Author: Drou, Nizar ; Gunsalus, Kristin C. ; Arnoux, Marc ; Shibl, Ahmed A. ; Voolstra, Christian R. ; Isaac, Ashley ; Fei, Cong ; Ochsenkühn, Michael A. ; Amin, Shady A. ; Santos, Miraflor P. ; Behringer, Gregory ; Cárdenas, Anny

SignificancePhytoplankton are major primary producers in the marine environment that excrete a wide range of metabolites. These exudates support the growth of surrounding bacteria that in turn provide phytoplankton cells with resources and growth cofactors to proliferate. Unlike multicellular eukaryotes with dedicated structures housing microbiomes, mechanisms enabling unicellular eukaryotic phytoplankton hosts to modulate potential symbionts and opportunists within a natural microbial community are unknown. Exposure of a host phytoplankton cell to its natural microbial community triggers major transcriptional and metabolic reprogramming to release unique secondary metabolites that selectively enable growth and attachment of symbiotic taxa while simultaneously suppressing the colonization of nonsymbiont bacteria. These results suggest strong and highly selective microbiome-modulating strategies shared across the unicellular and multicellular eukaryotic lineages.

15 Jun 2007·Free Radical Biology and MedicineQ2 · MEDICINE

Targeting lipoic acid to mitochondria: Synthesis and characterization of a triphenylphosphonium-conjugated α-lipoyl derivative

Q2 · MEDICINE

Article

Author: Michael P. Murphy ; Abdul-Rahman B. Manas ; Meredith F. Ross ; Robin A.J. Smith ; Alejandra Sanjuan-Pla ; Stephanie E. Brown

Lipoic acid (LA) is a widely used antioxidant that protects mitochondria from oxidative damage in vivo. Much of this protection is thought to be due to the reduction of LA to dihydrolipoic acid (LAH(2)). This reduction is catalyzed in vivo by thioredoxin, thioredoxin reductase (TrxR), and lipoamide dehydrogenase. We hypothesized that specifically targeting LA to mitochondria, the site of most cellular reactive oxygen species production, would make it a more effective antioxidant. To do this, we made a novel molecule, MitoLipoic acid, by attaching lipoic acid to the lipophilic triphenylphosphonium cation. MitoL was accumulated rapidly within mitochondria several-hundred fold driven by the membrane potential. MitoL was reduced to the active antioxidant dihydroMitoLipoic acid by thioredoxin and by lipoamide dehydrogenase but not by TrxR. In isolated mitochondria or cells MitoL was only slightly reduced (5-10%), while, in contrast, LA was extensively reduced. This difference was largely due to the reaction of LA with TrxR, which did not occur for MitoL. Furthermore, in cells MitoL was quantitatively converted to an S-methylated product. As a consequence of its lack of reduction, MitoL was not protective for mitochondria or cells against a range of oxidative stresses. These results suggest that the protective action of LA in vivo may require its reduction to LAH(2) and that this reduction is largely mediated by TrxR.

01 Jan 1973·Die Pharmazie

[Occurrence of flavonoids in Melissa officinalis L].

Article

Author: Kitze, C ; Thieme, H

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