ArticleInternational journal of medical sciences2008
Upregulation of Bax and Bcl-2 following prenatal cocaine exposure induces apoptosis in fetal rat brain.
Article in International journal of medical sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 41 citations in OpenAlex.
- The landscape of cocaine cytotoxicity and the role of sigma-1 receptor modulation and adulterant synergism.Archives of toxicology · 2026Review
- Dimethyltryptamine and harmine, components of ayahuasca, prevented cocaine-induced apoptosis in SH-SY5Y human neuroblastoma cells.Archives of toxicology · 2026Article
- Article
- CircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR-30a-3p and promoting PON2.Cell proliferation · 2022Article
- CD47 antibody protects mice from doxorubicin-induced myocardial damage by suppressing cardiomyocyte apoptosis.Experimental and therapeutic medicine · 2022Article
- Anhydroecgonine methyl ester, a cocaine pyrolysis product, contributes to cocaine-induced rat primary hippocampal neuronal death in a synergistic and time-dependent manner.Archives of toxicology · 2021Article
- Murine maternal dietary restriction affects neural Humanin expression and cellular profile.Journal of neuroscience research · 2020Article
- Hypercapnia induces IL-1β overproduction via activation of NLRP3 inflammasome: implication in cognitive impairment in hypoxemic adult rats.Journal of neuroinflammation · 2018Article
- Effect of docosahexaenoic acid on traumatic brain injury in rats.Experimental and therapeutic medicine · 2017Article
- Toxic effects of xylazine on endothelial cells in combination with cocaine and 6-monoacetylmorphine.Toxicology in vitro : an international journal published in association with BIBRA · 2014Article
- Cardiac Fas-dependent and mitochondria-dependent apoptosis after chronic cocaine abuse.International journal of molecular sciences · 2014Article
- Prenatal cocaine exposure and gray matter volume in adolescent boys and girls: relationship to substance use initiation.Biological psychiatry · 2013Article
- Delayed developmental changes in neonatal vocalizations correlates with variations in ventral medial hypothalamus and central amygdala development in the rodent infant: effects of prenatal cocaine.Behavioural brain research · 2012Article
- Mitochondria-specific accumulation of amyloid β induces mitochondrial dysfunction leading to apoptotic cell death.PloS one · 2012Article
- Maternal oral consumption of morphine increases Bax/Bcl-2 ratio and caspase 3 activity during early neural system development in rat embryos.Journal of molecular neuroscience : MN · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledCocaine abuse during pregnancy has been associated with numerous adverse perinatal outcomes.
aimsThe present study was to determine whether prenatal cocaine exposure induced apoptosis and the possible role of Bcl-2 family genes in the programming cell death in fetal rat brain. MAIN
methodsPregnant rats were treated with cocaine subcutaneously (30 & 60 mg/kg/day) from day 15 to 21 of gestation. Then the fetal and maternal brains were isolated. KEY
findingsCocaine produced a dose-dependent decrease in fetal brain weight and brain/body weight ratio (P<0.05). Apoptotic nuclei in fetal brain were increased from 2.6 +/- 0.1 (control) to 8.1+/- 0.6 (low dose) and 10.4 +/- 0.2% (high dose) (P<0.05). In accordance, cocaine dose dependently increased activities of caspase-3, caspase-8, and caspase-9 (% of control) in the fetal brain by 177%, 155%, 174%, respectively, at 30 mg/kg/day, and by 191%, 176%, 274%, respectively, at 60 mg/kg/day. In contrast, cocaine showed no effect on caspase activities in the maternal brain. Cocaine produced a dose-dependent increase in both Bcl-2 and Bax protein expression in the fetal brain, and increased the ratio of Bax/Bcl-2 at dose of 30 mg/kg/day (P<0.05). SIGNIFICANCE: Our study has demonstrated that prenatal cocaine exposure induces apoptosis in the fetal brain, and suggested that up-regulating Bax/Bcl-2 gene expression may be involved in cocaine-induced apoptosis. The increased apoptosis of neuronal cells in the fetal brain is likely to play a key role in cocaine-induced neuronal defects during fetal development.
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