Normobaric hyperoxia induces ischemic tolerance and upregulation of glutamate transporters in the rat brain and serum TNF-α level

Bigdeli, Mohammad Reza; Hajizadeh, Sohrab; Froozandeh, Mehdi; Heidarianpour, Ali; Rasoulian, Bahram; Asgari, Ali; Pourkhalili, Khalil; Khoshbaten, Ali

doi:10.1016/j.expneurol.2008.03.029

Cited by 43 publications

(34 citation statements)

References 46 publications

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“…[28] Free radicals have a major role in ischemia-reperfusion (IR) injury of various organs, and thus the mechanisms responsible for the reduction of IR injury may also work against cisplatin-induced free radical injury. It has been shown that pre-exposure to normobaric hyperoxia could be protective against subsequent brain, [29] heart, [30] spinal cord, [31] and renal IR injury. [9] Atasoyu et al concluded that the synchronous application of HBO therapy (60 min every day for seven days at 2.5 ATA) with cisplatin prevents kidney damage by decreasing necrosis scores.…”

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confidence: 99%

Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

et al. 2010

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Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatininduced acute renal failure was investigated in present study.Twenty-four rats were divided into four groups. The O 2 + CP and Air + CP groups were were subjected to i.p. injection of 5 mg/kg cisplatin, and in the Air + Saline and O 2 + Saline groups, saline was injected instead of cisplatin. O 2 + CP and O 2 + Saline groups were pretreated with oxygen (3h/d for two days), and the other two groups were pretreated with room air. Cisplatin was administered 24 h after last pretreatment session. Three days after cisplatin injection, plasma samples were obtained, and parts of kidney tissue were frozen for biochemical analysis or fixed in formalin for histological assessments. Preconditioning with oxygen prior to cisplatin administration led to reduced tubular necrosis and luminal cast formation and improvement of renal function, as was evidenced by significant reduction in plasma creatinine and urea levels. Oxygen pretreatment also significantly reversed cisplatin-induced reduction in renal catalase activity and glutathione level. It could be concluded that oxygen pretreatment could have a delayed protective effect against cisplatin nephrotoxicity, and that increased renal catalase activity may be involved in this protective effect of hyperoxia.

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Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

et al. 2010

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“…15,3 Of note, however, neuroprotection induced by oxygen-glucose deprivation promotes cellular glutamate reuptake by increasing expression of excitatory aminoacid transporters (EAATs) or glutamate transporters. 25,22,4 Meanwhile, tumor necrosis factor (TNF)-a may be an important mediator of IT, 13 and is released in soluble form by the action of a membrane-anchored zinc protease called TNF-a converting enzyme (TACE). At least 5 glutamate transporters exist: EAAT1 (formerly known as GLAST [GLutamate-ASpartate Transporter]), GLT1 (glutamate transporters 1 or EAAT2), EAAC1 (Excitatory amino-acid carrier 1 or EAAT3), EAAT4, and EAAT5 and their action-promoting glutamate reuptake into neurons and glial cells may be cytoprotective.…”

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confidence: 99%

Preconditioning with Sublethal Ischemia or Intermittent Normobaric Hyperoxia Up-regulates Glutamate Transporters and Tumor Necrosis Factor-α Converting Enzyme in the Rat Brain

Bigdeli

Rahnema

Khoshbaten

2009

Journal of Stroke and Cerebrovascular Diseases

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“…In addition, it has been shown that oxygen preconditioning can protect human renal tubular cells from cisplatin-induced cytotoxicity in vitro [5]. Likewise, in animal models, oxygen pretreatment reduces ischemia-reperfusion injuries in various vital organs such as the central nervous system [18–21], liver [22, 23], heart [24], and kidney [25, 26]. Moreover, it has been reported that hyperoxic preconditioning could attenuate hypoxia-induced apoptosis in cultured mesenchymal stem cells [27].…”

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confidence: 99%

Cellular Preoxygenation Partially Attenuates the Antitumoral Effect of Cisplatin despite Highly Protective Effects on Renal Epithelial Cells

Rasoulian

Kaeidi

Rezaei

et al. 2017

Oxidative Medicine and Cellular Longevity

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Our previous in vitro studies demonstrated that oxygen pretreatment significantly protects human embryonic renal tubular cell against acute cisplatin- (CP-) induced cytotoxicity. The present study was designed to investigate whether this protective effect is associated with decreasing therapeutic effects of cisplatin on malignant cells. For this purpose, cultured human embryonic kidney epithelial-like (AD293), cervical carcinoma epithelial-like (Hela), and ovarian adenocarcinoma epithelial-like (OVCAR-3) cells were subjected to either 2-hour pretreatment with oxygen (≥90%) or normal air and then to a previously determined 50% lethal dose of cisplatin for 24 hours. Cellular viability was evaluated via MTT and Neutral Red assays. Also, activated caspase-3 and Bax/Bcl-2 ratio, as the biochemical markers of cell apoptosis, were determined using immunoblotting. The hyperoxic preexposure protocol significantly protects renal AD293 cells against cisplatin-induced toxicity. Oxygen pretreatment also partially attenuated the cisplatin-induced cytotoxic effects on Hela and OVCAR-3 cells. However, it did not completely protect these cells against the therapeutic cytotoxic effects of cisplatin. In summary, the protective methods for reducing cisplatin nephrotoxic side effects like oxygen pretreatment might be associated with concurrent reduction of the therapeutic cytotoxic effects of cisplatin on malignant cells like cervical carcinoma (Hela) and ovarian adenocarcinoma (OVCAR-3) cells.

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Normobaric hyperoxia induces ischemic tolerance and upregulation of glutamate transporters in the rat brain and serum TNF-α level

Cited by 43 publications

References 46 publications

Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

Preconditioning with Sublethal Ischemia or Intermittent Normobaric Hyperoxia Up-regulates Glutamate Transporters and Tumor Necrosis Factor-α Converting Enzyme in the Rat Brain

Cellular Preoxygenation Partially Attenuates the Antitumoral Effect of Cisplatin despite Highly Protective Effects on Renal Epithelial Cells

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