@article { ISI:000294572800023,
	title = {Antifungal activity of novel synthetic peptides by accumulation of reactive oxygen species (ROS) and disruption of cell wall against Candida albicans},
	journal = {Peptides},
	volume = {32},
	number = {8},
	year = {2011},
	month = {AUG},
	pages = {1732-1740},
	publisher = {ELSEVIER SCIENCE INC},
	address = {360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA},
	abstract = {<p>In the present work, we investigated the antifungal activity of two de novo designed, antimicrobial peptides VS2 and VS3, incorporating unnatural amino acid alpha,beta-dehydrophenylalanine (Delta Phe). We observed that the low-hemolytic peptides could irreversibly inhibit the growth of various Candida species and multidrug resistance strains at MIC(80) values ranging from 15.62 mu M to 250 mu M. Synergy experiments showed that MIC(80) of the peptides was drastically reduced in combination with an antifungal drug fluconazole. The dye PI uptake assay was used to demonstrate peptide induced cell membrane permeabilization. Intracellular localization of the FITC-labeled peptides in Candida albicans was studied by confocal microscopy and FACS. Killing kinetics, PI uptake assay, and the intracellular presence of FITC-peptides suggested that growth inhibition is not solely a consequence of increased membrane permeabilization. We showed that entry of the peptide in Candida cells resulted in accumulation of reactive oxygen species (ROS) leading to cell necrosis. Morphological alteration in Candida cells caused by the peptides was visualized by electron microscopy. We propose that de novo designed VS2 and VS3 peptides have multiple detrimental effects on target fungi, which ultimately result in cell wall disruption and killing. Therefore, these peptides represent a good template for further design and development as antifungal agents. (C) 2011 Elsevier Inc. All rights reserved.</p>},
	keywords = {Antifungal peptides, Candida albicans, Cell wall, ROS},
	issn = {0196-9781},
	doi = {10.1016/j.peptides.2011.06.003},
	author = {Maurya, Indresh Kumar and Pathak, Sarika and Sharma, Monika and Sanwal, Hina and Chaudhary, Preeti and Tupe, Santosh and Deshpande, Mukund V. and Chauhan, Virander Singh and Prasad, Rajendra}
}
@article {49321,
	title = {SWATH-MS reveals that bisphenol A and its analogs regulate pathways leading to disruption in insulin signaling and fatty acid metabolism},
	journal = {Food and Chemical Toxicology},
	volume = {188},
	year = {2024},
	month = {JUN},
	pages = {114667},
	type = {Article},
	abstract = {<p>
	Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC), associated with obesity and insulin resistance. The FDA prohibited the use of BPA-based polycarbonate resins in infant formula packaging; thus, its analogs, viz. Bisphenol S (BPS) and Bisphenol F (BPF) were considered alternatives in epoxy resins, plastics, and food cans. As these analogs might evoke a similar response, we investigated the role of Bisphenols (BPA, BPF, and BPS), on insulin signaling in CHO-HIRc-myc-GLUT4eGFP cells at environmentally relevant concentrations of 2 nM and 200 nM. Insulin signaling demonstrated that Bisphenols reduced phosphorylation of IR and AKT2, GLUT4 translocation, and glucose uptake. This was accompanied by increased oxidative stress. Furthermore, SWATHMS-based proteomics of 3T3-L1 cells demonstrated that Bisphenol-treated cells regulate proteins in insulin resistance, adipogenesis, and fatty acid metabolism pathways differently. All three Bisphenols induced differentially expressed proteins enriched similar pathways, although their abundance differed for each Bisphenol. This might be due to their varying toxicity level, structural differences, and estrogen-mimetic activity. This study has important implications in addressing health concerns related to EDCs. Given that the analogs of BPA are considered alternatives to BPA, the findings of this study suggest they are equally potent in altering fatty acid metabolism and inducing insulin resistance.</p>
},
	keywords = {Bisphenols, Estrogen, Lipid droplet, Mitochondrial beta-oxidation, Oxidative stress, PPAR gamma},
	issn = {0278-6915},
	doi = {10.1016/j.fct.2024.114667},
	author = {Kulsange, Shabda E. and Sharma, Monika and Sonawane, Babasaheb and Jaiswal, Meera R. and Kulkarni, Mahesh J. and Santhakumari, B.}
}
