Document Detail

Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells.
MedLine Citation:
PMID:  19757036     Owner:  NLM     Status:  MEDLINE    
Investigations with astroglial cells carry more prominence in drug abuse studies. However, due to earlier perception that astroglial cells were only passive bystanders in neural signal transmission, not many investigations were conducted on the toxicity of various abused drugs, like cocaine. The present study was aimed to discern the effect of cocaine on rat astroglioma cells and analyzed qualitatively for morphological features as well as vacuolation by phase contrast microscope, quantitatively for cytotoxicity, mitochondrial membrane potential by rhodamine- 123 fluorometric assay, and cell cycle analysis by flow cytometry. Based on population cell doubling time studies, glial cells were grown in 10% FBS in RPMI 1640 medium and treated with cocaine for 24 or 48 h. Microscopic assessments clearly demonstrated massive vacuolation and significant disruption at general architecture of glial cell morphology with cocaine. Chronic cocaine treatment (24 or 48 h) caused significant loss of cell viability. The sublethal dose of cocaine was found to be 4.307 and 3.794 mM at 24 and 48 h, respectively. Cocaine reduced the mitochondrial membrane potential in a dose dependent manner with ED(50) of 4 mM after 24 h. Cell cycle analysis suggested dual inhibition at G0/G1 and G2/M phases after 24 and 48 h, respectively. In summary, our findings suggest that cocaine toxicity was due to loss of mitochondrial membrane potential, vacuolation, and dual inhibition of cell cycle phases. These results may shed light in understanding the onset of some early key events in cocaine-induced toxicity in glial cells.
Ramesh B Badisa; Selina F Darling-Reed; Carl B Goodman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2009-09-16
Journal Detail:
Title:  Neurochemical research     Volume:  35     ISSN:  1573-6903     ISO Abbreviation:  Neurochem. Res.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-21     Completed Date:  2010-03-23     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  7613461     Medline TA:  Neurochem Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  288-97     Citation Subset:  IM    
Science Research Center, College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Room # 308E, Tallahassee, FL 32307, USA.
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MeSH Terms
Apoptosis / drug effects
Cell Cycle / drug effects*
Cell Division / drug effects
Cell Line, Tumor
Cell Survival / drug effects
Cocaine / pharmacology*
G0 Phase / drug effects
G2 Phase / drug effects
Membrane Potential, Mitochondrial / drug effects*
Neuroglia / cytology,  drug effects
Vacuoles / drug effects
Grant Support
G12 RR003020/RR/NCRR NIH HHS; G12 RR003020-25/RR/NCRR NIH HHS; G12 RR003020-255370/RR/NCRR NIH HHS; G12 RR003020-255372/RR/NCRR NIH HHS; G12RR03020/RR/NCRR NIH HHS; GM08111/GM/NIGMS NIH HHS; SD34HP04018//PHS HHS
Reg. No./Substance:

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