Evidence for the biosynthesis and release of prostaglandins and related substances in pathophysiological states of ocular tissues is reviewed and their participation in ocular injury and acute inflammation discussed. Ocular tissues are capable of generating prostaglandins from the endogenous or exogenous precursor, arachidonic acid. Prostaglandins are released into the aqueous humour in response to paracentesis, mechanical or laser injury to the iris, and in experimental immunogenic and non-immunogenic ocular inflammation. Antidromic stimulation of the trigeminal nerve, formaldehyde or nitrogen mustard-induced irritation of the eye do not cause the release of prostaglandins, nor are the responses to these stimuli inhibited by prostaglandin synthetase inhibitors. Prostaglandins in small doses administered topically or intraocularly produce some of the responses of injury and inflammation, such as hyperaemia, miosis, breakdown of the blood-aqueous barrier and rise in intraocular pressure. Also, E-type prostaglandins administered topically together with histamine (but not the individual components) cause cellular infiltration and produce oedema in conjunctival tissues. Non-steroidal aspirin-like drugs at concentrations which inhibit prostaglandin biosynthesis markedly block injury responses but have only a moderate inhibitory effect on acute inflammatory reactions of the eye. The present evidence suggests that prostaglandins are involved in some of the injury and inflammatory responses. However, recent studies indicate that the intermediates of arachidonic acid metabolism, especially hydroxy fatty acids, may play a greater role in inflammatory responses.