“…Higher levels of glucocorticoids under cer tain conditions may act as a cocataractogenic factor [Bettman et al, 1968;Cremer-Bartels et al, 1969], induce ocular hypertension [Akingbehin, 1981;Becker, 1965;Schwartz and Seddon, 1981] or even provoke steroid glaucoma either by the stabilization of lysosomal membranes of the trabecular meshwork resulting in a decrease of aqueous humour outflow from the anterior chamber [François, 1975[François, , 1978 or by inhibition of phagocytosis of the trabecu lar endothelial cells cleaning continuously the debris entering this filter; supersensitiv ity of these cells to endogenous glucocor ticoids thus might be a basis for open-angle glaucoma [Bill, 1975]. Corticosteroid con centration increases in the aqueous humour after acid burns [Obenberger et al, 1983] and is higher in secondary aqueous humour in comparison with the primary ocular fluid [Obenberger et al, 1971].…”