Phytoalexins produced in plants act as toxins to the attacking organism. They may puncture the cell wall, delay maturation, disrupt metabolism or prevent reproduction of the pathogen in question. However, phytoalexins are often targeted to specific predators; a plant that has anti-insect phytoalexins may not have the ability to repel a fungal attack.
When a plant cell recognizes particles from damaged cells or particles from the pathogen, the plant launches a two-pronged resistance: a general short-term response and a delayed long-term specific response.
As part of the induced resistance, the short-term response, the plant deploys free radicals such as superoxide and hydrogen peroxide to kill invading cells. In pathogen interactions, the common short-term response is the hypersensitive response, wherein apoptosis-compromised cells commit suicide in order to create a physical barrier for the invader.
Long-term resistance, or systemic acquired resistance (SAR), involves communication of the damaged tissue with the rest of the plant using plant hormones such as jasmonic acid, ethylene, abscisic acid or salicylic acid. The reception of the signal leads to global changes within the plant, which induce genes that protect from further pathogen intrusion, including enzymes involved in the production of phytoalexins. Often, if jasmonates or ethylene (both gaseous hormones) is released from the wounded tissue, neighboring plants also manufacture phytoalexins in response. For herbivores, common vectors for disease, these and other wound response aromatics seem to act as a warning that the plant is no longer edible. Also, in accordance with the old adage, "an enemy of my enemy is my friend," the aromatics may alert natural enemies of the plant invaders to the presence thereof.