October 1985
Volume 26, Issue 10
Articles  |   October 1985
Metabolism of arachidonic acid in rabbit iris and retina.
Investigative Ophthalmology & Visual Science October 1985, Vol.26, 1336-1342. doi:
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      Y Preud'homme, D Demolle, J M Boeynaems; Metabolism of arachidonic acid in rabbit iris and retina.. Invest. Ophthalmol. Vis. Sci. 1985;26(10):1336-1342.

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      © ARVO (1962-2015); The Authors (2016-present)

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Both the iris and the retina of the rabbit released prostaglandins (PG) E2, F2 alpha, 6-keto-F1 alpha and thromboxane (Tx) B2, when incubated in vitro. PGE2 was the major cyclooxygenase product formed by each tissue. The kinetics of PGE2 release by the iris and the retina were similar: high initial output followed by a decline to a steady-state value. The production of PGE2 was inhibited by indomethacin and stimulated by ionophore A23187. The iris and the retina converted exogenous arachidonic acid into 12- and 15-hydroxy-eicosatetraenoic acid (HETE): inhibition by eicosatetraynoic acid (ETYA) indicated the involvement of lipoxygenase enzymes. This lipoxygenase activity was important relatively to cyclooxygenase in the retina, but was only a minor pathway in the iris. Leukotriene (LT) B4 was released by the iris and the retina in amounts smaller than PGE2, but compatible with a biological activity: ionophore A23187 stimulated LTB4 production in both tissues. Our data support the hypothesis that PGE2 and LTB4 could play a role in the initiation of ocular inflammation.


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