| Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells. | |
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MedLine Citation:
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PMID: 19757036 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Ramesh B Badisa; Selina F Darling-Reed; Carl B Goodman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. Date: 2009-09-16 |
Journal Detail:
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Title: Neurochemical research Volume: 35 ISSN: 1573-6903 ISO Abbreviation: Neurochem. Res. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-21 Completed Date: 2010-03-23 Revised Date: 2013-05-31 |
Medline Journal Info:
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Nlm Unique ID: 7613461 Medline TA: Neurochem Res Country: United States |
Other Details:
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Languages: eng Pagination: 288-97 Citation Subset: IM |
Affiliation:
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Science Research Center, College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Room # 308E, Tallahassee, FL 32307, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects Astrocytoma 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 Rats Vacuoles / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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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 |
| Chemical | |
Reg. No./Substance:
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50-36-2/Cocaine |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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