PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 12659939

Lipid membrane with low proton permeability.

Débora Nakai Biloti·Maria Helena Andrade Santana·Francisco Benedito Teixeira Pessine
View original source ↗Export metadata ↓

Abstract

This work reports the production of a liposomal formulation, having a lipidic membrane with known chemical composition and a low proton permeability, as confirmed by physicochemical characterization of the maintenance of a transmembranic pH gradient. These liposomes consist of DSPC, DSPE-PEG, DSPG and cholesterol, with low internal pH. To verify the low proton permeability of these liposomal bilayers, a study of proton migration according to the fluorescence quenching of 9-aminoacridine (9AA), as well as CPT-11 encapsulation, were used to monitor the acidification of the intravesicular space. Both experiments showed that this liposomal formulation is able to maintain a transmembranic proton gradient.

Explore related subjects

AminacrineCamptothecinFluorescent DyesHydrogen-Ion ConcentrationIrinotecanLiposomesMembrane LipidsPermeabilityProtonsSpectrometry, FluorescenceJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Débora Nakai Biloti, Maria Helena Andrade Santana, Francisco Benedito Teixeira Pessine. 2003-04-01. Lipid membrane with low proton permeability.. https://doi.org/10.1016/s0005-2736(03)00035-x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2006

Structure-activity relationship study of 9-aminoacridine compounds in scrapie-infected neuroblastoma cells.

A focused library of variously substituted 9-aminoacridine compounds was screened for bioactivity against accumulation of the infectious prion protein isoform, denoted PrP(Sc), in a cell model of prion replication. The efficacy of compounds against PrP(Sc) accumulation was influenced by both substituents of the distal tertiary amine and acridine heterocycle, while cellular cytotoxicity was encoded in the acridine heterocycle substituents.

Aminacrine↗
PubMed2006

Tautomerism of acridin-9-amines substituted at the exocyclic nitrogen atom: spectroscopic investigations and theoretical studies.

In the ground electronic state, the first two (1 and 2) of the compounds investigated--9-(methoxyamino)acridine (1), 9-hydrazinoacridine (2), N-(2-chloroethyl)acridin-9-amine (3) and N-(5-methylpyridin-2-yl)acridin-9-amine (4)--exist principally in the imino tautomeric form, while the other two (3 and 4) can coexist as amino and imino tautomers in solvents of various polarities and abilities to enter into specific interactions. These features of the molecules are reflected in the experimental absorption spectra and the predicted thermodynamic and spectral data. The predicted thermodynamic characteristics suggest that in the S1 state, the imino tautomers of 1, 2 and 4 and the amino tautomer of 3 are more stable than their tautomeric counterparts. However, the predicted rates of intersystem crossing suggest that the imino tautomers of 1-3 and the amino tautomer of 4 lose excitation energy very rapidly, so that only their counterpart tautomers in fact emit radiation. This explains why 1 and 2 do not fluoresce and why the amino form of 3 and the imino form of 4 are the emitters. 3 and 4 thus represent acridin-9-amines whose imino forms are preferred in the ground state, but whose respective amino and imino forms are preferred in the excited state. Because 3 and 4 are capable of tautomeric transformations in the ground and excited states, and also enter into specific interactions with solvents, these compounds could be potent spectral indicators or probes of environmental properties.

Aminacrine↗
PubMed2006

Isolation and characterization of dominant and recessive IL-3-independent hematopoietic transformants.

Retroviral integration mutagenesis and treatment with the frameshift mutagen ICR191 were used to transform v-H-ras expressing PB-3c cells to interleukin-3 (IL-3) independence. Six clones displayed viral integrations into the 3' region of the IL-3 gene thus acting post-transcriptionally by disrupting the AU-rich instability element. Two clones contained reverse orientation integration into the raf-1 gene revealing an enhancer insertion mechanism. Growth by this mechanism was sensitive to the Raf-1 inhibitor BAY 43-9006 and the Mek inhibitor U0126. Following treatment with ICR191, IL-3-independent clones were recovered and studied by cell fusion. With 21/22 clones, IL-3 independence resulted from a recessive mechanism as cellular hybrids with parental cells reverted to IL-3 dependence. Recessive clone D2c displayed increased phospho-Erk1/2 levels and was growth sensitive to U0126, but not to BAY43-9006. The single dominant clone, D5a, showed no signs of mitogen-activated protein kinases pathway activation but displayed constitutive phosphorylation of Stat5. We conclude that PB-3c has several options to acquire IL-3 growth autonomy involving transcriptional or post-transcriptional mechanisms affecting the distal regulators Erk or Stat5. The reported panel of independent dominant and recessive transformants should provide a useful tool for inhibitor profiling.

Aminacrine↗