Direct Measurement of Electron Transfer through a Hydrogen Bond between Single Molecules

Understanding electron transfer (ET) from a single molecule to another single molecule holds essential importance to realize bottom-up molecular devices in which constituent molecules are self-assembled via noncovalent interactions between each other. However, rather little is currently known about the ET properties at the single-molecule interface. Here we employ molecular tips to quantify the ET through a H-bond between single molecules. We found that a H-bond conducts electrons better than a covalent σ bond at short-range. Its conductance, however, decays steeply as the chain length of the H-bonded molecules increases. First-principle calculations were performed to reveal the electronic origin of the facile ET through the H-bond. Our results demonstrate that H-bonding in a molecular junction significantly affects its transport property

Immunohistochemical staining for 4-HNE in rat liver during chronic administration of ethanol (x100).

<p>(A1) Staining for 4-HNE was completely absent in rats received control liquid diet. (A2), (A3) & (A4) Animals received liquid diet containing 5% ethanol for 4, 6 and 8 weeks, respectively. Marked staining for 4-HNE in perivenular areas in increasing order from 4−8 weeks. CV−central vein. (B) Quantitative representation of the staining intensity of 4-HNE in A1−A4 stained sections (Mean ± S.D., <i>n = 5</i>).</p

Effect of AA-AGE on viability of cultured rat hepatocytes.

<p>(A) The 24 h old hepatocyte cultures were treated with media containing 25 µg/ml of AA-AGE or NEL and incubated for 48 h. Viability of hepatocytes cultured with AA-AGE was significantly decreased compared to the hepatocytes cultured with NEL. Neutralization of AA-AGE with AA-AGE antibody resulted in complete prevention of hepatocyte cell death induced by AA-AGE. ***<i>P</i><0.001 compared to the NEL treated cultures by Student’s <i>t</i>-test. (B) Alanine transaminase levels in rat serum after the start of chronic administration of alcohol for 8 weeks and also after abstinence. **<i>P</i><0.01 and ***<i>P</i><0.001 compared to control by ANOVA (n = 5).</p

Effect of alcohol abstinence on 4-HNE (×100).

<p>(A) Staining for 4-HNE during abstinence of alcohol, 4−12 weeks. Staining for 4-HNE was absent in rats received control liquid diet for 20 weeks. There was marked staining for 4-HNE in pericentral areas from 4−10 weeks of abstinence in sequentially decreasing order. Staining for 4-HNE was completely absent at 12 weeks of abstinence. CV−central vein. (B) Quantitative representation of the staining intensity of 4-HNE in A1−A6 stained sections. The data are mean ± S.D. of five liver samples (*<i>P</i><0.05).</p

Schematic representation of the formation of AA-AGE from acetaldehyde, production of ROS, and pathogenesis of ALD.

<p>This scheme was prepared based on our current data and previous work.</p

Effect of alcohol abstinence on AA-AGE (×100).

<p>(A) Staining for AA-AGE during abstinence of alcohol, 4−12 weeks. AA-AGE staining was absent in the liver of rats received control liquid diet for 20 weeks. Marked staining for AA-AGE was present in pericentral areas from 4−10 weeks of abstinence in sequentially decreasing order. Staining for AA-AGE was completely absent at 12 weeks of abstinence. CV−central vein (B) Quantitative representation of the staining intensity of AA-AGE in A1−A6 stained sections. The data are mean ± S.D. of five liver samples.</p

Immunohistochemical staining for 4-HNE in cultured rat hepatic stellate cells (×200).

<p>(A) Mild staining for 4-HNE was present in untreated control cells and cells treated with BSA. Marked staining for 4-HNE was present in stellate cells treated with both 5 µg/ml and 10 µg/ml AA-AGE. A few apoptotic cells (arrow) observed in cultures treated with both 5 µg/ml and 10 µg/ml AA-AGE. (B) Quantitative representation of the staining intensity of 4-HNE in cultured stellate cells (Mean ± S.D., <i>n = 5</i>).</p

Histopathological alterations in rat liver during chronic administration of ethanol (H&E ×100).

<p>(A1) Histopathological changes were not observed in rats received control liquid diet. (A2), (A3) & (A4) Animals received liquid diet containing ethanol for 4, 6, and 8 weeks, respectively. Fatty degeneration was observed in all ethanol treated animals in increasing order from 4−8 weeks. (B) Abstinence of alcohol for 12 weeks (H&E x100). There was no alteration in the liver of rats received control liquid diet for 20 weeks. Fatty degeneration was ameliorated from 4−12 weeks with complete disappearance of steatosis at 12 weeks. CV−central vein, PT−portal triad.</p

Glutathione levels in the liver during chronic administration of ethanol and after alcohol abstinence.

<p>A significant decrease was observed in total glutathione levels (GSH+GSSG) at 4th, 6th, and 8th week of ethanol administration through liquid diet. **<i>P</i><0.01 and ***P<0.001 compared to the untreated control by ANOVA (n = 5).</p

Immunohistochemical staining for α-smooth muscle actin (α-SMA) in the liver biopsy sections.

<p><b>(A)</b> The intensity of α-SMA staining in activated stellate cells coincided with the degree of fibrosis in F0, F1, F2, F3, and F4 group of patients with HCV infection. <b>(B)</b> Quantification of α-SMA staining. The data are mean ± S.D. in each group. Original magnification, x100.</p