Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1984;31(4):359-64.

Prophage induction by liver microsomal metabolites of aflatoxin B1 in lysogenic Pseudomonas aeruginosa

  • PMID: 6085605

Prophage induction by liver microsomal metabolites of aflatoxin B1 in lysogenic Pseudomonas aeruginosa

I R Patel et al. Acta Microbiol Hung. 1984.

Abstract

Microsomal metabolites of aflatoxin B1 (AFB1) causing induction of prophage in lysogenic strain of Pseudomonas aeruginosa SM was studied. Reduction of culture turbidity was determined at various concentrations of toxin. The effect of the toxin was also studied on deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and protein synthesis. AFB1 at the concentration of 50 micrograms/ml reduced initial turbidity to approximately 90% in 4 h. DNA synthesis stopped completely in the first hour but reappeared due to induction of the temperate phage. Soon after induction both RNA and protein synthesis continued but later little or no net synthesis of these macromolecules occurred. Plaque forming units (pfu) were increased approximately 90 times at 2 h as compared to the control. Testing of the effect of AFB1 on the non-lysogenic, sensitive strain demonstrated that although there was no significant decrease in culture turbidity at 50 micrograms/ml concentration of AFB1, DNA synthesis stopped completely within 1 h, while RNA and protein synthesis were increasing throughout the test interval. It has been concluded that the liver microsomal fraction of AFB1 caused induction of prophage in lysogenic cells and inhibited DNA synthesis significantly in non-lysogenic cells.

PubMed Disclaimer

Similar articles

Publication types