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Cinchona-based liquid formulation exhibits antifungal activity through Tryptophan starvation and disruption of mitochondrial respiration in Rhizoctonia Solani

Summary

Researchers found that an extract from Cinchona bark, containing the compound quinine, effectively kills rice-damaging fungus Rhizoctonia solani through two mechanisms: starving the fungus of the amino acid tryptophan and disrupting its energy-producing mitochondria. This natural plant-based treatment could serve as an eco-friendly alternative to synthetic fungicides, reducing crop losses from fungal diseases while avoiding the environmental damage and resistance problems associated with chemical pesticides.

Background

Rhizoctonia solani causes rice sheath blight disease, resulting in significant crop losses in southeastern Asia. Synthetic fungicides have led to resistant pathogen strains and environmental hazards. Natural sources like Cinchona bark contain quinoline alkaloids with potential antifungal properties.

Objective

This study investigates the antifungal properties and molecular mechanisms of a Cinchona-based formulation (CBF) against Rhizoctonia solani AG1-IA, focusing on tryptophan starvation and mitochondrial disruption as potential antifungal mechanisms.

Results

CBF exhibited EC50 of 217.14 µg/mL with 58.75% mycelial growth suppression. Quinine was identified as the primary active alkaloid. Molecular docking revealed strong quinine binding to amino acid permeases (−6.5 to −7.8 kcal/mol). Tryptophan supplementation reversed fungal growth inhibition. CBF elevated ROS levels, reduced mitochondrial membrane potential, and downregulated Cytochrome P450 expression.

Conclusion

CBF demonstrates dual antifungal mechanisms through tryptophan starvation and mitochondrial respiratory disruption. The combination of these mechanisms suggests CBF as a promising eco-friendly biopesticide for sustainable disease management with reduced resistance development potential.
  • Published in:Scientific Reports,
  • Study Type:Experimental Research,
  • Source: PMID: 41203652, DOI: 10.1038/s41598-025-23347-7
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