Amelioration of ethanol-induced growth retardation by all- trans-retinoic acid and α-tocopherol in shell-less culture of the chick embryo

The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all- trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 5...

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Published in:Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2004-05, Vol.18 (3), p.407-412
Main Authors: Satiroglu-Tufan, N.Lale, Tufan, A.Cevik
Format: Article
Language:English
Subjects:
Alcoholism and acute alcohol poisoning
All- trans-retinoic acid
Animals
Antioxidants - pharmacology
Biological and medical sciences
Body Weight - drug effects
Chick Embryo
Dose-Response Relationship, Drug
Embryo Culture Techniques
Embryology: invertebrates and vertebrates. Teratology
Ethanol
Ethanol - antagonists & inhibitors
Ethanol - toxicity
FAS
Fetal Growth Retardation - chemically induced
Fetal Growth Retardation - pathology
Fundamental and applied biological sciences. Psychology
Growth retardation
Malondialdehyde - metabolism
Medical sciences
Teratogens
Teratology. Teratogens
Toxicology
Tretinoin - pharmacology
Vitamin E - pharmacology
α-Tocopherol
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Summary:The mechanisms of teratogenic action of ethanol (EtOH) were investigated by testing the hypothesis that all- trans-retinoic acid and/or α-tocopherol ameliorates ethanol-induced embryonic growth retardation. Chicken embryos were explanted in shell-less cultures and a single dose of EtOH (15, 30, or 50%) or 50% EtOH with either all- trans-retinoic acid (10 −8 M) or α-tocopherol (0.05 M) or a mix of all- trans-retinoic acid (10 −8 M) and α-tocopherol (0.05 M) was applied to the center of the blastodisc. EtOH significantly increased the mortality rate and induced growth retardation in a dose-dependent manner. In addition, EtOH increased malondialdehyde (MDA) levels, an indicator of oxidative stress and cell damage, in a dose dependent manner. All- trans-retinoic acid, the active form of Vitamin A, and/or α-tocopherol, an antioxidant, co-treatment with EtOH significantly diminished both the EtOH-induced mortality and growth retardation. However, only α-tocopherol co-treatment reduced the MDA levels. Thus, the mechanisms of teratogenic action of EtOH appear to involve initiation of oxidative stress as well as perturbation of retinoic acid (RA) signaling. It also appears likely that these mechanisms work independently of each other.
ISSN:0890-6238
1873-1708
DOI:10.1016/j.reprotox.2004.01.005