{'fraction_non_alphanumeric': 0.024271844660194174, 'fraction_numerical': 0.00424757281553398, 'mean_word_length': 5.391472868217054, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Fatty Acid Remodeling of Membrane Glycerophospholipids Induced by Bleomycin and Iron Oxide Nanoparticles in Human Embryonic Kidney Cells.

Bleomycin has a long-studied mechanism of action through the formation of a complex with metals, such as iron. Bleomy-cin-iron complex was recently shown to induce membrane damage by free radical reactivity. Since the use of Fe nanoparticles is spreading as drug delivery strategies, molecular mechanisms of cell damage must include different compartments in order to observe the progression of the cell reactivity. In this study human embryonic kidney (HEK-293) cells were exposed for 24 h to bleomycin and polymeric iron oxide nanoparticles (Fe-NPs), alone or in combination. The fatty acid-based membrane lipidomic analysis evidenced the fatty acid remodeling in response to the treatments. Bleomycin alone caused increase of saturated fatty acid (SFA) moieties in cell membrane glycerophospholipids with concomitant diminution of monounsaturat-ed (MUFA) and polyunsaturated fatty acid (PUFA) levels. Under Fe-NPs treatment omega-6 PUFA decreased and trans fatty acid isomers increased. Under co-administration bleomycin and Fe-NPs all membrane remodeling changes disappeared com-pared to controls, remaining only an increase of omega-6 PUFA that elevates peroxidation index. Our results highlight the important role of fatty acid-based membrane lipidome monitoring to follow up the fatty acid reorganization induced by the drug, to be considered as a side effect of the pharmacological activity, suggesting the need of an integrated approach for the investigation of drug and carrier molecular mechanisms.