Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation will increase in lipopolysaccharide-induced inflammation in vitro model
With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced in...
Saved in:
Published in | Journal of neuroinflammation Vol. 12; no. 1; p. 105 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central Ltd
29.05.2015
BioMed Central |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase.
Spiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley® (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 μg/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay.
LPS (100 μg/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 μg/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 μg/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 μg/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 μg/ml) exposure, and H2O2 groups (P < 0.05, 0.01).
Short-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model. |
---|---|
AbstractList | With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase. Spiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley[R] (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 [mu]g/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay. LPS (100 [mu]g/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 [mu]g/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 [mu]g/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 [mu]g/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 [mu]g/ml) exposure, and H.sub.2O.sub.2 groups (P < 0.05, 0.01). Short-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model. With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase.BACKGROUNDWith the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase.Spiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley® (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 μg/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay.METHODSSpiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley® (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 μg/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay.LPS (100 μg/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 μg/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 μg/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 μg/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 μg/ml) exposure, and H2O2 groups (P < 0.05, 0.01).RESULTSLPS (100 μg/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 μg/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 μg/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 μg/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 μg/ml) exposure, and H2O2 groups (P < 0.05, 0.01).Short-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model.CONCLUSIONSShort-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model. With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase. Spiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley® (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 μg/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay. LPS (100 μg/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 μg/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 μg/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 μg/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 μg/ml) exposure, and H2O2 groups (P < 0.05, 0.01). Short-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model. Background With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain unclear. Apart from RF-EMR, humans are also exposed to various physical and chemical factors. We established a lipopolysaccharide (LPS)-induced inflammation in vitro model to investigate whether the possible sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation (at specific absorption rates: 2, 4 W/kg) will increase. Methods Spiral ganglion neurons (SGN) were obtained from neonatal (1- to 3-day-old) Sprague Dawley[R] (SD) rats. After the SGN were treated with different concentrations (0, 20, 40, 50, 100, 200, and 400 [mu]g/ml) of LPS, the Cell Counting Kit-8 (CCK-8) and alkaline comet assay were used to quantify cellular activity and DNA damage, respectively. The SGN were treated with the moderate LPS concentrations before RF-EMR exposure. After 24 h intermittent exposure at an absorption rate of 2 and 4 W/kg, DNA damage was examined by alkaline comet assay, ultrastructure changes were detected by transmission electron microscopy, and expression of the autophagy markers LC3-II and Beclin1 were examined by immunofluorescence and confocal laser scanning microscopy. Reactive oxygen species (ROS) production was quantified by the dichlorofluorescin-diacetate assay. Results LPS (100 [mu]g/ml) induced DNA damage and suppressed cellular activity (P < 0.05). LPS (40 [mu]g/ml) did not exhibit cellular activity changes or DNA damage (P > 0.05); therefore, 40 [mu]g/ml was used to pretreat the concentration before exposure to RF-EMR. RF-EMR could not directly induce DNA damage. However, the 4 W/kg combined with LPS (40 [mu]g/ml) group showed mitochondria vacuoles, karyopyknosis, presence of lysosomes and autophagosome, and increasing expression of LC3-II and Beclin1. The ROS values significantly increased in the 4 W/kg exposure, 4 W/kg combined with LPS (40 [mu]g/ml) exposure, and H.sub.2O.sub.2 groups (P < 0.05, 0.01). Conclusions Short-term exposure to radiofrequency electromagnetic radiation could not directly induce DNA damage in normal spiral ganglion neurons, but it could cause the changes of cellular ultrastructure at special SAR 4.0 W/kg when cells are in fragile or micro-damaged condition. It seems that the sensitivity of SGN to damage caused by mobile phone electromagnetic radiation will increase in a lipopolysaccharide-induced inflammation in vitro model. Keywords: Lipopolysaccharide, Spiral ganglion neurons, Sensitivity, Damage, Radiofrequency electromagnetic radiation |
ArticleNumber | 105 |
Audience | Academic |
Author | Hu, Yu-Juan Kong, Wen Zhao, Xue-Yan Kong, Wei-Jia Zuo, Wen-Qi Zhang, Yuan-Yuan Yang, Yang |
Author_xml | – sequence: 1 givenname: Wen-Qi surname: Zuo fullname: Zuo, Wen-Qi – sequence: 2 givenname: Yu-Juan surname: Hu fullname: Hu, Yu-Juan – sequence: 3 givenname: Yang surname: Yang fullname: Yang, Yang – sequence: 4 givenname: Xue-Yan surname: Zhao fullname: Zhao, Xue-Yan – sequence: 5 givenname: Yuan-Yuan surname: Zhang fullname: Zhang, Yuan-Yuan – sequence: 6 givenname: Wen surname: Kong fullname: Kong, Wen – sequence: 7 givenname: Wei-Jia surname: Kong fullname: Kong, Wei-Jia |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26022358$$D View this record in MEDLINE/PubMed |
BookMark | eNp1kk1rFTEUhgep2A_9AW4k4MbN1CST-doIpWgVCi7UdTg3OXNvJJOMyUzl_iT_ped2WmlFySIH8rxvztdpcRRiwKJ4Kfi5EF3zNgvZt6rkoi55xXkpnhQnolWylLxXRw_i4-I05--cV7Ju5LPiWDZcyqruTopfXzBkN7sbN-9ZHFieXALPthC23sXAAi4phszmyCyMsEVmYMlo2WbPxrhxHtm0o6wYejRzioQEnJ1hCayD-WDx03nPXDAJISMFzLspTtHvMxizg-Qsli7YxZCrC4OHcVyFhFJaKdJHFv3z4ukAPuOLu_us-Pbh_dfLj-X156tPlxfXpWl4M5dDL8xguOiwtS2gANHX0DXNhurdiMHUFrjqoG2HzlrVSaTAVNyCaI2Sqq_Oiner77RsRrQGw0wd0VNyI6S9juD045fgdnobb7RSdcdlQwZv7gxS_LFgnvXoskHvIWBcshZN1_S9qvgBfb2iW_CoqfhIjuaA64taiVqKiiuizv9B0bE4OkPNH2gMjwWvHpbwJ_f7sRPQroBJMeeEgzZuvm06OTuvBdeHBdPrgmlaMH1YMC1IKf5S3pv_X_MbIxXXQQ |
CitedBy_id | crossref_primary_10_1016_j_envint_2024_109104 crossref_primary_10_1016_j_heliyon_2024_e36140 crossref_primary_10_1186_s42826_020_00055_z crossref_primary_10_1016_j_neuroscience_2018_06_002 crossref_primary_10_1016_j_phymed_2024_156245 crossref_primary_10_3390_ijms22073772 crossref_primary_10_3390_ijms23158414 crossref_primary_10_3892_ijmm_2018_3539 crossref_primary_10_1016_j_freeradbiomed_2018_04_575 crossref_primary_10_2139_ssrn_3548385 crossref_primary_10_1002_bem_22388 crossref_primary_10_1080_15548627_2021_1905466 crossref_primary_10_1371_journal_pone_0201022 crossref_primary_10_1080_09553002_2018_1432913 crossref_primary_10_1016_j_heliyon_2024_e37223 crossref_primary_10_1016_j_mrgentox_2017_08_001 crossref_primary_10_1042_BSR20212584 crossref_primary_10_1002_bem_22032 crossref_primary_10_1016_j_envres_2018_01_034 crossref_primary_10_1002_bem_22255 crossref_primary_10_1080_15548627_2019_1569926 crossref_primary_10_3389_fpubh_2021_771508 crossref_primary_10_3390_ijms23020658 crossref_primary_10_1007_s12192_018_0945_7 crossref_primary_10_1016_j_mrgentox_2018_11_014 crossref_primary_10_3389_fpubh_2024_1419525 |
Cites_doi | 10.1093/jjco/hyt160 10.1111/j.1365-2249.2010.04292.x 10.1002/pmic.200600234 10.1167/iovs.07-1333 10.2307/3579911 10.1007/s00420-003-0446-5 10.1016/j.toxlet.2014.05.004 10.1016/S0731-7085(01)00492-7 10.1186/s12866-014-0236-0 10.3109/09553002.2012.711504 10.1016/j.mrgentox.2006.03.002 10.1371/journal.pone.0054906 10.4161/auto.25399 10.1016/j.biopha.2007.12.004 10.1093/mutage/ger034 10.3342/ceo.2008.1.3.117 10.1667/RR3127 10.1017/S0022215114000723 10.1099/jmm.0.015792-0 10.1289/ehp.6039 10.1016/j.pathophys.2012.11.001 10.1016/j.mrfmmm.2009.10.004 10.1042/BJ20061653 10.1186/1748-717X-7-61 10.1093/toxsci/kfh184 10.1080/09553000802460123 10.1038/cddis.2013.217 10.1016/j.fertnstert.2008.08.022 10.1093/mutage/ges018 10.1002/bem.20127 10.1523/JNEUROSCI.1014-14.2014 10.1016/j.tiv.2009.06.019 10.1523/JNEUROSCI.1735-05.2005 10.1016/j.mrfmmm.2009.10.012 10.1371/journal.pone.0109630 10.1002/bem.20580 |
ContentType | Journal Article |
Copyright | COPYRIGHT 2015 BioMed Central Ltd. Zuo et al. 2015 |
Copyright_xml | – notice: COPYRIGHT 2015 BioMed Central Ltd. – notice: Zuo et al. 2015 |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
DOI | 10.1186/s12974-015-0300-1 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1742-2094 |
ExternalDocumentID | PMC4458026 A541521304 26022358 10_1186_s12974_015_0300_1 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GroupedDBID | --- 0R~ 29L 2WC 4.4 53G 5GY 5VS 7X7 88E 8FI 8FJ AAFWJ AAJSJ AASML AAWTL AAYXX ABDBF ABUWG ACGFO ACGFS ACIHN ACPRK ACUHS ADBBV ADRAZ ADUKV AEAQA AENEX AFKRA AFPKN AHBYD AHMBA AHSBF AHYZX ALIPV ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C6C CCPQU CITATION CS3 DIK DU5 E3Z EBD EBLON EBS EJD ESX F5P FYUFA GROUPED_DOAJ GX1 H13 HMCUK HYE IAO IHR INH INR ITC KQ8 M1P M48 M~E O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO RBZ RNS ROL RPM RSV SBL SOJ TR2 TUS UKHRP WOQ WOW XSB ~8M CGR CUY CVF ECM EIF NPM PJZUB PPXIY PMFND 7X8 5PM |
ID | FETCH-LOGICAL-c606t-f91cfc018e7d7ae1a195a866b235b1fc5da048a77f8dd482e7f8c30da17c42493 |
IEDL.DBID | M48 |
ISSN | 1742-2094 |
IngestDate | Thu Aug 21 17:17:50 EDT 2025 Mon Jul 21 10:00:22 EDT 2025 Tue Jun 17 22:07:11 EDT 2025 Tue Jun 10 21:10:16 EDT 2025 Mon Jul 21 06:02:48 EDT 2025 Thu Apr 24 22:57:23 EDT 2025 Tue Jul 01 02:54:24 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Language | English |
License | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c606t-f91cfc018e7d7ae1a195a866b235b1fc5da048a77f8dd482e7f8c30da17c42493 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1186/s12974-015-0300-1 |
PMID | 26022358 |
PQID | 1686994306 |
PQPubID | 23479 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_4458026 proquest_miscellaneous_1686994306 gale_infotracmisc_A541521304 gale_infotracacademiconefile_A541521304 pubmed_primary_26022358 crossref_citationtrail_10_1186_s12974_015_0300_1 crossref_primary_10_1186_s12974_015_0300_1 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2015-05-29 |
PublicationDateYYYYMMDD | 2015-05-29 |
PublicationDate_xml | – month: 05 year: 2015 text: 2015-05-29 day: 29 |
PublicationDecade | 2010 |
PublicationPlace | England |
PublicationPlace_xml | – name: England – name: London |
PublicationTitle | Journal of neuroinflammation |
PublicationTitleAlternate | J Neuroinflammation |
PublicationYear | 2015 |
Publisher | BioMed Central Ltd BioMed Central |
Publisher_xml | – name: BioMed Central Ltd – name: BioMed Central |
References | YM Moustafa (300_CR35) 2001; 26 B Avci (300_CR14) 2012; 88 Y Al Dhaheri (300_CR17) 2014; 9 S Xu (300_CR25) 2013; 8 A Agarwal (300_CR2) 2009; 92 S Ivancsits (300_CR38) 2003; 76 F Focke (300_CR39) 2010; 683 KK Kesari (300_CR1) 2013; 51 LG Salford (300_CR3) 2003; 111 ID Kim (300_CR32) 2009; 23 M Eguchi (300_CR33) 2011; 163 P Vecchia (300_CR37) 2007; 43 Q Zeng (300_CR26) 2006; 6 C Seidel (300_CR21) 2012; 7 P Galloni (300_CR8) 2005; 26 J Luukkonen (300_CR10) 2010; 31 K Liu (300_CR27) 2014; 228 AD Garg (300_CR16) 2013; 9 E Lee (300_CR28) 2004; 81 K Yao (300_CR5) 2008; 49 GJ Hook (300_CR7) 2004; 161 Z Zhou (300_CR19) 2005; 25 C Ersson (300_CR22) 2011; 26 TQ Huang (300_CR9) 2008; 84 S Franzellitti (300_CR24) 2010; 683 E Seckin (300_CR30) 2014; 128 EM Bailey (300_CR29) 2014; 34 SK Juhn (300_CR12) 2008; 1 YS Lu (300_CR15) 2012; 2012 VK Wong (300_CR34) 2013; 4 AL Smit (300_CR11) 2010; 59 TS Kumaravel (300_CR23) 2006; 605 RS Malyapa (300_CR6) 1998; 149 Q Deng (300_CR18) 2013; 43 M Kruszewski (300_CR20) 2012; 27 J Friedman (300_CR13) 2007; 405 L Hardell (300_CR36) 2008; 62 L Hardell (300_CR4) 2013; 20 EA Britta (300_CR31) 2014; 14 18436834 - Invest Ophthalmol Vis Sci. 2008 May;49(5):2009-15 20093374 - J Med Microbiol. 2010 Apr;59(Pt 4):377-83 24813634 - Toxicol Lett. 2014 Aug 4;228(3):216-24 19896957 - Mutat Res. 2010 Jan 5;683(1-2):74-83 9611103 - Radiat Res. 1998 Jun;149(6):637-45 22511614 - Mutagenesis. 2012 Sep;27(5):551-8 12802592 - Int Arch Occup Environ Health. 2003 Jul;76(6):431-6 19822160 - Mutat Res. 2010 Jan 5;683(1-2):35-42 16037958 - Bioelectromagnetics. 2005 Oct;26(7):536-47 20564172 - Bioelectromagnetics. 2010 Sep;31(6):417-24 16888767 - Proteomics. 2006 Sep;6(17):4732-8 16107643 - J Neurosci. 2005 Aug 17;25(33):7558-66 22520045 - Radiat Oncol. 2012;7:61 23678539 - Indian J Exp Biol. 2013 Mar;51(3):187-200 17938457 - Ann Ist Super Sanita. 2007;43(3):260-7 22788526 - Int J Radiat Biol. 2012 Nov;88(11):799-805 11516912 - J Pharm Biomed Anal. 2001 Nov;26(4):605-8 23800749 - Autophagy. 2013 Sep;9(9):1292-307 15178808 - Toxicol Sci. 2004 Sep;81(1):121-32 16621680 - Mutat Res. 2006 Jun 16;605(1-2):7-16 22778799 - Oxid Med Cell Longev. 2012;2012:740280 24784924 - J Laryngol Otol. 2014 May;128(5):400-5 14731070 - Radiat Res. 2004 Feb;161(2):193-200 23355902 - PLoS One. 2013;8(1):e54906 23846222 - Cell Death Dis. 2013;4:e720 21778357 - Mutagenesis. 2011 Nov;26(6):689-95 18242044 - Biomed Pharmacother. 2008 Feb;62(2):104-9 17456048 - Biochem J. 2007 Aug 1;405(3):559-68 18804757 - Fertil Steril. 2009 Oct;92(4):1318-25 24186908 - Jpn J Clin Oncol. 2013 Dec;43(12):1261-8 19540912 - Toxicol In Vitro. 2009 Sep;23(6):1014-9 12782486 - Environ Health Perspect. 2003 Jun;111(7):881-3; discussion A408 23261330 - Pathophysiology. 2013 Apr;20(2):85-110 25253283 - BMC Microbiol. 2014;14:236 21166666 - Clin Exp Immunol. 2011 Feb;163(2):260-9 25253857 - J Neurosci. 2014 Sep 24;34(39):13110-26 19016139 - Int J Radiat Biol. 2008 Nov;84(11):909-15 25299698 - PLoS One. 2014;9(10):e109630 19434244 - Clin Exp Otorhinolaryngol. 2008 Sep;1(3):117-38 |
References_xml | – volume: 2012 start-page: 740280 year: 2012 ident: 300_CR15 publication-title: Oxid Med Cell Longev – volume: 43 start-page: 1261 year: 2013 ident: 300_CR18 publication-title: Jpn J Clin Oncol doi: 10.1093/jjco/hyt160 – volume: 163 start-page: 260 year: 2011 ident: 300_CR33 publication-title: Clin Exp Immunol doi: 10.1111/j.1365-2249.2010.04292.x – volume: 51 start-page: 187 year: 2013 ident: 300_CR1 publication-title: Indian J Exp Biol – volume: 6 start-page: 4732 year: 2006 ident: 300_CR26 publication-title: Proteomics doi: 10.1002/pmic.200600234 – volume: 49 start-page: 2009 year: 2008 ident: 300_CR5 publication-title: Invest Ophthalmol Vis Sci doi: 10.1167/iovs.07-1333 – volume: 149 start-page: 637 year: 1998 ident: 300_CR6 publication-title: Radiat Res doi: 10.2307/3579911 – volume: 76 start-page: 431 year: 2003 ident: 300_CR38 publication-title: Int Arch Occup Environ Health doi: 10.1007/s00420-003-0446-5 – volume: 228 start-page: 216 year: 2014 ident: 300_CR27 publication-title: Toxicol Lett doi: 10.1016/j.toxlet.2014.05.004 – volume: 26 start-page: 605 year: 2001 ident: 300_CR35 publication-title: J Pharm Biomed Anal doi: 10.1016/S0731-7085(01)00492-7 – volume: 14 start-page: 236 year: 2014 ident: 300_CR31 publication-title: BMC Microbiol doi: 10.1186/s12866-014-0236-0 – volume: 88 start-page: 799 year: 2012 ident: 300_CR14 publication-title: Int J Radiat Biol doi: 10.3109/09553002.2012.711504 – volume: 605 start-page: 7 year: 2006 ident: 300_CR23 publication-title: Mutat Res doi: 10.1016/j.mrgentox.2006.03.002 – volume: 8 start-page: e54906 year: 2013 ident: 300_CR25 publication-title: PLoS One doi: 10.1371/journal.pone.0054906 – volume: 9 start-page: 1292 year: 2013 ident: 300_CR16 publication-title: Autophagy doi: 10.4161/auto.25399 – volume: 62 start-page: 104 year: 2008 ident: 300_CR36 publication-title: Biomed Pharmacother doi: 10.1016/j.biopha.2007.12.004 – volume: 26 start-page: 689 year: 2011 ident: 300_CR22 publication-title: Mutagenesis doi: 10.1093/mutage/ger034 – volume: 1 start-page: 117 year: 2008 ident: 300_CR12 publication-title: Clin Exp Otorhinolaryngol doi: 10.3342/ceo.2008.1.3.117 – volume: 161 start-page: 193 year: 2004 ident: 300_CR7 publication-title: Radiat Res doi: 10.1667/RR3127 – volume: 128 start-page: 400 year: 2014 ident: 300_CR30 publication-title: J Laryngol Otol doi: 10.1017/S0022215114000723 – volume: 59 start-page: 377 year: 2010 ident: 300_CR11 publication-title: J Med Microbiol doi: 10.1099/jmm.0.015792-0 – volume: 111 start-page: 881 year: 2003 ident: 300_CR3 publication-title: Environ Health Perspect doi: 10.1289/ehp.6039 – volume: 20 start-page: 85 year: 2013 ident: 300_CR4 publication-title: Pathophysiology doi: 10.1016/j.pathophys.2012.11.001 – volume: 683 start-page: 35 year: 2010 ident: 300_CR24 publication-title: Mutat Res doi: 10.1016/j.mrfmmm.2009.10.004 – volume: 405 start-page: 559 year: 2007 ident: 300_CR13 publication-title: Biochem J doi: 10.1042/BJ20061653 – volume: 7 start-page: 61 year: 2012 ident: 300_CR21 publication-title: Radiat Oncol doi: 10.1186/1748-717X-7-61 – volume: 81 start-page: 121 year: 2004 ident: 300_CR28 publication-title: Toxicol Sci doi: 10.1093/toxsci/kfh184 – volume: 84 start-page: 909 year: 2008 ident: 300_CR9 publication-title: Int J Radiat Biol doi: 10.1080/09553000802460123 – volume: 4 start-page: e720 year: 2013 ident: 300_CR34 publication-title: Cell Death Dis doi: 10.1038/cddis.2013.217 – volume: 92 start-page: 1318 year: 2009 ident: 300_CR2 publication-title: Fertil Steril doi: 10.1016/j.fertnstert.2008.08.022 – volume: 27 start-page: 551 year: 2012 ident: 300_CR20 publication-title: Mutagenesis doi: 10.1093/mutage/ges018 – volume: 43 start-page: 260 year: 2007 ident: 300_CR37 publication-title: Ann Ist Super Sanita – volume: 26 start-page: 536 year: 2005 ident: 300_CR8 publication-title: Bioelectromagnetics doi: 10.1002/bem.20127 – volume: 34 start-page: 13110 year: 2014 ident: 300_CR29 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.1014-14.2014 – volume: 23 start-page: 1014 year: 2009 ident: 300_CR32 publication-title: Toxicol In Vitro doi: 10.1016/j.tiv.2009.06.019 – volume: 25 start-page: 7558 year: 2005 ident: 300_CR19 publication-title: J Neurosci doi: 10.1523/JNEUROSCI.1735-05.2005 – volume: 683 start-page: 74 year: 2010 ident: 300_CR39 publication-title: Mutat Res doi: 10.1016/j.mrfmmm.2009.10.012 – volume: 9 start-page: e109630 year: 2014 ident: 300_CR17 publication-title: PLoS One doi: 10.1371/journal.pone.0109630 – volume: 31 start-page: 417 year: 2010 ident: 300_CR10 publication-title: Bioelectromagnetics doi: 10.1002/bem.20580 – reference: 16888767 - Proteomics. 2006 Sep;6(17):4732-8 – reference: 22788526 - Int J Radiat Biol. 2012 Nov;88(11):799-805 – reference: 18804757 - Fertil Steril. 2009 Oct;92(4):1318-25 – reference: 19016139 - Int J Radiat Biol. 2008 Nov;84(11):909-15 – reference: 16621680 - Mutat Res. 2006 Jun 16;605(1-2):7-16 – reference: 25253857 - J Neurosci. 2014 Sep 24;34(39):13110-26 – reference: 22511614 - Mutagenesis. 2012 Sep;27(5):551-8 – reference: 11516912 - J Pharm Biomed Anal. 2001 Nov;26(4):605-8 – reference: 17938457 - Ann Ist Super Sanita. 2007;43(3):260-7 – reference: 12802592 - Int Arch Occup Environ Health. 2003 Jul;76(6):431-6 – reference: 24186908 - Jpn J Clin Oncol. 2013 Dec;43(12):1261-8 – reference: 22778799 - Oxid Med Cell Longev. 2012;2012:740280 – reference: 23355902 - PLoS One. 2013;8(1):e54906 – reference: 23800749 - Autophagy. 2013 Sep;9(9):1292-307 – reference: 12782486 - Environ Health Perspect. 2003 Jun;111(7):881-3; discussion A408 – reference: 20564172 - Bioelectromagnetics. 2010 Sep;31(6):417-24 – reference: 24813634 - Toxicol Lett. 2014 Aug 4;228(3):216-24 – reference: 25253283 - BMC Microbiol. 2014;14:236 – reference: 22520045 - Radiat Oncol. 2012;7:61 – reference: 16107643 - J Neurosci. 2005 Aug 17;25(33):7558-66 – reference: 23846222 - Cell Death Dis. 2013;4:e720 – reference: 23261330 - Pathophysiology. 2013 Apr;20(2):85-110 – reference: 25299698 - PLoS One. 2014;9(10):e109630 – reference: 24784924 - J Laryngol Otol. 2014 May;128(5):400-5 – reference: 19434244 - Clin Exp Otorhinolaryngol. 2008 Sep;1(3):117-38 – reference: 18436834 - Invest Ophthalmol Vis Sci. 2008 May;49(5):2009-15 – reference: 20093374 - J Med Microbiol. 2010 Apr;59(Pt 4):377-83 – reference: 9611103 - Radiat Res. 1998 Jun;149(6):637-45 – reference: 18242044 - Biomed Pharmacother. 2008 Feb;62(2):104-9 – reference: 17456048 - Biochem J. 2007 Aug 1;405(3):559-68 – reference: 21166666 - Clin Exp Immunol. 2011 Feb;163(2):260-9 – reference: 15178808 - Toxicol Sci. 2004 Sep;81(1):121-32 – reference: 16037958 - Bioelectromagnetics. 2005 Oct;26(7):536-47 – reference: 21778357 - Mutagenesis. 2011 Nov;26(6):689-95 – reference: 19896957 - Mutat Res. 2010 Jan 5;683(1-2):74-83 – reference: 14731070 - Radiat Res. 2004 Feb;161(2):193-200 – reference: 19540912 - Toxicol In Vitro. 2009 Sep;23(6):1014-9 – reference: 23678539 - Indian J Exp Biol. 2013 Mar;51(3):187-200 – reference: 19822160 - Mutat Res. 2010 Jan 5;683(1-2):35-42 |
SSID | ssj0032562 |
Score | 2.2750807 |
Snippet | With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system remain... Background With the increasing popularity of mobile phones, the potential hazards of radiofrequency electromagnetic radiation (RF-EMR) on the auditory system... |
SourceID | pubmedcentral proquest gale pubmed crossref |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 105 |
SubjectTerms | Analysis Animals Animals, Newborn Apoptosis Regulatory Proteins - metabolism Beclin-1 Care and treatment Cell Phone Cells, Cultured Disease Models, Animal DNA Damage - drug effects Dose-Response Relationship, Drug Electric waves Electromagnetic Phenomena Electromagnetic radiation Electromagnetic waves Electromagnetism Ganglion Health aspects In Vitro Techniques Inflammation Inflammation - etiology Inflammation - metabolism Inflammation - physiopathology Lipopolysaccharides - adverse effects Lipopolysaccharides - pharmacology Microtubule-Associated Proteins - metabolism Mitogens Neurons Neurons - cytology Neurons - drug effects Neurons - physiology Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Risk factors Spiral Ganglion - cytology Spiral Ganglion - drug effects Spiral Ganglion - physiology Time Factors |
Title | Sensitivity of spiral ganglion neurons to damage caused by mobile phone electromagnetic radiation will increase in lipopolysaccharide-induced inflammation in vitro model |
URI | https://www.ncbi.nlm.nih.gov/pubmed/26022358 https://www.proquest.com/docview/1686994306 https://pubmed.ncbi.nlm.nih.gov/PMC4458026 |
Volume | 12 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1bi9QwFA7rLogv4t3qOkQQBCHaS5qkDyKr7LIIs4g6MG8hzWUd6LbrdAacn-S_9Jy2M0xl9a2Q05L2fOfWnAshr4xJlA-5YWANHONpcMxkwjGR2hjnFebc4_-O6YU4n_HP83x-QLbjrYYP2N4Y2uE8qdmyevvr5-YDCPz7TuCVeNeCzZKYS5EzgGzMIBg6AsMkUU6nfHeokIF1T4eDzRtvw8bAAmxahvPf96zU37p6z1iNEyn3LNPZPXJ3cCnpSY-B--TA1w_I7elwaP6Q_P6GSer9lAjaBNqdrVf00mAFb1PTrqVl3dJVQ525Av1CrVm33tFyQ6-aEtQGxQR2T4eROUBSY-kjXWJfA2QsBYe7oosaPdDWwwWtFtc4fWHTGot1XQvnGQT_ACMHqwFQ2FdMIilsa9nQbiLPIzI7O_3-6ZwNExqYhcBnxUKR2GBjYLd00vjEJEVulBAlfMMyCTZ3BjSEkTIo57hKPVzYLHYmkZZD4Jc9Joc1vMBTQr3gRemKwiYhcDCZZabyYJwqpQMdYeKIxFuOaDu0L8cpGpXuwhgldM9PDfzUyE-dROTN7pbrvnfH_4hfI5s1Ig2ea81QngC7ww5Z-iTvXJ0s5hE5HlGCPNrR8sstUDQuYRJb7Zt1qxOhRIHt7kVEnvTA2e1rC7yIyBGkdgTYBny8Ui9-dO3AOc8VRNLP_vnM5-RO2qE8Z2lxTA5Xy7V_Aa7UqpyQW3IuJ-To4-nFl6-T7ofEpBOaP7ROIZ8 |
linkProvider | Scholars Portal |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Sensitivity+of+spiral+ganglion+neurons+to+damage+caused+by+mobile+phone+electromagnetic+radiation+will+increase+in+lipopolysaccharide-induced+inflammation+in+vitro+model&rft.jtitle=Journal+of+neuroinflammation&rft.au=Zuo%2C+Wen-Qi&rft.au=Hu%2C+Yu-Juan&rft.au=Yang%2C+Yang&rft.au=Zhao%2C+Xue-Yan&rft.date=2015-05-29&rft.eissn=1742-2094&rft.volume=12&rft.spage=105&rft_id=info:doi/10.1186%2Fs12974-015-0300-1&rft_id=info%3Apmid%2F26022358&rft.externalDocID=26022358 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1742-2094&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1742-2094&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1742-2094&client=summon |