NDLI: Persistent mitoK$_{ATP}$ Activation Is Involved in the Isoflurane-induced Cytotoxicity

Content Provider	Springer Nature Link
Author	Yang, Yan Chen, Xiufang Min, Haiyan Song, Shiyu Zhang, Juan Fan, Shanshan Yi, Long Wang, Hongwei Gu, Xiaoping Ma, Zhengliang Gao, Qian
Copyright Year	2016
Abstract	Isoflurane exposure induces apoptosis in cultured cells and in the developing brain, while the underlying mechanism remains largely unclarified. This study was designed to determine whether the disruption of mitoK$_{ATP}$-mediated ATP balance was involved in the cytotoxicity of isoflurane. Human neuroglioma cells U251 and 7-day-old mice were treated with isoflurane. A specific mitoK$_{ATP}$ antagonist 5-HD was used, and the cellular ATP levels, NAD$^{+}$/NADH ratios, and mitochondrial transmembrane potential (ΔΨ$_{m}$) were measured. Our data showed that the blockage of mitoK$_{ATP}$ by 5-HD mitigated the isoflurane-induced ΔΨ$_{m}$ disruption, reactive oxygen species (ROS) accumulation, and apoptosis in U251 cells. Moreover, we found that the toxic effect of isoflurane was not observed in the first 2-h exposure; instead, the cellular ATP levels and NAD$^{+}$/NADH ratios were markedly increased. The reduction of ATP levels and NAD$^{+}$/NADH ratios was only detected after this initial phase. This dynamical effect of isoflurane was blocked by 5-HD. In contrast, a ROS scavenger NAC sustained the isoflurane-induced ATP elevation. Similar results were observed in animal studies. And again, 5-HD attenuated isoflurane-induced cognitive disorders in the Intellicage test, a system that assesses place learning behavior in a social environment. Our study uncovered a potential mechanism underlying isoflurane’s toxicity with a therapeutic future.
Starting Page	1101
Ending Page	1110
Page Count	10
File Format	PDF
ISSN	08937648
Journal	Molecular Neurobiology
Volume Number	54
Issue Number	2
e-ISSN	15591182
Language	English
Publisher	Springer US
Publisher Date	2016-01-23
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Isoflurane MitoK$_{ATP}$ Cytotoxicity ROS Intellicage Neurosciences Neurobiology Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Mitochondrial K$_{ATP}$ Channels Control Glioma Radioresistance by Regulating ROS-Induced ERK Activation

Vitamin C Attenuates Isoflurane-Induced Caspase-3 Activation and Cognitive Impairment

Anesthetic Isoflurane Induces DNA Damage Through Oxidative Stress and p53 Pathway

JNK Activation Contributes to Oxidative Stress-Induced Parthanatos in Glioma Cells via Increase of Intracellular ROS Production

Liver X Receptor β Is Involved in Formalin-Induced Spontaneous Pain

Calpain-Dependent ErbB4 Cleavage Is Involved in Brain Ischemia-Induced Neuronal Death

FBXW7-Induced MTOR Degradation Forces Autophagy to Counteract Persistent Prion Infection

Erratum to: Activation of Glycogen Synthase Kinase-3 Mediates the Olfactory Deficit-Induced Hippocampal Impairments

Molecular Alterations Associated with the NMDA Preconditioning-Induced Neuroprotective Mechanism Against Glutamate Cytotoxicity

Persistent mitoK$_{ATP}$ Activation Is Involved in the Isoflurane-induced Cytotoxicity

Similar Documents

Mitochondrial K$_{ATP}$ Channels Control Glioma Radioresistance by Regulating ROS-Induced ERK Activation

Vitamin C Attenuates Isoflurane-Induced Caspase-3 Activation and Cognitive Impairment

Anesthetic Isoflurane Induces DNA Damage Through Oxidative Stress and p53 Pathway

JNK Activation Contributes to Oxidative Stress-Induced Parthanatos in Glioma Cells via Increase of Intracellular ROS Production

Liver X Receptor β Is Involved in Formalin-Induced Spontaneous Pain

Calpain-Dependent ErbB4 Cleavage Is Involved in Brain Ischemia-Induced Neuronal Death

FBXW7-Induced MTOR Degradation Forces Autophagy to Counteract Persistent Prion Infection

Erratum to: Activation of Glycogen Synthase Kinase-3 Mediates the Olfactory Deficit-Induced Hippocampal Impairments

Molecular Alterations Associated with the NMDA Preconditioning-Induced Neuroprotective Mechanism Against Glutamate Cytotoxicity

Persistent mitoK$_{ATP}$ Activation Is Involved in the Isoflurane-induced Cytotoxicity