ArticleNeurochemical research2010
Cocaine induces alterations in mitochondrial membrane potential and dual cell cycle arrest in rat c6 astroglioma cells.
Article in Neurochemical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- The landscape of cocaine cytotoxicity and the role of sigma-1 receptor modulation and adulterant synergism.Archives of toxicology · 2026Review
- Evaluation of Cocaine Effect on Endogenous Metabolites of HepG2 Cells Using Targeted Metabolomics.Molecules (Basel, Switzerland) · 2021Article
- Cocaine potentiates an inflammatory response in C6 astroglia-like cells.Biomedical reports · 2021Article
- Identification of cytotoxic markers in methamphetamine treated rat C6 astroglia-like cells.Scientific reports · 2019Article
- Identification of biochemical and cytotoxic markers in cocaine treated PC12 cells.Scientific reports · 2018Article
- Cellular and molecular responses to acute cocaine treatment in neuronal-like N2a cells: potential mechanism for its resistance in cell death.Cell death discovery · 2018Article
- The Alterations in Mitochondrial DNA Copy Number and Nuclear-Encoded Mitochondrial Genes in Rat Brain Structures after Cocaine Self-Administration.Molecular neurobiology · 2017Article
- Cardiovascular Mitochondrial Dysfunction Induced by Cocaine: Biomarkers and Possible Beneficial Effects of Modulators of Oxidative Stress.Oxidative medicine and cellular longevity · 2017Review
- N-acetyl cysteine mitigates the acute effects of cocaine-induced toxicity in astroglia-like cells.PloS one · 2015Article
- Milk thistle seed extract protects rat C6 astroglial cells from acute cocaine toxicity.Molecular medicine reports · 2014Article
- Role of methamphetamine on glioblastoma cytotoxicity induced by doxorubicin and methotrexate.Neurotoxicity research · 2014Article
- Selective anticancer activity of neurotoxin 1-methyl-4-phenylpyridinium on non-small cell lung adenocarcinoma A549 cells.Anticancer research · 2014Article
- Attenuating effect of N-acetyl-L-cysteine against acute cocaine toxicity in rat C6 astroglial cells.International journal of molecular medicine · 2013Article
- Effects of chronic cocaine in rat C6 astroglial cells.International journal of molecular medicine · 2012Article
- Cerebrolysin Attenuates Heat Shock Protein (HSP 72 KD) Expression in the Rat Spinal Cord Following Morphine Dependence and Withdrawal: Possible New Therapy for Pain Management.Current neuropharmacology · 2011Article
- The protective role of D-glucose against 1-methyl-4-phenylpyridinium ion (MPP+): induced mitochondrial dysfunction in C6 astroglial cells.Neurochemical research · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.