Nicotine, a major toxic component in tobacco smoke, leads to severe embryonic damage during organogenesis in embryos. We investigated whether resveratrol would positively influence nicotine-induced teratogenesis in mouse embryos (embryonic day 8.5) cultured for 48 h using a whole embryo culture system. Embryos exposed to nicotine (1mM) revealed significantly severe morphological anomalies, increased levels of caspase-3 mRNA and lipid peroxidation, and decreased levels of cytoplasmic superoxide dismutase (SOD), mitochondrial manganese SOD, cytosolic glutathione peroxidase, phospholipid hydroperoxide glutathione peroxidase, hypoxia-inducible factor 1α, Bcl-x(L), and sirtuin1 (SIRT1) mRNAs and SOD activity compared to those in the normal control group. However, when resveratrol (1×10(-8) μM or 1×10(-7) μM) was added concurrently to the embryos exposed to nicotine, all the parameters in above improved conspicuously. These findings indicate that resveratrol has a noted protective effect against nicotine-induced teratogenesis in mouse embryos through its antioxidative and anti-apoptotic effects.
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http://dx.doi.org/10.1016/j.reprotox.2012.05.097 | DOI Listing |
Comp Biochem Physiol C Toxicol Pharmacol
April 2023
Centre for the Research and Technology of Agro-Environmental and Biological Sciences (CITAB), UTAD, Vila Real, Portugal; Institute for Innovation, Capacity Building and Sustainability of Agri-Food Production (Inov4Agro), UTAD, Vila Real, Portugal. Electronic address:
Nicotine is a highly addictive substance that can cause teratogenic impacts in the embryo through redox-dependent pathways. As antioxidants, naturally occurring chemicals can protect cells from redox imbalance. The purpose of this study was to evaluate the effectiveness of 24-epibrassinolide (24-EPI), a natural brassinosteroid with well-known antioxidant properties, in protecting zebrafish embryos against nicotine's teratogenic effects.
View Article and Find Full Text PDFWound Repair Regen
November 2022
Allen Discovery Center at Tufts University, Medford, Massachusetts, USA.
Organogenesis is a complex process that can be disrupted by embryonic exposure to teratogens or mutation-induced alterations in signalling pathways, both of which result in organ mispatterning. Building on prior work in Xenopus laevis that showed that increased HCN2 ion channel activity rescues nicotine-induced brain and eye morphogenesis, we demonstrate much broader HCN2-based rescue of organ patterning defects. Induced HCN2 expression in both local or distant tissues can rescue CNS (brain and eye) as well as non-CNS (heart and gut) organ defects induced by three different teratogenic conditions: nicotine exposure, ethanol exposure or aberrant Notch protein.
View Article and Find Full Text PDFEvid Based Complement Alternat Med
July 2013
College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, Republic of Korea.
After maternal intake, nicotine crosses the placental barrier and causes severe embryonic disorders and fetal death. In this study, we investigated whether β -carotene has a beneficial effect against nicotine-induced teratogenesis in mouse embryos (embryonic day 8.5) cultured for 48 h in a whole embryo culture system.
View Article and Find Full Text PDFReprod Toxicol
November 2012
College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju 361-763, South Korea.
Nicotine, a major toxic component in tobacco smoke, leads to severe embryonic damage during organogenesis in embryos. We investigated whether resveratrol would positively influence nicotine-induced teratogenesis in mouse embryos (embryonic day 8.5) cultured for 48 h using a whole embryo culture system.
View Article and Find Full Text PDFBrain Res
March 1997
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710, USA.
Neurobehavioral teratogenesis caused by prenatal nicotine exposure is associated with deficiencies in brain cell numbers that reflect, in part, effects on cell replication but that also involve delayed cell loss. In the current study, pregnant rats were given nicotine by implanted minipump infusion either from gestational days 4-12 or 4-21 and fetal and neonatal brain regions were examined for expression of the mRNA encoding c-fos, a nuclear transcription factor that becomes chronically elevated when cell injury or apoptosis are occurring. Fetuses exposed to nicotine on gestational days 4-12 did not show elevations of c-fos mRNA on gestational day 18 whereas animals undergoing exposure through day 21 did.
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