Innovative biofilm inhibition and anti-microbial behavior of molybdenum sulfide nanostructures generated by microwave-assisted solvothermal route

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• 作者：Nilam Qureshi (1)
  Rajendra Patil (2)
  Manish Shinde (1)
  Govind Umarji (1)
  Valerio Causin (3)
  Wasudev Gade (2)
  Uttam Mulik (1)
  Anand Bhalerao (4)
  Dinesh P. Amalnerkar (1)
  
  1. Centre for Materials for Electronics Technology (C-MET) ; Panchwati Off Pashan Road ; Pune ; 411008 ; India
  2. Department of Biotechnology ; University of Pune ; Ganeshkhind Road ; Pune ; 411007 ; India
  3. Dipartimento di Scienze Chimiche ; Universit脿 di Padova ; via Marzolo 1 ; Padua ; 35131 ; Italy
  4. College of Engineering ; Bharati Vidyapeeth University ; Pune ; 411043 ; India
  
• 关键词：Biofilm ; Antimicrobial ; ROS ; Molybdenum Sulfide ; Solvothermal
• 刊名：Applied Nanoscience
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：5
• 期：3
• 页码：331-341
• 全文大小：5,655 KB
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• 刊物类别：Chemistry and Materials Science
• 刊物主题：Materials Science
  Nanotechnology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：2190-5517

文摘

The incessant use of antibiotics against infectious diseases has translated into a vicious circle of developing new antibiotic drug and its resistant strains in short period of time due to inherent nature of micro-organisms to alter their genes. Many researchers have been trying to formulate inorganic nanoparticles-based antiseptics that may be linked to broad-spectrum activity and far lower propensity to induce microbial resistance than antibiotics. The way-out approaches in this direction are nanomaterials based (1) bactericidal and (2) bacteriostatic activities. We, herein, present hitherto unreported observations on microbial abatement using non-cytotoxic molybdenum disulfide nanostructures (MSNs) which are synthesized using microwave assisted solvothermal route. Inhibition of biofilm formation using MSNs is a unique feature of our study. Furthermore, this study evinces antimicrobial mechanism of MSNs by reactive oxygen species (ROS) dependent generation of superoxide anion radical via disruption of cellular functions.