Redox and respiratory chain related alterations in the lophirones B and C-mediated bacterial lethality

• Lophirones B and C perturbs redox status of Escherichia coli, Pseudomonas aeruginosa and Staphylococcus.
• Lophirones B and C inhibits respiratory chain complex of Escherichia coli, Pseudomonas aeruginosa and Staphylococcus.
• Lophirones B and C promotes oxidant generation in Escherichia coli, Pseudomonas aeruginosa and Staphylococcus.
• Lophirones B and C depletes cellular glutathione level in Escherichia coli, Pseudomonas aeruginosa and Staphylococcus.

The influence of chalcone dimers, lophirones B and C on redox status and respiratory chain activity of Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa was investigated. Minimum inhibitory concentrations (MIC) of lophirones B and C against E. coli, P. aeruginosa and S. aureus are 200-; 100-; 200- and 150-μg/mL respectively. Similarly, the minimum bactericidal concentrations (MBC) of lophirones B and C are 250; 200; 300 and 200-μg/mL respectively. The optical densities and colony forming units of lophirones B and C-treated bacteria decreased in time-dependent manner. Superoxide anion content of E. coli, P. aeruginosa and S. aureus exposed to lophirones B and C (4× MIC) increased significantly. Superoxide dismutase and catalase in the chalcone dimers-treated bacteria increased significantly. Conversely, reduced glutathione in lophirones B and C-treated bacteria decrease significantly with corresponding increase in glutathione disulfide. Furthermore, malondialdehyde and fragmented DNA increased significantly following exposure to the chalcone dimers. The respiratory complex I and II decreased significantly in the chalcone dimers-treated bacteria. From the findings, lophirones B and C altered intracellular redox status via enhanced oxidant generation possibly by autoxidation, Fenton chemistry and inhibiting electron transport chain resulting to lipid peroxidation and DNA fragmentation and consequentially bacterial cell death.

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