Amphiphilic bilayer membrane structures (vesicles) have been postulated to have been abiotically formed and spontaneously assemble on the prebiotic Earth, providing compartmentalization for the origin of life. These vesicles are similar to modern cellular membranes and can serve to contain water-soluble species, concentrate species, and have the potential to catalyze reactions. The origin of the use of photochemical energy in metabolism (i.e. energy transduction) is one of the central issues in the origin of life. This includes such questions as how energy transduction may have occurred before complex enzymatic systems, such as required by contemporary photosynthesis, had developed and how simple a photochemical system is possible. It has been postulated that vesicle structures developed the ability to capture and transduce light, providing energy for reactions. It has also been shown that pH gradients across the membrane surface can be photochemically created, but coupling these to drive chemical reactions has been difficult. Colloidal semiconducting mineral particles are known to photochemically drive redox chemistry. We propose that encapsulation of these particles has the potential to provide a source of energy transduction inside vesicles, and thereby drive protocellular chemistry, and represents a model system for early photosynthesis. In our experiments we show that TiO2 particles, in the approximately 20 nm size range, can be incorporated into vesicles and retain their photoactivity through the dehydration/rehydration cycles that have been shown to concentrate species inside a vesicle.
Cationic lipids, particularly those with nitrogen containing heterocycles, such as a pyridinium headgroup, display various bactericidal, bacteriostatic and disinfectant activity as reported in various works, all dependent on the length of their respective alkyl chains. Two quaternary alkyl pyridinium amphiphiles, vis. 4‐amino‐1‐decyl (1) and 4‐amino‐1‐dodecyl (2), were evaluated for their cytotoxic activity in a human cervical cancer cell line. These two compounds were assessed for their cytotoxicity and the following CC50's, 15.68 μM and 4.58 μM respectively were established. 1 proves to be a poor candidate as an anti‐cancer therapeutic agent as its cytotoxicity induced necrotic death. At a low concentration, 2 displayed a pro‐apoptotic profile demonstrated by phosphatidylserine externalization suggesting induction via an extrinsic pathway since it did not disrupt mitochondrial polarity. Of both compounds, 2, acts as a cell cycle progression disruptor causing slight S‐phase arrest and a decrease in G2/M phase along with eliciting DNA fragmentation. An explicit difference of two carbons between both 1 and 2 warrants further investigation to elucidate alkyl‐chain length role in anti‐cancer drugs. Furthermore, a series of these cationic amphiphiles with different lengths for their hydrophobic moiety has been synthesized and will be studied on a wider panel of cancer cell lines and have their mechanism of death further elucidated.Support or Funding InformationThe Cytometry, Screening and Imaging Core Facility that was used in this work was supported by the National Institute on Minority Health and Health Disparities (NIMHD) through a Research Centers for Minority Institutions (RCMI) grants 8G12MD007592 and 5G12MD007592, a component of the National Institutes of Health (NIH).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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