Neuropharmacological Alterations by a Rice Contaminant Stenotrophomonas maltophilia: a Detailed Bio-molecular and

Moitreyee Chattopadhyay1, Souvik Basak2, Atish Barua3

  • 1Department of Pharmaceutical Science and Technology, Maulana Abul Kalam Azad University of Technology, Kalyani, Nadia, West Bengal, India. pharmacol2015@gmail.com.

Insights

Unsaturated fatty acids (UFAs) from Stenotrophomonas maltophilia in rice cause neurotoxicity. This contamination leads to decreased activity, increased depression, and brain cell damage in rodents.

Area of Science:

  • Microbiology
  • Neuroscience
  • Toxicology

Background:

  • Stored rice contamination by Stenotrophomonas maltophilia is a significant food safety concern.
  • Previous research identified S. maltophilia as a major rice contaminant.

Purpose of the Study:

  • To investigate the neurotoxic potential of unsaturated fatty acids (UFAs) from S. maltophilia.
  • To determine the effects of S. maltophilia cell lysate on rodent behavior and brain biochemistry.

Main Methods:

  • Analysis of fatty acid composition in S. maltophilia cell lysate.
  • Assessment of rodent locomotor activity and depression following exposure to cell lysate.
  • Measurement of bioamine levels in rodent brains.
  • In vitro evaluation of cell lysate's effect on murine microglial cell viability and reactive oxygen species (ROS) production.

Main Results:

  • Mono- and di-unsaturated fatty acids (UFAs) were identified as major components of S. maltophilia cell lysate.
  • Exposure to cell lysate decreased locomotor activity and increased depression in rodents.
  • Significant depletion of key bioamines (dopamine, noradrenaline, adrenaline, serotonin, GABA) was observed in rodent brains.
  • UFA-rich cell lysate inhibited microglial cell viability and increased ROS production in vitro.
  • Evidence suggests UFA-induced neurotoxicity through microglial cell destruction and neuroinflammation.

Conclusions:

  • Unsaturated fatty acids derived from Stenotrophomonas maltophilia contribute to neurotoxicity.
  • These UFAs may cause neurotoxicity by depleting brain bioamines and damaging microglial cells, leading to increased oxidative stress and inflammation.

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