Influence of Altering Chlorine Substitution Positions on Photovoltaic Property of Small Molecule Donors for All-Small-Molecule Organic Solar Cells

To deeply investigate the structure-property relationship in organic solar cells (OSCs), one widely used strategy is to design a series of organic photovoltaic materials with same chemical formular but different...

Microbial dechlorination of polychrolinated biphenyls

Polychlorinated biphenyls (PCBs) are organic xenobiotics contaminating environment for at least 50 years. They could be eventually eliminated by various organisms under different conditions. The degree of chlorine substitution per biphenyl molecule influences biodegradability which decreases with increasing chlorination. Our work is focused on the PCBs biodegradation under anaerobic conditions. The suitable high chlorinated biphenyls are converted via reductive dechlorination to the chlorinated biphenyls with lower extent of chlorine, which could be eventually fully mineralized by aerobic bacteria. Microbial consortium was isolated from sediment of Strážský Creek (located near by plant producing PCBs in the past). This consortium was able to dechlorinate polychlorinated biphenyls under anoxic conditions. The effectiveness of this process was tested under different cultivation condition – different energetic sources (Aroclor 1248 or Aroclor 1260 or Delor 103 or Delor 106), addition of potential electron donors (pyruvate, lactate or acetate with hydrogen) and further if there is necessary to add yeast extract into fresh low sulphur cultivation media. Our microbial consortia so far do not need supplementation by non-contaminated sediment to maintain dechlorination activity. Addition of yeast extract is non essential, but needs to be further proved in serial transfers. In all cases (except acetate without yeast extract) dechlorination proceeds at meta- and flanked paraposition.

Crystal and molecular structures of some phosphane-substituted cymantrenes [(C5H4 X)Mn(CO)LL′] (X = H or Cl, L = CO, L′ = PPh3 or PCy3, and LL' = Ph2PCH2CH2PPh2)

UV irradiation of tetrahydrofuran solutions of [CpMn(CO)3] (Cp = π-C5H5 or π-C5H4Cl) in the presence of the phosphanes PPh3 or PCy3 (Cy = cyclohexyl) and Ph2PCH2CH2PPh2 yields the substitution products [CpMn(CO)2PR 3] (R = Ph or Cy) and [CpMn(CO)(Ph2PCH2CH2PPh2)], namely, dicarbonyl(η5-cyclopentadienyl)(triphenylphosphane-κP)manganese(I), [Mn(C5H5)(C18H15P)(CO)2], 1a, dicarbonyl(η5-1-chlorocyclopentadienyl)(triphenylphosphane-κP)manganese(I), [Mn(C5H4Cl)(C18H15P)(CO)2], 1b, dicarbonyl(η5-cyclopentadienyl)(tricyclohexylphosphane-κP)manganese(I), [Mn(C5H5)(C18H33P)(CO)2], 2a, dicarbonyl(η5-1-chlorocyclopentadienyl)(tricyclohexylphosphane-κP)manganese(I), [Mn(C5H4Cl)(C18H33P)(CO)2], 2b, carbonyl(η5-cyclopentadienyl)[1,2-bis(diphenylphosphanyl)ethane-κ2 P,P′]manganese(I), [Mn(C5H5)(C26H24P2)(CO)], 3a, and carbonyl(η5-1-chlorocyclopentadienyl)[1,2-bis(diphenylphosphanyl)ethane-κ2 P,P′]manganese(I), [Mn(C5H4Cl)(C26H24P2)(CO)], 3b, The crystal structure determinations show a very small influence of the chlorine substitution and a moderate influence of the phosphane substitution on the bond lengths. The PR 3 groups avoid being eclipsed with the C—Cl bonds. All the compounds employ weak C—H...O interactions for intermolecular association, which are enhanced by C—H...Cl contacts in the chlorinated products.

Investigation of the complex vibronic structure in the first excited and ionic ground state of 3-chloropyridine by means of REMPI and MATI spectroscopy and Franck-Condon analysis

3-Chloropyridine (3-CP) has been investigated by means of resonance-enhanced multi photon ionization (REMPI) and mass-analyzed threshold ionization (MATI) spectroscopy to elucidate the effect of m-chlorine substitution on the vibronic structure...

The Antiproliferative Effects of Flavonoid MAO Inhibitors on Prostate Cancer Cells

Prostate cancer (PCa) patients commonly experience clinical depression. Recent reports indicated that monoamine oxidase-A (MAO-A) levels elevate in PCa, and antidepressant MAO-Is show anti-PCa properties. In this work, we aimed to find potential drugs for PCa patients suffering from depression by establishing novel anti-PCa reversible monoamine oxidase-A inhibitors (MAO-AIs/RIMA); with an endeavor to understand their mechanism of action. In this investigation, twenty synthesized flavonoid derivatives, defined as KKR compounds were screened for their inhibitory potentials against human MAO-A and MAO-B isozymes. Meanwhile, the cytotoxic and antiproliferative effects were determined in three human PCa cell lines. MAO-A-kinetics, molecular docking, SAR, cell morphology, and cell migration were investigated for the most potent compounds. The screened KKRs inhibited MAO-A more potently than MAO-B, and non-toxically inhibited LNCaP cell proliferation more than the DU145 and PC3 cell lines, respectively. The results showed that the three top MAO-AI KKRs compounds (KKR11, KKR20, and KKR7 (IC50s 0.02–16 μM) overlapped with the top six antiproliferative KKRs against LNCaP (IC50s ~9.4 μM). While KKR21 (MAO-AI) and KKR2A (MAO-I) were ineffective against the PCa cells. Furthermore, KKR21 and KKR11 inhibited MAO-A competitively (Kis ≤ 7.4 nM). Molecular docking of the two compounds predicted shared hydrophobic and distinctive hydrophilic interactions—between the KKR molecule and MAO-A amino acid residues—to be responsible for their reversibility. The combined results and SAR observations indicated that the presence of specific active groups—such as chlorine and hydroxyl groups—are essential in certain MAO-AIs with anti-PCa effects. Additionally, MAO-A inhibition was found to be associated more with anti-PCa property than MAO-B. Distinctively, KKR11 [(E)-3-(3,4-dichlorophenyl)-1-(2-hydroxy-4,6-dimethoxyphenyl)prop-2-en-1-one] exhibited anti-metastatic effects on the DU145 cell line. The chlorine substitution groups might play vital roles in the KKR11 multiple actions. The obtained results indicated that the flavonoid derivative KKR11 could present a novel candidate for PCa patients with depression, through safe non-selective potent inhibition of MAOs.