Toxin- and cadmium-induced cell death events in tomato suspension cells resemble features of hypersensitive response

Elicitors of different origin (fumonisin B1, fungal toxin), camptothecin (alkaloid from Camptotheca acuminata), mastoparan (wasp venom) and the heavy metal (cadmium) were tested for their ability to induce programmed cell death (PCD) in a model system of tomato cell culture, line MsK8. By employing a pharmacological approach the involvement of proteolysis, oxidative stress and ethylene in the suicidal cascade is shown. The caspase-specific peptide inhibitors: irreversible caspase-1 (ICE)-inhibitor acyl-Tyr-Val-Ala-Asp-chloromethylketone and the broad range caspase inhibitor benzyoxycarbonyl-Asp-2,6-dichlorobenzoyloxymethylketone effectively reduced cell lethality providing a sound indication that in tomato suspension cells the applied inducers promote cell death that resembles features typical for PCD. A lack of inhibition occurred at mastoparan-induced cell death in response to the caspase inhibitors, while the serine protease inhibitor aminoethylbenzenesulphonyl fluoride caused substantial reduction of cell mortality. Significant inhibition was detected after administration of ethylene inhibitor, aminoethoxyvinyl glicine and the antioxidants Lgalactonic acid -¿-galactone and catalase. The results indicate that the cell death response at the exposure to biotic and abiotic stressors may employ an activation of similar cell death pathways and that caspase-like- and non-caspase-like-dependent biochemical processes may be operative. In addition, the presented comparative study suggests that the reaction of tomato suspension cells to diverse cell death stimulating compounds at least partially coincides with the cell death machinery involved in the plant hypersensitive response and during PCD in animal cells