This work evaluated the genotoxic potential of the soluble organic material (SOM) extracted from the particulate matter (PM) emitted by an automotive diesel engine. The engine was modified to operate with a home-made multipoint-port injection system to substitute 10% of ultralow-sulfur diesel (ULSD) fuel in energy basis by hydrous ethanol (h-Et) or n-butanol (n-Bu) injected into the manifold during the intake stroke. A low engine load mode named M4 (43 N·m at 2410 min−1) and a medium-load mode M2 (95 N·m at 2410 min−1) were selected from the vehicle homologation cycle. PM was collected with a stainless steel filter located 1.5 m downstream the exhaust manifold. The SOM of the PM was extracted to evaluate the genotoxic activity on human lymphocytes using the comet assay. Results indicated that independently of the mode, the SOM coming from alcohols led more genotoxicity than ULSD, following the order h-Et > n-Bu > ULSD. The low engine load operation exhibited much more deoxyribonucleic acid (DNA) damage than mode M2, especially the PM produced by hydrous ethanol port-injection. Although further research is still necessary, these findings suggest that the biology activity of the SOM coming from alcohols PM could be a barrier for the implementation of alcohol port-injection technology.
Drug nanoencapsulation increases the availability, pharmacokinetics, and concentration efficiency for therapeutic regimes. Azobenzene light-responsive molecules experience a hydrophobicity change from a polar to an apolar tendency by trans–cis photoisomerization upon UV irradiation. Polymeric photoresponse nanoparticles (PPNPs) based on azobenzene compounds and biopolymers such as chitosan derivatives show prospects of photodelivering drugs into cells with accelerated kinetics, enhancing their therapeutic effect. PPNP biocompatibility studies detect the safe concentrations for their administration and reduce the chance of side effects, improving the effectiveness of a potential treatment. Here, we report on a PPNP biocompatibility evaluation of viability and the first genotoxicity study of azobenzene-based PPNPs. Cell line models from human ventricular cardiomyocytes (RL14), as well as mouse fibroblasts (NIH3T3) as proof of concept, were exposed to different concentrations of azobenzene-based PPNPs and their precursors to evaluate the consequences on mitochondrial metabolism (MTT assay), the number of viable cells (trypan blue exclusion test), and deoxyribonucleic acid (DNA) damage (comet assay). Lethal concentrations of 50 (LC50) of the PPNPs and their precursors were higher than the required drug release and synthesis concentrations. The PPNPs affected the cell membrane at concentrations higher than 2 mg/mL, and lower concentrations exhibited lesser damage to cellular genetic material. An azobenzene derivative functionalized with a biopolymer to assemble PPNPs demonstrated biocompatibility with the evaluated cell lines. The PPNPs encapsulated Nile red and dofetilide separately as model and antiarrhythmic drugs, respectively, and delivered upon UV irradiation, proving the phototriggered drug release concept. Biocompatible PPNPs are a promising technology for fast drug release with high cell interaction opening new opportunities for azobenzene biomedical applications.
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