NDLI: Antiapoptotic effects of nicotine in its protection against salsolinol-induced cytotoxicity

Content Provider	Springer Nature Link
Author	Copeland, Robert L. Das, Jharna R. Kanaan, Yasmine M. Taylor, Robert E. Tizabi, Yousef
Copyright Year	2007
Abstract	Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), a metabolite of dopamine, may act as an endogenous neurotoxin and contribute to the etiology of Parkinson’s disease (PD). The inverse relationship between smoking and PD prompted our previous investigation and the report of protective effects of nicotine against salsolinol-induced toxicity in cultured SH-SY5Y cells (Copelandet al., Neurotox. Res. 8:289, 2005). These cells, derived from human neuroblastoma cells, express dopaminergic activity and are used as a model of nigral dopaminergic cells, the major site of pathology in PD. The purpose of the current study was to investigate whether apoptotic or antiapoptotic mechanisms were responsible for the observed effects of salsolinol and nicotine, respectively. Moreover, it was of interest to determine whether the actions of nicotine are mediated through nicotinic receptors. SH-SY5Y cells were exposed to 0.4 or 0.7 mM salsolinol with and without pretreatment in combination of 0.1 mM nicotine and 0.1 mM mecamylamine, and were exposed for 24 and 48 h. Various parameters including cell cycle perturbations (reflected in propidium iodide DNA staining); cell cycle regulator retinoblastoma protein (reflected in the Western blot), apoptosis (reflected in annexin V/propidium iodide staining followed by flow cytometry) were analyzed. Salsolinol caused an arrest of the cells in G$_{1}$-phase of cell cycle and an increase in apoptotic indices, whereas pretreatment with nicotine attenuated or completely blocked the effects of salsolinol. Nicotine effects in turn, were totally blocked by mecamylamine (0.1 mM). The results suggest that apoptosis is a major mechanism for salsolinol-induced toxicity and that antiapoptotic effects of nicotine, mediated by nicotinic receptors, may play a primary role in its neuroprotective effects. Hence, nicotinic agonists in combination with other antiapoptotic agents may be of substantial benefit in at least a subpopulation of Parkinson patients.
Starting Page	61
Ending Page	69
Page Count	9
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	12
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2007-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Salsolinol Nicotine Mecamylamine Apoptosis Neuroprotection Neuroblastoma SH-SY5Y Cell Cycle Parkinson’s disease Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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

Additive Protective Effects of Donepezil and Nicotine Against Salsolinol-Induced Cytotoxicity in SH-SY5Y Cells

Neuroprotective effects of nicotine against salsolinol-induced cytotoxicity: Implications for parkinson’s disease

Protective Effects of Curcumin Against Rotenone and Salsolinol-Induced Toxicity: Implications for Parkinson’s Disease

PACAP Protects Against Salsolinol-Induced Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

PACAP Protects Against Inflammatory-Mediated Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells

Toxic Effects of Low Alcohol and Nicotine Combinations in SH-SY5Y Cells are Apoptotically Mediated

PACAP Protects Against Ethanol and Nicotine Toxicity in SH-SY5Y Cells: Implications for Drinking-Smoking Co-morbidity

Effects of Antidepressants on DSP4/CPT-Induced DNA Damage Response in Neuroblastoma SH-SY5Y Cells

Antiapoptotic effects of nicotine in its protection against salsolinol-induced cytotoxicity

Similar Documents

Additive Protective Effects of Donepezil and Nicotine Against Salsolinol-Induced Cytotoxicity in SH-SY5Y Cells

Neuroprotective effects of nicotine against salsolinol-induced cytotoxicity: Implications for parkinson’s disease

Protective Effects of Curcumin Against Rotenone and Salsolinol-Induced Toxicity: Implications for Parkinson’s Disease

PACAP Protects Against Salsolinol-Induced Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

PACAP Protects Against Inflammatory-Mediated Toxicity in Dopaminergic SH-SY5Y Cells: Implication for Parkinson’s Disease

Autophagy Activation Alleviates Amyloid-β-Induced Oxidative Stress, Apoptosis and Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells

Toxic Effects of Low Alcohol and Nicotine Combinations in SH-SY5Y Cells are Apoptotically Mediated

PACAP Protects Against Ethanol and Nicotine Toxicity in SH-SY5Y Cells: Implications for Drinking-Smoking Co-morbidity

Effects of Antidepressants on DSP4/CPT-Induced DNA Damage Response in Neuroblastoma SH-SY5Y Cells

Antiapoptotic effects of nicotine in its protection against salsolinol-induced cytotoxicity