Acute Alcohol Exposure Induces Apoptosis and Increases Histone H3K9/18 Acetylation in the Mid-Gestation Mouse Lung.

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Title: Acute Alcohol Exposure Induces Apoptosis and Increases Histone H3K9/18 Acetylation in the Mid-Gestation Mouse Lung.
Authors: Xiangyuan Wang1, Gomutputra, Prasra2,3, Wolgemuth, Debra J.1,2,3, Baxi, Laxmi V.1,4 lvb1@columbia.edu
Source: Reproductive Sciences. Apr2010, Vol. 17 Issue 4, p384-390. 7p. 2 Color Photographs, 1 Chart, 1 Graph.
Subject Terms: *ALCOHOL drinking, *APOPTOSIS, *HISTONES, *ACETYLATION, *FETUS, *LUNGS, *PREGNANCY
Abstract: Objective: Alcohol consumption causes cellular injury and excessive cell death. Recent studies indicate that ethanol can induce epigenetic alterations, particularly acetylation and methylation of histones and hypomethylation and hypermethylation of DNA. In the current study, we tested the hypothesis that acute exposure of pregnant mice to alcohol during mid-gestation can induce apoptosis and increase histone H3K9/18 acetylation in the fetal lung. The increased expression of histone H3K9/18 acetylation could alter the expression of genes that induce apoptosis. Study Design: C57BL/6J mice at day 13.5 of gestation were injected intraperitoneally with 2 doses of 25% ethanol (experimental) or Ringer solution (control) at 4-hour intervals. The fetuses were retrieved at 1, 3, 12, and 24 hours after alcohol exposure. The lungs were processed for detection of apoptosis by the terminal deoxynucleotidyl transferase biotin-deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assay and for levels of acetylated histone H3K9/18 by immunohistochemistry. Results: In the control lungs, apoptosis was observed in 0.22% and 0.25% of the mesenchymal and epithelial cells, respectively. In contrast, at 24 hours after alcohol injection at E13.5, 3.4% of the mesenchymal and 4.0% of the epithelial cells in the lung were undergoing apoptosis (TUNEL-positive; P < .005). The number of positively stained cells and levels of acetylated histone H3K9/18 staining significantly increased 1 hour after alcohol injection (P < .05) and returned to basal levels after 12 hours. Conclusions: Acute alcohol exposure of pregnant mice at mid-gestation results in increased apoptosis in the fetal lung, and elevated levels of acetylated histone H3K9/18 precede the observation of apoptosis. [ABSTRACT FROM AUTHOR]
Copyright of Reproductive Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Acute Alcohol Exposure Induces Apoptosis and Increases Histone H3K9/18 Acetylation in the Mid-Gestation Mouse Lung.
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Reproductive+Sciences%22&quot;&gt;Reproductive Sciences&lt;/searchLink&gt;. Apr2010, Vol. 17 Issue 4, p384-390. 7p. 2 Color Photographs, 1 Chart, 1 Graph.
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  Data: Objective: Alcohol consumption causes cellular injury and excessive cell death. Recent studies indicate that ethanol can induce epigenetic alterations, particularly acetylation and methylation of histones and hypomethylation and hypermethylation of DNA. In the current study, we tested the hypothesis that acute exposure of pregnant mice to alcohol during mid-gestation can induce apoptosis and increase histone H3K9/18 acetylation in the fetal lung. The increased expression of histone H3K9/18 acetylation could alter the expression of genes that induce apoptosis. Study Design: C57BL/6J mice at day 13.5 of gestation were injected intraperitoneally with 2 doses of 25% ethanol (experimental) or Ringer solution (control) at 4-hour intervals. The fetuses were retrieved at 1, 3, 12, and 24 hours after alcohol exposure. The lungs were processed for detection of apoptosis by the terminal deoxynucleotidyl transferase biotin-deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL) assay and for levels of acetylated histone H3K9/18 by immunohistochemistry. Results: In the control lungs, apoptosis was observed in 0.22% and 0.25% of the mesenchymal and epithelial cells, respectively. In contrast, at 24 hours after alcohol injection at E13.5, 3.4% of the mesenchymal and 4.0% of the epithelial cells in the lung were undergoing apoptosis (TUNEL-positive; P &lt; .005). The number of positively stained cells and levels of acetylated histone H3K9/18 staining significantly increased 1 hour after alcohol injection (P &lt; .05) and returned to basal levels after 12 hours. Conclusions: Acute alcohol exposure of pregnant mice at mid-gestation results in increased apoptosis in the fetal lung, and elevated levels of acetylated histone H3K9/18 precede the observation of apoptosis. [ABSTRACT FROM AUTHOR]
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  Data: &lt;i&gt;Copyright of Reproductive Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder&#39;s express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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