Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake
Perigestational alcohol consumption by CF-1 mouse, from before mating up to the period of embryo organogenesis, leads to retarded early embryo development and neural tube defects. Here, we addressed if perigestational alcohol ingestion up to Day 10 of pregnancy induces oxidative stress and changes i...
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2017
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paper:paper_1040452X_v84_n10_p1086_Coll2023-06-08T16:00:46Z Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake apoptosis mouse embryo organogenesis nitrosylation oxidative stress perigestational alcohol 3 nitrotyrosine alcohol caspase 3 catalase drinking water glutathione nitrite superoxide dismutase thiobarbituric acid reactive substance alcohol antioxidant adult alcohol consumption animal tissue apoptosis Article caloric intake cardiac muscle cell adhesion cell damage controlled study ectoderm embryo endocardium enzyme activity female fetus development fetus growth immunohistochemistry immunoreactivity ingestion lipid peroxidation macromolecule mesoderm mouse neural tube nonhuman organogenesis oxidative stress priority journal tissue injury TUNEL assay Western blotting animal DNA damage drinking behavior drug effect embryo development genetics mammalian embryo metabolism outbred strain oxidative stress pathology pregnancy prenatal exposure Alcohol Drinking Animals Animals, Outbred Strains Antioxidants Apoptosis DNA Damage Embryo, Mammalian Embryonic Development Ethanol Female Mice Organogenesis Oxidative Stress Pregnancy Prenatal Exposure Delayed Effects Perigestational alcohol consumption by CF-1 mouse, from before mating up to the period of embryo organogenesis, leads to retarded early embryo development and neural tube defects. Here, we addressed if perigestational alcohol ingestion up to Day 10 of pregnancy induces oxidative stress and changes in macromolecules and organ tissues of early organogenic embryos. Adult CF-1 female mice were administered 10% ethanol in their drinking water for 17 days prior to mating and until Day 10 of gestation, whereas control females were administered ethanol-free water. Our results demonstrated significantly reduced Catalase abundance and activity and increased glutathione content in the embryos of ethanol-treated females. The nitrite level was significantly reduced, but TBARS (thiobarbituric acid reactive substances) content, an index of lipid peroxidation, did not change. Embryos derived from ethanol-treated females also showed higher abundance of 3-nitrotyrosine (3-NT)-containing proteins in all tissues, compared to the control group. Apoptosis was significantly increased in the ectoderm and mesoderm, but not in the heart—although this organ did contain more cleaved Caspase-3-positive cardiomyocytes per area of ventricular myocardium than controls. In sum, moderate perigestational alcohol ingestion up to Day 10 of gestation in mice induces oxidative stress by altering radical nitrogen species and antioxidant enzymatic and non-enzymatic mechanisms in embryos. Further, generalized protein nitration, due to unbalanced nitric oxide levels associated with tissue-specific apoptosis, was detected in embryos, suggesting that oxidative mechanisms may play an important role in the perigestational alcohol-induced malformation of organogenic embryos exposed to ethanol. © 2017 Wiley Periodicals, Inc. 2017 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_1040452X_v84_n10_p1086_Coll http://hdl.handle.net/20.500.12110/paper_1040452X_v84_n10_p1086_Coll |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
apoptosis mouse embryo organogenesis nitrosylation oxidative stress perigestational alcohol 3 nitrotyrosine alcohol caspase 3 catalase drinking water glutathione nitrite superoxide dismutase thiobarbituric acid reactive substance alcohol antioxidant adult alcohol consumption animal tissue apoptosis Article caloric intake cardiac muscle cell adhesion cell damage controlled study ectoderm embryo endocardium enzyme activity female fetus development fetus growth immunohistochemistry immunoreactivity ingestion lipid peroxidation macromolecule mesoderm mouse neural tube nonhuman organogenesis oxidative stress priority journal tissue injury TUNEL assay Western blotting animal DNA damage drinking behavior drug effect embryo development genetics mammalian embryo metabolism outbred strain oxidative stress pathology pregnancy prenatal exposure Alcohol Drinking Animals Animals, Outbred Strains Antioxidants Apoptosis DNA Damage Embryo, Mammalian Embryonic Development Ethanol Female Mice Organogenesis Oxidative Stress Pregnancy Prenatal Exposure Delayed Effects |
| spellingShingle |
apoptosis mouse embryo organogenesis nitrosylation oxidative stress perigestational alcohol 3 nitrotyrosine alcohol caspase 3 catalase drinking water glutathione nitrite superoxide dismutase thiobarbituric acid reactive substance alcohol antioxidant adult alcohol consumption animal tissue apoptosis Article caloric intake cardiac muscle cell adhesion cell damage controlled study ectoderm embryo endocardium enzyme activity female fetus development fetus growth immunohistochemistry immunoreactivity ingestion lipid peroxidation macromolecule mesoderm mouse neural tube nonhuman organogenesis oxidative stress priority journal tissue injury TUNEL assay Western blotting animal DNA damage drinking behavior drug effect embryo development genetics mammalian embryo metabolism outbred strain oxidative stress pathology pregnancy prenatal exposure Alcohol Drinking Animals Animals, Outbred Strains Antioxidants Apoptosis DNA Damage Embryo, Mammalian Embryonic Development Ethanol Female Mice Organogenesis Oxidative Stress Pregnancy Prenatal Exposure Delayed Effects Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| topic_facet |
apoptosis mouse embryo organogenesis nitrosylation oxidative stress perigestational alcohol 3 nitrotyrosine alcohol caspase 3 catalase drinking water glutathione nitrite superoxide dismutase thiobarbituric acid reactive substance alcohol antioxidant adult alcohol consumption animal tissue apoptosis Article caloric intake cardiac muscle cell adhesion cell damage controlled study ectoderm embryo endocardium enzyme activity female fetus development fetus growth immunohistochemistry immunoreactivity ingestion lipid peroxidation macromolecule mesoderm mouse neural tube nonhuman organogenesis oxidative stress priority journal tissue injury TUNEL assay Western blotting animal DNA damage drinking behavior drug effect embryo development genetics mammalian embryo metabolism outbred strain oxidative stress pathology pregnancy prenatal exposure Alcohol Drinking Animals Animals, Outbred Strains Antioxidants Apoptosis DNA Damage Embryo, Mammalian Embryonic Development Ethanol Female Mice Organogenesis Oxidative Stress Pregnancy Prenatal Exposure Delayed Effects |
| description |
Perigestational alcohol consumption by CF-1 mouse, from before mating up to the period of embryo organogenesis, leads to retarded early embryo development and neural tube defects. Here, we addressed if perigestational alcohol ingestion up to Day 10 of pregnancy induces oxidative stress and changes in macromolecules and organ tissues of early organogenic embryos. Adult CF-1 female mice were administered 10% ethanol in their drinking water for 17 days prior to mating and until Day 10 of gestation, whereas control females were administered ethanol-free water. Our results demonstrated significantly reduced Catalase abundance and activity and increased glutathione content in the embryos of ethanol-treated females. The nitrite level was significantly reduced, but TBARS (thiobarbituric acid reactive substances) content, an index of lipid peroxidation, did not change. Embryos derived from ethanol-treated females also showed higher abundance of 3-nitrotyrosine (3-NT)-containing proteins in all tissues, compared to the control group. Apoptosis was significantly increased in the ectoderm and mesoderm, but not in the heart—although this organ did contain more cleaved Caspase-3-positive cardiomyocytes per area of ventricular myocardium than controls. In sum, moderate perigestational alcohol ingestion up to Day 10 of gestation in mice induces oxidative stress by altering radical nitrogen species and antioxidant enzymatic and non-enzymatic mechanisms in embryos. Further, generalized protein nitration, due to unbalanced nitric oxide levels associated with tissue-specific apoptosis, was detected in embryos, suggesting that oxidative mechanisms may play an important role in the perigestational alcohol-induced malformation of organogenic embryos exposed to ethanol. © 2017 Wiley Periodicals, Inc. |
| title |
Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| title_short |
Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| title_full |
Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| title_fullStr |
Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| title_full_unstemmed |
Oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| title_sort |
oxidative stress and cellular and tissue damage in organogenic outbred mouse embryos after moderate perigestational alcohol intake |
| publishDate |
2017 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_1040452X_v84_n10_p1086_Coll http://hdl.handle.net/20.500.12110/paper_1040452X_v84_n10_p1086_Coll |
| _version_ |
1768545888453525504 |