The cornea and the lens have some common features: both organs are avascular, have a high protein concentration, and are transparent, having relatively high indices of refraction. Because experiments done by various investigators have differed with respect to tissue preparation, incubation time, the amount of AA used as substrate, the cofactors used, and so forth, it is difficult to make a direct comparison of the ability of the lens and the cornea to synthesize eicosanoids. Nevertheless, based on the preceding review, we can conclude that the cornea has a higher capacity than does the lens to produce PGs and lipoxygenase products. One important difference between these two tissues is that the cornea is innervated, whereas the lens is not. This raises the question of the possible influence of neuronal elements on the synthesis and effects of eicosanoids. There is substantial evidence that neuronal mechanisms play a role in various aspects of corneal physiology. In rabbits, there is decreased ability for corneal wound healing after surgical interruption of the trigeminal ganglion (Beuerman and Schimmelpfennig, 1980). The cornea contains beta-adrenergic receptors (Neufeld et al., 1978) and cAMP mediates the initial events in the healing process in the corneal epithelium (Jumblatt et al., 1980). PGE2 is an activator of this pathway (Schaeffer et al., 1982). However, it is not known how neuronal mechanisms may influence the synthesis of PGs in the cornea. It must also be kept in mind that the responses of the cornea to inflammation involve the interplay of several mediators, some of which come from the corneal cells and others from recruited inflammatory cells. The lens is also avascular and in contrast to the cornea, which has some peripheral blood vessels, the lens remains avascular even after injury. When it is injured, the lens, in the absence of a blood supply, responds instead to the composition of the aqueous humor. Secondary aqueous humor formed after ocular trauma or paracentesis has been shown to trigger mitosis of the lens cells (Reddan et al., 1979). It has also been clearly demonstrated that injury to the eye produces increased release of PGs in the aqueous humor (Unger, 1989). There is also evidence that some PGs, mainly PGF2 alpha, can act as mitogens in some cells (Jimenez de Asua et al, 1983). Therefore, the low capacity of the lens to synthesize PGs can be compensated for by the presence of these eicosanoids in the aqueous humor.(ABSTRACT TRUNCATED AT 400 WORDS)