Plants have evolved many secondary metabolites involved in plant defense, which are collectively known as antiherbivory compounds and can be classified into three sub-groups: nitrogen compounds (including alkaloids, cyanogenic glycosides, glucosinolates and benzoxazinoids), terpenoids, and phenolics.
Alkaloids are derived from various amino acids. Over 3000 known alkaloids exist, examples include nicotine, caffeine, morphine, cocaine, colchicine, ergolines, strychnine, and quinine. Alkaloids have pharmacological effects on humans and other animals. Some alkaloids can inhibit or activate enzymes, or alter carbohydrate and fat storage by inhibiting the formation phosphodiester bonds involved in their breakdown. Certain alkaloids bind to nucleic acids and can inhibit synthesis of proteins and affect DNA repair mechanisms. Alkaloids can also affect cell membrane and cytoskeletal structure causing the cells to weaken, collapse, or leak, and can affect nerve transmission. Although alkaloids act on a diversity of metabolic systems in humans and other animals, they almost uniformly invoke an aversively bitter taste.
Cyanogenic glycosides are stored in inactive forms in plant vacuoles. They become toxic when herbivores eat the plant and break cell membranes allowing the glycosides to come into contact with enzymes in the cytoplasm releasing hydrogen cyanide which blocks cellular respiration. Glucosinolates are activated in much the same way as cyanogenic glucosides, and the products can cause gastroenteritis, salivation, diarrhea, and irritation of the mouth. Benzoxazinoids, such as DIMBOA, are secondary defence metabolites characteristic of certain grasses (Poaceae). Like cyanogenic glycosides, they are stored as inactive glucosides in the plant vacuole. Upon tissue disruption they get into contact with β-glucosidases from the chloroplasts, which enzymatically release the toxic aglucones. Whereas some benzoxazinoids are constitutively present, others are only synthesized following herbivore infestation, and thus, considered inducible plant defenses against herbivory.
The terpenoids, sometimes referred to as isoprenoids, are organic chemicals similar to terpenes, derived from five-carbon isoprene units. There are over 10,000 known types of terpenoids. Most are multicyclic structures which differ from one another in both functional groups, and in basic carbon skeletons. Monoterpenoids, containing 2 isoprene units, are volatile essential oils such as citronella, limonene, menthol, camphor, and pinene. Diterpenoids, 4 isoprene units, are widely distributed in latex and resins, and can be quite toxic. Diterpenes are responsible for making Rhododendron leaves poisonous. Plant steroids and sterols are also produced from terpenoid precursors, including vitamin D, glycosides (such as digitalis) and saponins (which lyse red blood cells of herbivores).
Phenolics, sometimes called phenols, consist of an aromatic 6-carbon ring bonded to a hydroxy group. Some phenols have antiseptic properties, while others disrupt endocrine activity. Phenolics range from simple tannins to the more complex flavonoids that give plants much of their red, blue, yellow, and white pigments. Complex phenolics called polyphenols are capable of producing many different types of effects on humans, including antioxidant properties. Some examples of phenolics used for defense in plants are: lignin, silymarin and cannabinoids. Condensed tannins, polymers composed of 2 to 50 (or more) flavonoid molecules, inhibit herbivore digestion by binding to consumed plant proteins and making them more difficult for animals to digest, and by interfering with protein absorption and digestive enzymes.
In addition, some plants use fatty acid derivatives, amino acids and even peptides as defenses. The cholinergic toxin, cicutoxin of water hemlock, is a polyyne derived from the fatty acid metabolism. Oxalyldiaminopropionic acid is a neurotoxic amino acid produced as a defensive metabolite in the grass pea (Lathyrus sativus). The synthesis of fluoroacetate in several plants is an example of the use of small molecules to disrupt the metabolism of herbivores, in this case the citric acid cycle.