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A pivotal role of metabolic reprogramming in urothelial carcinoma is hallmarked by the dependence of two-fold faster proliferation of urothelial carcinoma cell line T24 than benign cell line TRT-HU1 on five-fold higher glucose (basal) 16 mM vs. 3 mM in McCoy’s 5A media and Keratinocyte Serum Free media, respectively. Here, we report that an additional 10% increase to 17.6 mM and 3.3 mM glucose significantly shortens the doubling time by 3 h and 1 h for T24 and TRT-HUI, respectively. T24 grown at 17.6 mM glucose lowers the confocal localization of the fatty acid mimetic, Betulinic Acid (BA) conjugated to FITC (BA-FITC) with Mito Tracker Red (mitochondrial marker), which doubles the IC50 of BA and BA-FITC by lowering cell cycle arrest in the G0/G1 phase from 54.2% to 43.8% and caspase-3/7 mediated apoptosis and by reversing caspase-3, p53, PTEN, GAPDH, and XIAP gene expression induced by BA in T24 grown at basal glucose (16 mM). Besides slowing the glycogen and pH decline of T24 at basal glucose, BA exhibited an eight-fold higher IC50 than Mitomycin C (MC) on TRT-HU1 by not mimicking the glucose-insensitive cycle arrest and apoptosis of MC. Overall, the glucose sensitivity of the lower IC50 of BA-FITC and BA on T24 vs. TRT-HU1 supports the safety of BA conjugates for theragnostic purposes.

Antibiotic resistance is the never‐ending war among medical researchers and microbial life forms. The extensive evolving potential of the microorganisms, in combination with improper usage, storage and disposal of the marketed antibiotics generated from natural or artificial sources, always calls for the need for novel antimicrobial agents with different modes of action. In this project, azo‐oxime complexes of iron and manganese (seven in total) have been applied to wild multidrug‐resistant pathogenic bacterial strains (isolated from sewage water of hospital). All complexes were inhibitory to bacterial strains present in the sewage water sample, which have been authenticated by a significant reduction in colony count upon their application to the microbial population of the water sample. Four of the most abundant colonies were isolated for further investigation about the bacterial characteristics, as well as to comprehend the molecular mechanism of action of these complexes to inhibit bacterial growth. Biochemical experiments in the form of the Catalase test, Coagulase test and lipase assay point towards the pathogenicity of bacterial strains. The strains were treated with various broad‐spectrum antibiotics, namely, Penicillin G, Oxacillin, Cephalothin, Clindamycin, Erythromycin, Amoxyclav, Cefotaxime, Levofloxacin, Aztreonam, Imipenem, Amikacin, Ceftazidime, and found to be resistant against many of them, viz., Clindamycin, Ceftazidime, Erythromycin, Amoxyclav, and some others, thereby signifying that the molecular mechanism of action of the aforesaid complexes is multidimensional. These complexes were producing ROS in sufficient amounts that can cause lipid peroxidation, and subsequent damage to the bacterial cell membrane and translation machinery was found to be inhibited by RNA. Bacterial genomic DNA was also affected by the chelates, and this has been authenticated by the decreased genomic DNA concentration and presence of DNA debris on agarose gel electrophoresis of the DNA of bacterial cultures treated with the complexes.