Role of Catalase in Pre- and Postjunctional Responses of Mammalian Irides to Hydrogen Peroxide

Matutte, Beverly; Awe, S. Olubusayo; Ameh, Ferdy A.; LeDay, Angela M.; Rice, Justin C.; Opere, Catherine A.; Ohia, Sunny E.

doi:10.1089/jop.2000.16.429

Cited by 4 publications

(1 citation statement)

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“…The enzyme CAT which is involved in the metabolism of H 2 O 2 has also been linked to neurotransmission regulation by peroxides in ocular tissues. Matutte et al showed that the inhibition of catalase unmasked an excitatory action of H 2 O 2 on evoked NE release and an inhibitory effect on muscarinic receptor-induced contraction of iris smooth muscle (Matutte et al, 2000). These studies establish that inhibiting peroxide metabolism causes both sympathetic nerves and smooth muscles of the anterior uvea to be more susceptible to the harmful effects of H 2 O 2 .…”

Section: Role Of Oxidant-derived Metabolites In Pathogenesis Of Eye Dmentioning

confidence: 99%

Lipid peroxidation: pathophysiological and pharmacological implications in the eye

et al. 2013

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Oxygen-derived free radicals such as hydroxyl and hydroperoxyl species have been shown to oxidize phospholipids and other membrane lipid components leading to lipid peroxidation. In the eye, lipid peroxidation has been reported to play an important role in degenerative ocular diseases (age-related macular degeneration, cataract, glaucoma, diabetic retinopathy). Indeed, ocular tissues are prone to damage from reactive oxygen species due to stress from constant exposure of the eye to sunlight, atmospheric oxygen and environmental chemicals. Furthermore, free radical catalyzed peroxidation of long chain polyunsaturated acids (LCPUFAs) such as arachidonic acid and docosahexaenoic acid leads to generation of LCPUFA metabolites including isoprostanes and neuroprostanes that may further exert pharmacological/toxicological actions in ocular tissues. Evidence from literature supports the presence of endogenous defense mechanisms against reactive oxygen species in the eye, thereby presenting new avenues for the prevention and treatment of ocular degeneration. Hydrogen peroxide (H2O2) and synthetic peroxides can exert pharmacological and toxicological effects on tissues of the anterior uvea of several mammalian species. There is evidence suggesting that the retina, especially retinal ganglion cells can exhibit unique characteristics of antioxidant defense mechanisms. In the posterior segment of the eye, H2O2 and synthetic peroxides produce an inhibitory action on glutamate release (using [3H]-D-aspartate as a marker), in vitro and on the endogenous glutamate and glycine concentrations in vivo. In addition to peroxides, isoprostanes can elicit both excitatory and inhibitory effects on norepinephrine (NE) release from sympathetic nerves in isolated mammalian iris ciliary bodies. Whereas isoprostanes attenuate dopamine release from mammalian neural retina, in vitro, these novel arachidonic acid metabolites exhibit a biphasic regulatory effect on glutamate release from retina and can regulate amino acid neurotransmitter metabolism without inducing cell death in the retina. Furthermore, there appears to be an inhibitory role for neuroprostanes in the release of excitatory amino acid neurotransmitters in mammalian retina. The ability of peroxides and metabolites of LCPUFA to alter the integrity of neurotransmitter pools provides new potential target sites and pathways for the treatment of degenerative ocular diseases.

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Section: Role Of Oxidant-derived Metabolites In Pathogenesis Of Eye Dmentioning

confidence: 99%