Effects of inhalation anesthetics halothane, sevoflurane, and isoflurane on human cell lines

Kvolik, Slavica; Glavaš‐Obrovac, Ljubica; Bares, Vesna; Karner, Ivan

doi:10.1016/j.lfs.2004.12.052

Cited by 108 publications

(73 citation statements)

References 44 publications

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“…Current evidence suggests that some inhaled anesthetics are capable of causing apoptosis, neuronal damage and durable cognitive dysfunction (Culley et al, 2003(Culley et al, , 2004aJevtovicTodorovic et al, 2003;Kvolik et al, 2005;Loop et al, 2005;Muravchick and Smith, 1995;Wei et al, 2005;Yon et al, 2005). Potential mechanisms are varied but a recent study shows that anesthetics can enhance protein misfolding and aggregation.…”

Section: Introductionmentioning

confidence: 99%

Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics

Bianchi

Tran

Liu

et al. 2008

Neurobiology of Aging

216

187

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Inhaled anesthetics have been shown to increase the aggregation of amyloid beta in vitro through the stabilization of intermediate toxic oligomers, which are thought to contribute to neurocognitive dysfunction in Alzheimer's disease. Inhaled anesthetics may escalate cognitive dysfunction through enhancement of these intermediate oligomer concentrations. We intermittently exposed 12-month-old Tg2576 transgenic mice and nontransgenic littermates to isoflurane and halothane for 5 days. Cognitive function was measured before and after anesthetic exposures using the Morris Water Maze; amyloid beta plaque burden and caspase-3 mediated apoptosis were quantified by immunohistochemistry. At 12 months of age, anesthetic exposure did not further enhance cognitive decline in the transgenic mice. Immunohistochemistry, however, revealed that the halothane-exposed Tg2576 mice had more amyloidopathy than the isoflurane treated mice or the nonexposed transgenic mice. Isoflurane exposure impaired cognitive function in the nontransgenic mice, implying an alternative pathway for neurodegeneration. These findings indicate that inhaled anesthetics influence cognition and amyloidogenesis, but that the mechanistic relationship remains unclear.

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Section: Introductionmentioning

confidence: 99%

Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics

Bianchi

Tran

Liu

et al. 2008

Neurobiology of Aging

216

187

View full text Add to dashboard Cite

show abstract

“…A recent study also reported that patients undergoing coronary artery bypass graft surgery under general anesthesia were at increased risk for AD compared with those having percutaneous transluminal coronary angioplasty under local anesthesia (Lee et al, 2005). Isoflurane, one of the most commonly used inhalation anesthetics, has been reported to enhance aggregation and cytotoxicity of A␤ (Eckenhoff et al, 2004) and induce caspase activation and apoptosis (Matsuoka et al, 2001;Jevtovic-Todorovic et al, 2003;Kvolik et al, 2005;Loop et al, 2005;Wei et al, 2005;Yon et al, 2005). Our recent studies have shown that a clinically relevant isoflurane treatment causes caspase-3 activation and apoptosis, decreases cell viability, affects APP processing, and increases A␤ generation in human neuroglioma cells stably transfected to express human APP (H4-APP cells) (Xie et al, 2006a(Xie et al, ,b, 2007.…”

Section: Introductionmentioning

confidence: 99%

Isoflurane-Induced Caspase-3 Activation Is Dependent on Cytosolic Calcium and Can Be Attenuated by Memantine

Zhang¹,

Dong²,

Zhang³

et al. 2008

J. Neurosci.

104

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Increasing evidence indicates that caspase activation and apoptosis are associated with a variety of neurodegenerative disorders, including Alzheimer's disease. We reported that anesthetic isoflurane can induce apoptosis, alter processing of the amyloid precursor protein (APP), and increase amyloid-␤ protein (A␤) generation. However, the mechanism by which isoflurane induces apoptosis is primarily unknown. We therefore set out to assess effects of extracellular calcium concentration on isoflurane-induced caspase-3 activation in H4 human neuroglioma cells stably transfected to express human full-length APP (H4-APP cells). In addition, we tested effects of RNA interference (RNAi) silencing of IP 3 receptor, NMDA receptor, and endoplasmic reticulum (ER) calcium pump, sacro-/ER calcium ATPase (SERCA1). Finally, we examined the effects of the NMDA receptor partial antagonist, memantine, in H4-APP cells and brain tissue of naive mice. EDTA (10 mM), BAPTA (10 M), and RNAi silencing of IP 3 receptor, NMDA receptor, or SERCA1 attenuated capase-3 activation. Memantine (4 M) inhibited isoflurane-induced elevations in cytosolic calcium levels and attenuated isoflurane-induced caspase-3 activation, apoptosis, and cell viability. Memantine (20 mg/kg, i.p.) reduced isoflurane-induced caspase-3 activation in brain tissue of naive mice. These results suggest that disruption of calcium homeostasis underlies isoflurane-induced caspase activation and apoptosis. We also show for the first time that the NMDA receptor partial antagonist, memantine, can prevent isoflurane-induced caspase-3 activation and apoptosis in vivo and in vitro. These findings, indicating that isoflurane-induced caspase activation and apoptosis are dependent on cytosolic calcium levels, should facilitate the provision of safer anesthesia care, especially for Alzheimer's disease and elderly patients.

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“…Isoflurane has both anti-apoptotic and pro-apoptotic effects under different conditions [1]. It is cytotoxic in a concentration and time-dependent manner in vitro , inducing neuronal apoptosis in the developing brain and impairing memory and learning ability in rodents at clinically relevant concentrations [2,3,4,5]. However, isoflurane inhibits apoptosis in cardiac myocytes and protects the brain against ischemic injury [6,7].…”

Section: Introductionmentioning

confidence: 99%

Isoflurane Preconditioning Promotes the Survival and Migration of Bone Marrow Stromal Cells

Sun

Jia

et al. 2015

Cell Physiol Biochem

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Background: Preconditioning with the volatile anesthetic isoflurane exerts protective effects in animal models of ischemia. The cytoprotective effects of isoflurane are dependent on the expression of hypoxia inducible factor-1 (HIF-1), a dimeric transcription factor that mediates cellular responses to hypoxia. Methods: We investigated the effect of isoflurane preconditioning on bone marrow stromal cell (BMSC) survival and function. Results: Short exposures to low isoflurane concentrations promoted in vitro survival and migration of BMSCs, whereas long exposures and high doses had the opposite effect. At specific doses and times, isoflurane upregulated the expression of HIF-1α and the stromal-derived factor-1 receptor CXCR4, and induced the activation of Akt, similar to hypoxia, and the effect of isoflurane was abrogated by silencing of HIF-1α or inhibition of PI3K/Akt signaling. In vivo experiments showed that isoflurane preconditioning increased the engraftment of BMSCs into the ischemic brain and improved functional recovery in a mouse model of stroke. Conclusion: Isoflurane preconditioning at specific doses and times improves the survival and function of BMSCs through the upregulation of CXCR4 via a mechanism involving HIF-1α expression and the PI3K/Akt pathway, suggesting that anesthetic preconditioning could be developed as a strategy to improve the efficiency of cell therapy.

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Effects of inhalation anesthetics halothane, sevoflurane, and isoflurane on human cell lines

Cited by 108 publications

References 44 publications

Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics

Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics

Isoflurane-Induced Caspase-3 Activation Is Dependent on Cytosolic Calcium and Can Be Attenuated by Memantine

Isoflurane Preconditioning Promotes the Survival and Migration of Bone Marrow Stromal Cells

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