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Current Alzheimer Research

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

Sevoflurane But Not Propofol Provided Dual Effects of Cell Survival in Human Neuroblastoma SH-SY5Y Cells

Author(s): Xue Gao, Xiu Wang , Lei Zhang , Ge Liang , Rachel Mund and Huafeng Wei *

Volume 17, Issue 14, 2020

Page: [1311 - 1319] Pages: 9

DOI: 10.2174/1567205018666210218162856

Price: $65

Abstract

Background: We have hypothesized that the most commonly used intravenous (propofol) and inhalational (sevoflurane) general anesthetics affect cell survival concentration and duration dependently with different potency associated with their differential potency to affect intracellular Ca+2 homeostasis.

Methods: Human neuroblastoma SH-SY5Y cells stably transfected with either wild type or M146L mutant human presenilin 1 were cultured and exposed to equipotent of propofol or sevoflurane. Cell viability, cytosolic and mitochondrial calcium were measured.

Results: Sevoflurane but not propofol, at clinically relevant concentrations and durations, promoted cell survival. Prolonged exposure (24 hours) of 1% sevoflurane resulted in significant cell damage in both types of cells. Both sevoflurane and propofol had significantly higher cell response rates to the elevation of cytosolic Ca+2 or mitochondrial Ca+2 in the presence of extracellular calcium. With the contribution of Ca+2 influx, sevoflurane but not equipotent 1 MAC propofol, caused a significantly greater increase in peak and overall Ca+2 in Alzheimer’s mutation cell than in wild type cells, but significantly more increase in overall mitochondrial Ca+2 concentrations in wild type than mutation cells. In the absence of extracellular Ca+2 influx, sevoflurane, but not propofol, caused more significant elevations of overall mitochondrial Ca+2 concentration in mutation cells than control cells.

Conclusion: Calcium influx contributed to the general anesthetics mediated elevation of cytosolic or mitochondrial Ca+2, which is especially true for propofol. Sevoflurane has a greater potency to either promote or inhibit cell survival than propofol, which may be associated with its ability to affect cytosolic or mitochondrial Ca+2 concentrations.

Keywords: Anesthetics, Alzheimer's disease, calcium, neurodegeneration, apoptosis, cell death.

« Previous Next »
[1]
Twaroski DM, Yan Y, Zaja I, Clark E, Bosnjak ZJ, Bai X. Altered mitochondrial dynamics contributes to propofol-induced cell death in human stem cell-derived neurons. Anesthesiology 2015; 123(5): 1067-83.
[http://dx.doi.org/10.1097/ALN.0000000000000857] [PMID: 26352374]
[2]
Ren G, Zhou Y, Liang G, et al. General anesthetics regulate autophagy via modulating the inositol 1,4,5-trisphosphate receptor: Implications for dual effects of cytoprotection and cytotoxicity. Sci Rep 2017; 7(1): 12378.
[http://dx.doi.org/10.1038/s41598-017-11607-0] [PMID: 28959036]
[3]
Sohn H-M, Kim HY, Park S, Han S-H, Kim J-H. Isoflurane decreases proliferation and differentiation, but none of the effects persist in human embryonic stem cell-derived neural progenitor cells. J Anesth 2017; 31(1): 36-43.
[http://dx.doi.org/10.1007/s00540-016-2277-z] [PMID: 27817157]
[4]
Liang G, Ward C, Peng J, Zhao Y, Huang B, Wei H. Isoflurane causes greater neurodegeneration than an equivalent exposure of sevoflurane in the developing brain of neonatal mice. Anesthesiology 2010; 112(6): 1325-34.
[http://dx.doi.org/10.1097/ALN.0b013e3181d94da5] [PMID: 20460994]
[5]
Huang B-Y, Huang H-B, Zhang Z-J, et al. Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8. CNS Neurosci Ther 2019; 25(5): 612-20.
[http://dx.doi.org/10.1111/cns.13090] [PMID: 30676695]
[6]
Liu F, Rainosek SW, Frisch-Daiello JL, et al. Potential adverse effects of prolonged sevoflurane exposure on developing monkey brain: From abnormal lipid metabolism to neuronal damage. Toxicol Sci 2015; 147(2): 562-72.
[http://dx.doi.org/10.1093/toxsci/kfv150] [PMID: 26206149]
[7]
Tao KM, Yang LQ, Liu YT, et al. Volatile anesthetics might be more beneficial than propofol for postoperative liver function in cirrhotic patients receiving hepatectomy. Med Hypotheses 2010; 75(6): 555-7.
[http://dx.doi.org/10.1016/j.mehy.2010.07.028] [PMID: 20709457]
[8]
Yang M, Wang Y, Liang G, Xu Z, Chu CT, Wei H. Alzheimer’s Disease Presenilin-1 Mutation Sensitizes Neurons to Impaired Autophagy Flux and Propofol Neurotoxicity: Role of Calcium Dysregulation. J Alzheimers Dis 2019; 67(1): 137-47.
[http://dx.doi.org/10.3233/JAD-180858] [PMID: 30636740]
[9]
Bianchi SL, Tran T, Liu C, et al. Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics. Neurobiol Aging 2008; 29(7): 1002-10.
[http://dx.doi.org/10.1016/j.neurobiolaging.2007.02.009] [PMID: 17346857]
[10]
Perucho J, Rubio I, Casarejos MJ, et al. Anesthesia with isoflurane increases amyloid pathology in mice models of Alzheimer’s disease. J Alzheimers Dis 2010; 19(4): 1245-57.
[http://dx.doi.org/10.3233/JAD-2010-1318] [PMID: 20308791]
[11]
Yang H, Liang G, Hawkins BJ, Madesh M, Pierwola A, Wei H. Inhalational anesthetics induce cell damage by disruption of intracellular calcium homeostasis with different potencies. Anesthesiology 2008; 109(2): 243-50.
[http://dx.doi.org/10.1097/ALN.0b013e31817f5c47] [PMID: 18648233]
[12]
Wei H, Liang G, Yang H, et al. The common inhalational anesthetic isoflurane induces apoptosis via activation of inositol 1,4,5-trisphosphate receptors. Anesthesiology 2008; 108(2): 251-60.
[http://dx.doi.org/10.1097/01.anes.0000299435.59242.0e] [PMID: 18212570]
[13]
Joseph JD, Peng Y, Mak DO, et al. General anesthetic isoflurane modulates inositol 1,4,5-trisphosphate receptor calcium channel opening. Anesthesiology 2014; 121(3): 528-37.
[http://dx.doi.org/10.1097/ALN.0000000000000316] [PMID: 24878495]
[14]
Wang H, Dong Y, Zhang J, et al. Isoflurane induces endoplasmic reticulum stress and caspase activation through ryanodine receptors. Br J Anaesth 2014; 113(4): 695-707.
[http://dx.doi.org/10.1093/bja/aeu053] [PMID: 24699520]
[15]
Kelliher M, Fastbom J, Cowburn RF, et al. Alterations in the ryanodine receptor calcium release channel correlate with Alzheimer’s disease neurofibrillary and beta-amyloid pathologies. Neuroscience 1999; 92(2): 499-513.
[http://dx.doi.org/10.1016/S0306-4522(99)00042-1] [PMID: 10408600]
[16]
Cheung KH, Shineman D, Müller M, et al. Mechanism of Ca2+ disruption in Alzheimer’s disease by presenilin regulation of InsP3 receptor channel gating. Neuron 2008; 58(6): 871-83.
[http://dx.doi.org/10.1016/j.neuron.2008.04.015] [PMID: 18579078]
[17]
Hitomi J, Katayama T, Taniguchi M, Honda A, Imaizumi K, Tohyama M. Apoptosis induced by endoplasmic reticulum stress depends on activation of caspase-3 via caspase-12. Neurosci Lett 2004; 357(2): 127-30.
[http://dx.doi.org/10.1016/j.neulet.2003.12.080] [PMID: 15036591]
[18]
Zhang Y, Zhen Y, Dong Y, et al. Anesthetic propofol attenuates the isoflurane-induced caspase-3 activation and Aβ oligomerization. PLoS One 2011; 6(11)e27019
[http://dx.doi.org/10.1371/journal.pone.0027019] [PMID: 22069482]
[19]
Berridge MJ. Calcium signalling and cell proliferation. BioEssays 1995; 17(6): 491-500.
[http://dx.doi.org/10.1002/bies.950170605] [PMID: 7575490]
[20]
Waldron RT, Short AD, Meadows JJ, Ghosh TK, Gill DL. Endoplasmic reticulum calcium pump expression and control of cell growth. J Biol Chem 1994; 269(16): 11927-33.
[http://dx.doi.org/10.1016/S0021-9258(17)32661-3] [PMID: 8163492]
[21]
Yang M, Wei H. Anesthetic neurotoxicity: Apoptosis and autophagic cell death mediated by calcium dysregulation. Neurotoxicol Teratol 2017; 60: 59-62.
[http://dx.doi.org/10.1016/j.ntt.2016.11.004] [PMID: 27856359]
[22]
Ureshino RP, Rocha KK, Lopes GS, Bincoletto C, Smaili SS. Calcium signaling alterations, oxidative stress, and autophagy in aging. Antioxid Redox Signal 2014; 21(1): 123-37.
[http://dx.doi.org/10.1089/ars.2013.5777] [PMID: 24512092]
[23]
Klein GL, Castro SM, Garofalo RP. The calcium-sensing receptor as a mediator of inflammation. Semin Cell Dev Biol 2016; 49: 52-6.
[http://dx.doi.org/10.1016/j.semcdb.2015.08.006] [PMID: 26303192]
[24]
Müller M, Cárdenas C, Mei L, Cheung KH, Foskett JK. Constitutive cAMP response element binding protein (CREB) activation by Alzheimer’s disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling. Proc Natl Acad Sci USA 2011; 108(32): 13293-8.
[http://dx.doi.org/10.1073/pnas.1109297108] [PMID: 21784978]
[25]
Filadi R, Greotti E, Turacchio G, Luini A, Pozzan T, Pizzo P. Mitofusin 2 ablation increases endoplasmic reticulum-mitochondria coupling. Proc Natl Acad Sci USA 2015; 112(17): E2174-81.
[http://dx.doi.org/10.1073/pnas.1504880112] [PMID: 25870285]
[26]
Bonora M, Giorgi C, Bononi A, et al. Subcellular calcium measurements in mammalian cells using jellyfish photoprotein aequorin-based probes. Nat Protoc 2013; 8(11): 2105-18.
[http://dx.doi.org/10.1038/nprot.2013.127] [PMID: 24113784]
[27]
Bellanti F, Mirabella L, Mitarotonda D, et al. Propofol but not sevoflurane prevents mitochondrial dysfunction and oxidative stress by limiting HIF-1α activation in hepatic ischemia/reperfusion injury. Free Radic Biol Med 2016; 96: 323-33.
[http://dx.doi.org/10.1016/j.freeradbiomed.2016.05.002] [PMID: 27154980]
[28]
Humeau J, Bravo-San Pedro JM, Vitale I, et al. Calcium signaling and cell cycle: Progression or death. Cell Calcium 2018; 70: 3-15.
[http://dx.doi.org/10.1016/j.ceca.2017.07.006] [PMID: 28801101]
[29]
Andropoulos DB, Greene MF. Anesthesia and developing brains - implications of the FDA warning. N Engl J Med 2017; 376(10): 905-7.
[http://dx.doi.org/10.1056/NEJMp1700196] [PMID: 28177852]
[30]
Grover LA, Mitchell RB, Szmuk P. Anesthesia Exposure and neurotoxicity in children-understanding the FDA warning and implications for the otolaryngologist. JAMA Otolaryngol Head Neck Surg 2017; 143(11): 1071-2.
[http://dx.doi.org/10.1001/jamaoto.2017.1570] [PMID: 28910434]
[31]
Luo T, Wu J, Kabadi SV, et al. Propofol limits microglial activation after experimental brain trauma through inhibition of nicotinamide adenine dinucleotide phosphate oxidase. Anesthesiology 2013; 119(6): 1370-88.
[http://dx.doi.org/10.1097/ALN.0000000000000020] [PMID: 24121215]
[32]
Davidson AJ, Disma N, de Graaff JC, et al. Neurodevelopmental outcome at 2 years of age after general anaesthesia and awake-regional anaesthesia in infancy (GAS): An international multicentre, randomised controlled trial. Lancet 2016; 387(10015): 239-50.
[http://dx.doi.org/10.1016/S0140-6736(15)00608-X] [PMID: 26507180]
[33]
Sun LS, Li G, Miller TL, et al. Association between a single general anesthesia exposure before age 36 months and neurocognitive outcomes in later childhood. JAMA 2016; 315(21): 2312-20.
[http://dx.doi.org/10.1001/jama.2016.6967] [PMID: 27272582]
[34]
Xu Z, Dong Y, Wu X, et al. The potential dual effects of anesthetic isoflurane on Aβ-induced apoptosis. Curr Alzheimer Res 2011; 8(7): 741-52.
[http://dx.doi.org/10.2174/156720511797633223] [PMID: 21244349]
[35]
Swyers T, Redford D, Larson DF. Volatile anesthetic-induced preconditioning. Perfusion 2014; 29(1): 10-5.
[http://dx.doi.org/10.1177/0267659113503975] [PMID: 24002781]
[36]
Kato R, Foëx P. Myocardial protection by anesthetic agents against ischemia-reperfusion injury: an update for anesthesiologists. Can J Anaesth 2002; 49(8): 777-91.
[http://dx.doi.org/10.1007/BF03017409] [PMID: 12374705]
[37]
Wilder RT, Flick RP, Sprung J, et al. Early exposure to anesthesia and learning disabilities in a population-based birth cohort. Anesthesiology 2009; 110(4): 796-804.
[http://dx.doi.org/10.1097/01.anes.0000344728.34332.5d] [PMID: 19293700]

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