dror; Pratt, Hillel; Sharoni, Zohara; Hochman, Ayala

doi:10.1097/00129492-200403000-00019

Cited by 2 publications

(6 citation statements)

References 63 publications

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“…Animal studies indicate that the optimal timing for ITD would be about 40 minutes before Cisplatin delivery. 10,18,42,43 In the clinical realm we found it difficult to follow the ideal timing for ITD injection prior to Cisplatin treatment. This might decrease the potential maximal protective effect of Dexamethasone.…”

Section: Discussionmentioning

confidence: 99%

“…This results in lipid, protein, and nucleic acids peroxidation with Caspase system activation and apoptosis of inner ear cells. 4,[10][11][12] The outer hair cells at the basal turn of the cochlea are initially lost to be followed by the remaining outer hair cells, inner hair cells, supporting cells, and spiral gangalion neurons. 13 Advanced ototoxicity damages the stria vascularis and decreases the cochlear blood supply, resulting in reduced endocochlear potential.…”

Section: Introductionmentioning

confidence: 99%

“…The pathogenesis of CIHL is attributed to the creation of reactive oxygen species (ROS) and depletion of antioxidant enzymes. This results in lipid, protein, and nucleic acids peroxidation with Caspase system activation and apoptosis of inner ear cells 4,10‐12 . The outer hair cells at the basal turn of the cochlea are initially lost to be followed by the remaining outer hair cells, inner hair cells, supporting cells, and spiral gangalion neurons 13 .…”

Section: Introductionmentioning

confidence: 99%

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Prevention of Cisplatin‐Induced Hearing Loss by Intratympanic Dexamethasone: A Randomized Controlled Study

Marshak

Steiner

Kaminer

et al. 2014

Otolaryngol.--head neck surg.

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109

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Prevention of Cisplatin‐Induced Hearing Loss by Intratympanic Dexamethasone: A Randomized Controlled Study

Marshak

Steiner

Kaminer

et al. 2014

Otolaryngol.--head neck surg.

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109

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“…Although a variety of prevention methods have been proposed, few measures have been applied to practice except controlling the pressure and duration of HBO exposure. [29][30][31][32] In earlier studies, GGA, an anti-ulcer drug, was found to increase HSP70 expression in the gastrointestinal mucosa, liver, heart, and other tissues. 33 It was reported that GGA could also induce HSP70 expression in the CNS.…”

Section: Discussionmentioning

confidence: 99%

“…Although a variety of prevention methods have been proposed, few measures have been applied to practice except controlling the pressure and duration of HBO exposure. 29–32…”

Section: Discussionmentioning

confidence: 99%

HSP70 protects rats and hippocampal neurons from central nervous system oxygen toxicity by suppression of NO production and NF-κB activation

Huang

Zhang

et al. 2018

Exp Biol Med (Maywood)

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During diving, central nervous system oxygen toxicity may cause drowning or barotrauma, which has dramatically limited the working benefits of hyperbaric oxygen in underwater operations and clinical applications. The aim of this study is to understand the effects and the underlying mechanism of heat shock protein 70 on central nervous system oxygen toxicity and its mechanisms in vivo and in vitro. Rats were given geranylgeranylacetone (800 mg/kg) orally to induce hippocampal expression of heat shock protein 70 and then treated with hyperbaric oxygen. The time course of hippocampal heat shock protein 70 expression after geranylgeranylacetone administration was measured. Seizure latency and first electrical discharge were recorded to evaluate the effects of HSP70 on central nervous system oxygen toxicity. Effects of inhibitors of nitric oxide synthase and nuclear factor-κB on the seizure latencies and changes in nitric oxide, nitric oxide synthase, and nuclear factor-κB levels in the hippocampus tissues were examined. In cell experiments, hippocampal neurons were transfected with a virus vector carrying the heat shock protein 70 gene (H3445) before hyperbaric oxygen treatment. Cell viability, heat shock protein 70 expression, nitric oxide, nitric oxide synthase, and NF-κB levels in neurons were measured. The results showed that heat shock protein 70 expression significantly increased and peaked at 48 h after geranylgeranylacetone was given. Geranylgeranylacetone prolonged the first electrical discharge and seizure latencies, which was reversed by neuronal nitric oxide synthase, inducible nitric oxide synthase and NF-κB inhibitors. Nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels in the hippocampus were significantly increased after hyperbaric oxygen exposure, but reversed by geranylgeranylacetone, while heat shock protein 70 inhibitor quercetin could inhibit this effect of geranylgeranylacetone. In the in vitro study, heat shock protein 70-overexpression decreased the nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels as well as the cytoplasm/nucleus ratio of nuclear factor-κB and protected neurons from hyperbaric oxygen-induced cell injury. In conclusion, overexpression of heat shock protein 70 in hippocampal neurons may protect rats from central nervous system oxygen toxicity by suppression of neuronal nitric oxide synthase and inducible nitric oxide synthase-mediated nitric oxide production and translocation of nuclear factor-κB to nucleus. Impact statement Because the pathogenesis of central nervous system oxygen toxicity (CNS-OT) remains unclear, there are few interventions available. To develop an efficient strategy against CNS-OT, it is necessary to understand its pathogenesis and in particular, the relevant key factors involved. This study examined the protective effects of heat shock protein 70 (HSP70) on CNS-OT via in vivo and in vitro experiments. Our results indicated that overexpression of HSP70 in hippocampal neurons may protect rats from CNS...

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Attenuation of Cerebral Oxygen Toxicity by Sound Conditioning

Abstract: Our data show that sound conditioning prolongs the latency to oxygen-induced convulsions. This effect was not accompanied by significant changes in whole-brain antioxidant enzyme activity or the magnitude of lipid peroxidation.

Cited by 2 publications

References 63 publications

Prevention of Cisplatin‐Induced Hearing Loss by Intratympanic Dexamethasone: A Randomized Controlled Study

Prevention of Cisplatin‐Induced Hearing Loss by Intratympanic Dexamethasone: A Randomized Controlled Study

HSP70 protects rats and hippocampal neurons from central nervous system oxygen toxicity by suppression of NO production and NF-κB activation

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