Effects of Early Ethanol Exposure on Lithobates pipiens Tadpole Development

1984 ◽

Vol 42 ◽

pp. 716-717

Author(s):

C. Uphoff ◽

C. Nyquist-Battie

Keyword(s):

Prenatal Exposure ◽

Heart Development ◽

Membrane Integrity ◽

Ethanol Exposure ◽

Prenatal Ethanol Exposure ◽

Pathological Changes ◽

Prenatally Exposed ◽

Inner Mitochondrial Membrane ◽

Fetal Alcohol ◽

Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

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Alterations in Ultrastructure of Skeletal Muscle From Newborn Guinea Pigs Following in Utero Exposure to Ethanol

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100120126 ◽

1985 ◽

Vol 43 ◽

pp. 686-687

Author(s):

C. Uphoff ◽

C. Nyquist-Battie ◽

T.B. Cole

Keyword(s):

Skeletal Muscle ◽

Guinea Pigs ◽

Muscle Development ◽

In Utero ◽

Ethanol Exposure ◽

Prenatally Exposed ◽

Chronic Alcoholic ◽

Test Kit ◽

Food And Water Intake ◽

Post Intubation

Ultrastructural alterations of skeletal muscle have been observed in adult chronic alcoholic patients. However, no such study has been performed on individuals prenatally exposed to ethanol. In order to determine if ethanol exposure in utero in the latter stages of muscle development was deleterious, skeletal muscle was obtained from newborn guinea pigs treated in the following manner. Six Hartly strain pregnant guinea pigs were randomly assigned to either the ethanol or the pair-intubated groups. Twice daily the 3 ethanol-treated animals were intubated with Ensure (Ross Laboratories) liquid diet containing 30% ethanol (6g/Kg pre-pregnant body weight per day) from day 35 of gestation until parturition at day 70±1 day. Serum ethanol levels were determined at 1 hour post-intubation by the Sigma alcohol test kit. For pair-intubation the Ensure diet contained sucrose substituted isocalorically for ethanol. Both food and water intake were monitored.

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HDAC inhibitor as a therapeutic strategy against the Central Nervous System alterations associated with prenatal and lactation ethanol exposure.

10.26226/morressier.5b31ec542afeeb001345b868 ◽

2018 ◽

Author(s):

Sandra Montagud Romero ◽

Miguel Angel Lujan Perez

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Hdac Inhibitor ◽

Therapeutic Strategy ◽

Ethanol Exposure ◽

The Central Nervous System

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Faculty Opinions recommendation of Pressure loading and ethanol exposure differentially modulate rat hepatic stellate cell activation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1098697.554818 ◽

2007 ◽

Author(s):

David Adams

Keyword(s):

Hepatic Stellate Cell ◽

Cell Activation ◽

Stellate Cell ◽

Ethanol Exposure ◽

Pressure Loading ◽

Hepatic Stellate Cell Activation

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THE EFFECTS OF PREGNANCY (P) ON THE RESPONSE OF THE CYTOCHROME P-450-DEPENDENT MIXED-FUNCTION MONOOXYGENASE SYSTEM (P450) TO ETHANOL EXPOSURE AND DIET CHANGE

Pediatric Research ◽

10.1203/00006450-198404001-00370 ◽

1984 ◽

Vol 18 ◽

pp. 155A-155A

Author(s):

George H Lambert ◽

Helen Leitz ◽

Alvin N Kotake

Keyword(s):

Ethanol Exposure ◽

Monooxygenase System ◽

Diet Change ◽

Cytochrome P 450

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Maternal Ethanol Exposure Acutely Elevates Src Family Kinase Activity in the Fetal Cortex

Molecular Neurobiology ◽

10.1007/s12035-021-02467-x ◽

2021 ◽

Author(s):

Dandan Wang ◽

Brian W. Howell ◽

Eric C. Olson

Keyword(s):

Tyrosine Phosphorylation ◽

Cortical Neurons ◽

Molecular Mechanisms ◽

Fetal Brain ◽

Ethanol Exposure ◽

Src Family Kinase ◽

Cortical Cells ◽

Signaling Systems ◽

Sustained Reduction ◽

Reelin Signaling

AbstractFetal alcohol syndrome (FAS) is characterized by disrupted fetal brain development and postnatal cognitive impairment. The targets of alcohol are diverse, and it is not clear whether there are common underlying molecular mechanisms producing these disruptions. Prior work established that acute ethanol exposure causes a transient increase in tyrosine phosphorylation of multiple proteins in cultured embryonic cortical cells. In this study, we show that a similar tyrosine phosphorylation transient occurs in the fetal brain after maternal dosing with ethanol. Using phospho-specific antibodies and immunohistochemistry, we mapped regions of highest tyrosine phosphorylation in the fetal cerebral cortex and found that areas of dendritic and axonal growth showed elevated tyrosine phosphorylation 10 min after maternal ethanol exposure. These were also areas of Src expression and Src family kinase (SFK) activation loop phosphorylation (pY416) expression. Importantly, maternal pretreatment with the SFK inhibitor dasatinib completely prevents both the pY416 increase and the tyrosine phosphorylation response. The phosphorylation response was observed in the perisomatic region and neurites of immature migrating and differentiating primary neurons. Importantly, the initial phosphotyrosine transient (~ 30 min) targets both Src and Dab1, two critical elements in Reelin signaling, a pathway required for normal cortical development. This initial phosphorylation response is followed by sustained reduction in Ser3 phosphorylation of n-cofilin, a critical actin severing protein and an identified downstream effector of Reelin signaling. This biochemical disruption is associated with sustained reduction of F-actin content and disrupted Golgi apparatus morphology in developing cortical neurons. The finding outlines a model in which the initial activation of SFKs by ethanol has the potential to disrupt multiple developmentally important signaling systems for several hours after maternal exposure.

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