Effectiveness of <i>p</i> ‐Coumaric Acid Against <i>Alternaria</i> Rot in Tomato Fruits: Possible Dual Mode of Action on Succinate Dehydrogenase Enzyme and Fungal Cell Membrane Damage

Postharvest black rot caused by Alternaria alternata significantly reduces tomato shelf‐life worldwide. This study assessed the efficacy of p ‐coumaric acid and the ethanolic extract of Trichoderma longibrachiatum (Ext14) on the growth of A. alternata under in vitro conditions and in tomato fruits and explored the compound's mode of action against the pathogen. Spores were exposed to p ‐coumaric acid (0.5–2 mg.mL −1 ) for 48 h to measure the in vitro inhibition of spore germination. Tomatoes were treated, with Ext14 and p ‐coumaric acid (1.5–6 mg.mL −1 ), inoculated with A. alternata and maintained at 25°C and 80%–90% relative humidity (R.H.) to determine the in vivo antifungal effect of treatments. Alternaria's spore membrane integrity was evaluated by fluorescence microscopy, and molecular docking explored p ‐coumaric acid binding to succinate dehydrogenase (SDH). P‐ coumaric acid maintained 100% inhibition of spore germination at 1.5–2 mg.mL −1 throughout 48 h. On fruit, Ext14 reduced lesion diameter by 61% at 96 h, surpassing p ‐coumaric acid treatment at a concentration of 6 mg.mL −1 , which delayed disease only to 72 h ( p ≤ 0.05). Fluorescence imaging showed a spore membrane disruption in p ‐coumaric acid treated spores. Docking positioned p ‐coumaric acid in the ubiquinone (UQ) pocket of SDH, stabilized by two hydrogen bonds (Asn281, Tyr628) and π‐alkyl contacts, with a binding energy of −5.0 kcal.mol −1 versus −4.7 kcal.mol −1 for UQ. These findings indicate that p ‐coumaric acid inhibits the spore germination of A. alternata and plays an antifungal role by disrupting cell membranes and possibly competes for the SDH active site. These results suggest potential application of P ‐coumaric acid in ecofriendly postharvest protection.