Controlling Vibrational Energy Flow in Liquid Alkylbenzenes

Ultrafast infrared (IR) Raman spectroscopy was used to study vibrational energy in ϕ–S alkylbenzenes, where ϕ = C₆H₅ and substituents S were CH₃– (toluene), (CH₃)₂CH– (isopropylbenzene, IPB), or (CH₃)₃C– (<i>t</i>-butylbenzene, TBB). Using methods described previously, the normal modes were classified as phenyl (ϕ), substituent (S), or global (G). IR pulses were tuned to find conditions that maximized the localization of initial CH-stretch excitations on ϕ or S. Anti-Stokes Raman spectroscopy measured transient energy content of Raman-active S, ϕ, and G modes, to determine the rates of phenyl to substituent (Φ → S) or substituent to phenyl (S → Φ) transfer during the first few picoseconds, when energy transfer was mainly intramolecular. Since phenyl CH-stretches were 90–130 cm^–1 uphill in energy from substituent CH-stretches, of interest were S → Φ processes where molecular structure and local couplings were more important than energy differences. The Φ → S process efficiencies were small and about equal with all three substituents. The S → Φ transfer efficiencies could be increased by increasing substituent size. This was opposite to what would be predicted on the basis of the larger density of states of larger substituents, and it provides a path toward controlling forward-to-backward vibrational energy transfer ratios. The S → Φ transfer efficiency is understood as resulting from an increase in the local anharmonic couplings. A heavier substituent, when vibrating, transfers energy more effectively to the phenyl group

Unidirectional Vibrational Energy Flow in Nitrobenzene

Experiments were performed on nitrobenzene liquid at ambient temperature to probe vibrational energy flow from the nitro group to the phenyl group and vice versa. The IR pump, Raman probe method was used. Quantum chemical calculations were used to sort the normal modes of nitrobenzene into three categories: phenyl modes, nitro modes, and global modes. IR wavelengths in the 2500–3500 cm^–1 range were found that best produced excitations initially localized on nitro or phenyl. Pulses at 2880 cm^–1 excited a nitro stretch combination band. Pulses at 3080 cm^–1 excited a phenyl C–H stretch plus some nitro stretch. With nitro excitation there was no detectable energy transfer to phenyl. With phenyl excitation there was no direct transfer to nitro, but there was some transfer to global modes such as phenyl-nitro stretching, so some of the vibrational amplitude on phenyl moved onto nitro. Thus energy transfer from nitro to phenyl was absent, but there was weak energy transfer from phenyl to nitro. The experimental methods described here can be used to study vibrational energy flow from one part of a molecule to another, which could assist in the design of molecules for molecular electronics and phononics. The vibrational isolation of the nitro group when attached to a phenyl moiety suggests that strongly nonthermal reaction pathways may play an important role in impact initiation of energetic materials having peripheral nitro groups

Mitochondrial ROS-induced cardiac damage during sepsis and the mechanism of action of mitochondria-targeted antioxidants (MTAs).

<p>Mitochondrial ROS-induced cardiac damage during sepsis and the mechanism of action of mitochondria-targeted antioxidants (MTAs).</p

Mitochondrial ROS-dependent activation of myocardial inflammation after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A.</b> NF-κB p65 subunit was detected in cytosolic and nuclear fractions by Western blot using GAPDH and c-Jun as a loading control respectively. Results were quantified by densitometry. <b>B.</b> Heart sections were co-stained with anti-ASC (brown) and haematoxylin (blue). Negative control was stained with secondary antibody alone. Images are representative of a random selection of at least 3 sections of N = 6. <b>C.</b> Activated form of caspase 1 was determined in heart tissue lysates by Western blot using GAPDH as a loading control, and results were quantified by densitometry. <b>D.</b> Production of IL–1β was measured in heart tissue lysates by ELISA. All values are means ±SE, and statistical significances are shown as * between sham and sepsis and Δ between vehicle and Mito-Vit-E (<i>p</i><0.02, n = 6).</p

Mitochondrial ROS dependent activation of RAGE pathway in the heart after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A</b>. Heart sections were stained with anti-RAGE (brown) and haematoxylin (blue). Negative control was stained with secondary antibody alone. Images are representative of a random selection of at least 3 sections of N = 6. <b>B</b>. RAGE-TFAM interaction was determined by co-immunoprecipitation in total heart lysate. Shown result was reprehensive of three independent experiments (N = 6).</p

Mitochondrial ROS dependent functional deficiency and structural impairment in cardiac mitochondria after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A.</b> Mitochondrial fractions were subjected to the measurements of complex I-V activities. <b>B.</b> Ultrastructure of myocardial mitochondria was observed by transmission electron microscope (TEM). Biochemically, mitochondrial outer membrane damage was measured using the mitochondrial fractions. All values are means ±SE. Significant differences are shown as * between sham and sepsis and Δ between vehicle and Mito-Vit-E (<i>p</i><0.02, n = 6).</p

Effects of Mito-Vit-E and TLR9 inhibitor OND-I in LPS-challenged cardiomyocytes.

<p>Cultured neonatal cardiomyocytes from rats were treated with ±LPS (100 ng/ml), ±Mito-Vit-E (MVE) (1μM), or ±ODN-I (0.5 μM) 4 hours prior to harvesting. <b>A.</b> Mitochondrial superoxide was labeled with MitoSox Red and quantified by flow cytometry. <b>B</b>. Mitochondrial biogenesis was quantified in live cells using MitoBiogenesis In-Cell ELISA assay. <b>C.</b> Levels of mtDNA in cell medium and in cytoplasm were measured by real-time PCR. <b>D</b>. Cells apoptosis was evaluated by TUNEL assay (green). Cell nucleuses were identified by DAPI staining (blue). <b>E.</b> Expression of MyD88, RAGE, ASC and activated form of caspase 1 were determined in cell lysates by western blot using GAPDH as a loading control, and results were quantified by densitometry. <b>F.</b> Cellular production of IL–1β was measured by ELISA. All the measurements were normalized by cell numbers and obtained in triplicate. All values are means ±SE. Significant differences are shown as * between control and LPS and Δ between vehicle and drug-treated groups (<i>p</i><0.02 for A-C and p<0.01 for E-F, n = 4).</p

Mitochondrial ROS dependent activation of mtDNA-TLR9 pathway in the heart after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A</b>. Levels of mtDNA in cytosol fractions were measured by real-time PCR. <b>B</b>. Expression of TLR9, IRAK4 and MyD88 were determined in total tissue lysates by western blot using GAPDH as a loading control, and the results were quantified by densitometry. All values are means ±SE. Significant differences are shown as * between sham and sepsis and Δ between vehicle and Mito-Vit-E (<i>p</i><0.02, n = 6).</p

Mitochondrial ROS dependent mtDNA damage in the heart after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE), vitamin E (VE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A.</b> 0.4 ng genomic DNA from the heart tissue was amplified for 25 cycles by LPCR. Mouse DNA was included as an internal control. The PCR products were digested, separated on 1% agarose gel, and analyzed by densitometry. Levels of 8-hydroxy-2-deoxy guanosine (8-OH-dG) (<b>B</b>) and apurinic/apyrimidinic (AP) sites (<b>C</b>) were measured in DNA isolated from mitochondrial fractions. All values are means ±SE. Significant differences are shown as * between sham and sepsis, Δ between vehicle and drug-treated, and <b>⏏</b> between vitamin E and Mito-Vit-E (<i>p</i><0.01, n = 6).</p

Mito-Vit-E attenuates myocardial damage after sepsis.

<p>Rats were infected by <i>S</i>. <i>pneumoniae</i> or given PBS sham control. 21.5 μmoles/kg Mito-Vit-E (MVE) or vehicle was administered orally 30 minutes post-inoculation, and heart tissues were harvested 24 hours later. <b>A</b>. Serum levels of troponin I (cTnI) were measured by ELISA assay. All values are means ±SE. Significant differences are shown as * between sham and sepsis and Δ between vehicle and Mito-Vit-E (<i>p</i><0.05, n = 6). In addition, heart tissue sections were applied to H&E staining (<b>B)</b> and TUNEL assay (green) (<b>C</b>). In <b>C</b>, cell nucleuses were identified by propidium iodide (PI) staining (Red). The original magnification is 40 fold, and images are representative of a random selection of at least 3 sections of N = 6.</p