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PubMed1975

The uptake of a substituted acridone by rat mast cells in relationship to histamine release: a possible indicator of exocytosis-induced expansion of the plasma membrane.

A substituted acridone, 10-(2-dimethylaminopropyl)-9-acridone HCl (M-129), was taken up by isolated rat peritoneal and pleural mast cells in direct relationship to the degree of selective histamine release induced by compound 48/80. Other selective releasing agents, i.e., polymyxin B and anti-rat mast cell serum, also augmented uptake of M-129. Augmented uptake of M-129 was inhibited by measures that inhibited selective histamine release, i.e., cold, brief heating of the mast cells, N-ethylmaleimide and ninhydrin. 48/80 did not agument uptake of M-129 in rat erythrocytes or in rat serous fluid cells from which mast cells had been removed. M-129 taken up by mast cells was readily removed by two to three washes. Augmented uptake induced by 48/80 was specific for M-129 and acridone itself. Related compounds, i.e., a quaternary acridone derivative [10-(2-triethylaminoethyl)-9-acridone iodide] (M-231), acridine and acridan did not show augmented uptake. There was no relationship between heptane-water partition coefficients and uptake. It is postulated, based on estimates of cell membrane area, that M-129 is loosely bound to plasma membrane and that the augmented uptake associated with selective histamine release from rat mast cells is due to expanded plasma membrane that results from irreversible or slowly reversible exocytosis.

Acridines↗
PubMedDate not supplied

Photodynamic activity of substituted zinc trisulfophthalocyanines: role of plasma membrane damage.

We recently reported that variations in cellular phototoxicity among a series of alkynyl-substituted zinc trisulfophthalocyanines (ZnPcS3Cn) correlates with their hydrophobicity, with the most amphiphilic derivatives showing the highest cell uptake and phototoxicity. In this study we address the role of the plasma membrane in the photodynamic response as it relates to the overall hydrophobicity of the photosensitizer. The membrane tracker dye 1-[4(trimethylamino)phenyl]-6-phenylhexa-1,3,5-triene (TMA-DPH), which is incorporated into plasma membranes by endocytosis, was used to establish plasma membrane uptake by EMT-6 cells of the ZnPcS3C, by colocalization, and TMA-DPH membrane uptake rates after photodynamic therapy were used to quantify membrane damage. TMA-DPH colocalization patterns show plasma membrane uptake of the photosensitizers after short 1 h incubation periods. TMA-DPH plasma membrane uptake rates after illumination of the photosensitizer-treated cells show a parabolic relationship with photosensitizer hydrophobicity that correlates well with the phototoxicity of the ZnPcS3C,. After a 1 h incubation period, overall phototoxicity correlates closely with the postillumination rate of TMA-DPH incorporation into the cell membrane, suggesting a major role of plasma membrane damage in the overall PDT effect. In contrast, after a 24 h incubation, phototoxicity shows a stronger but imperfect correlation with total cellular photosensitizer uptake rather than TMA-DPH membrane uptake, suggesting a partial shift in the cellular damage responsible for photosensitization from the plasma membrane to intracellular targets. We conclude that plasma membrane localization of the amphiphilic ZnPcS3C6-C9 is a major factor in their overall photodynamic activity.

Animals↗