Regulation of uveal sympathetic neurotransmission by peroxides

Catherine A. Opere, Lin Tang, Michael Imler, Judy Kim, Matthias Okoye, Sunny Ohia

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Purpose. To investigate the effect of naturally occurring and synthetic peroxides on norepinephrine release from isolated iris-ciliary bodies of several mammalian species. Methods. Hemiirides (bovine) and iris-ciliary bodies (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) for 60 minutes. After incubation, tissues were set up for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited through electrical field stimulation. Results. In bovine irides, hydrogen peroxide (H2O2), cumene hydroperoxide (cuOOH), and tert-butyl hydroperoxide (buOOH) caused a concentration- dependent potentiation of field-stimulated [3H]NE release with the following rank order of potency: cuOOH > H2O2 > buOOH. Furthermore, the free radical scavenger, melatonin (2 mM), prevented the enhancement of evoked [3H]NE overflow elicited by H2O2 and cuOOH. At equimolar concentrations, H2O2 (1 mM) increased stimulated [3H]NE release from rabbit, human (mean age, 29.7; range, 15 to 48 years), and Fischer 344 rat (4 months old) iris-ciliary bodies by 98%, 50%, and 40%, respectively. However, H2O2 (1 mM) caused a 9% increase in evoked [3H]NE release in tissues from aged Fischer 344 rats (30 months old) and a 5% decrease in neurotransmitter release in tissues from old human donors (mean age, 72.3 years; range, 69 to 74 years). Conclusions. Peroxides such as H2O2 can potentiate sympathetic neurotransmission in the anterior uvea of several mammalian species. In bovine irides, H2O2 induced enhancement of neurotransmitter release can be mimicked by synthetic peroxides and may involve the generation of reactive oxygen species.

Original languageEnglish
Pages (from-to)842-847
Number of pages6
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number5
StatePublished - 1997

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Peroxides
Iris
Synaptic Transmission
Ciliary Body
Inbred F344 Rats
Neurotransmitter Agents
Norepinephrine
Uvea
Rabbits
tert-Butylhydroperoxide
Free Radical Scavengers
Melatonin
Hydrogen Peroxide
Electric Stimulation
Reactive Oxygen Species

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Opere, C. A., Tang, L., Imler, M., Kim, J., Okoye, M., & Ohia, S. (1997). Regulation of uveal sympathetic neurotransmission by peroxides. Investigative Ophthalmology and Visual Science, 38(5), 842-847.

Regulation of uveal sympathetic neurotransmission by peroxides. / Opere, Catherine A.; Tang, Lin; Imler, Michael; Kim, Judy; Okoye, Matthias; Ohia, Sunny.

In: Investigative Ophthalmology and Visual Science, Vol. 38, No. 5, 1997, p. 842-847.

Research output: Contribution to journalArticle

Opere, CA, Tang, L, Imler, M, Kim, J, Okoye, M & Ohia, S 1997, 'Regulation of uveal sympathetic neurotransmission by peroxides', Investigative Ophthalmology and Visual Science, vol. 38, no. 5, pp. 842-847.
Opere, Catherine A. ; Tang, Lin ; Imler, Michael ; Kim, Judy ; Okoye, Matthias ; Ohia, Sunny. / Regulation of uveal sympathetic neurotransmission by peroxides. In: Investigative Ophthalmology and Visual Science. 1997 ; Vol. 38, No. 5. pp. 842-847.
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abstract = "Purpose. To investigate the effect of naturally occurring and synthetic peroxides on norepinephrine release from isolated iris-ciliary bodies of several mammalian species. Methods. Hemiirides (bovine) and iris-ciliary bodies (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) for 60 minutes. After incubation, tissues were set up for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited through electrical field stimulation. Results. In bovine irides, hydrogen peroxide (H2O2), cumene hydroperoxide (cuOOH), and tert-butyl hydroperoxide (buOOH) caused a concentration- dependent potentiation of field-stimulated [3H]NE release with the following rank order of potency: cuOOH > H2O2 > buOOH. Furthermore, the free radical scavenger, melatonin (2 mM), prevented the enhancement of evoked [3H]NE overflow elicited by H2O2 and cuOOH. At equimolar concentrations, H2O2 (1 mM) increased stimulated [3H]NE release from rabbit, human (mean age, 29.7; range, 15 to 48 years), and Fischer 344 rat (4 months old) iris-ciliary bodies by 98{\%}, 50{\%}, and 40{\%}, respectively. However, H2O2 (1 mM) caused a 9{\%} increase in evoked [3H]NE release in tissues from aged Fischer 344 rats (30 months old) and a 5{\%} decrease in neurotransmitter release in tissues from old human donors (mean age, 72.3 years; range, 69 to 74 years). Conclusions. Peroxides such as H2O2 can potentiate sympathetic neurotransmission in the anterior uvea of several mammalian species. In bovine irides, H2O2 induced enhancement of neurotransmitter release can be mimicked by synthetic peroxides and may involve the generation of reactive oxygen species.",
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AU - Ohia, Sunny

PY - 1997

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N2 - Purpose. To investigate the effect of naturally occurring and synthetic peroxides on norepinephrine release from isolated iris-ciliary bodies of several mammalian species. Methods. Hemiirides (bovine) and iris-ciliary bodies (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) for 60 minutes. After incubation, tissues were set up for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited through electrical field stimulation. Results. In bovine irides, hydrogen peroxide (H2O2), cumene hydroperoxide (cuOOH), and tert-butyl hydroperoxide (buOOH) caused a concentration- dependent potentiation of field-stimulated [3H]NE release with the following rank order of potency: cuOOH > H2O2 > buOOH. Furthermore, the free radical scavenger, melatonin (2 mM), prevented the enhancement of evoked [3H]NE overflow elicited by H2O2 and cuOOH. At equimolar concentrations, H2O2 (1 mM) increased stimulated [3H]NE release from rabbit, human (mean age, 29.7; range, 15 to 48 years), and Fischer 344 rat (4 months old) iris-ciliary bodies by 98%, 50%, and 40%, respectively. However, H2O2 (1 mM) caused a 9% increase in evoked [3H]NE release in tissues from aged Fischer 344 rats (30 months old) and a 5% decrease in neurotransmitter release in tissues from old human donors (mean age, 72.3 years; range, 69 to 74 years). Conclusions. Peroxides such as H2O2 can potentiate sympathetic neurotransmission in the anterior uvea of several mammalian species. In bovine irides, H2O2 induced enhancement of neurotransmitter release can be mimicked by synthetic peroxides and may involve the generation of reactive oxygen species.

AB - Purpose. To investigate the effect of naturally occurring and synthetic peroxides on norepinephrine release from isolated iris-ciliary bodies of several mammalian species. Methods. Hemiirides (bovine) and iris-ciliary bodies (human, rabbit, and rat) were incubated in Krebs solution containing [3H]-norepinephrine ([3H]NE) for 60 minutes. After incubation, tissues were set up for studies of [3H]NE release using the superfusion method. Release of [3H]NE was elicited through electrical field stimulation. Results. In bovine irides, hydrogen peroxide (H2O2), cumene hydroperoxide (cuOOH), and tert-butyl hydroperoxide (buOOH) caused a concentration- dependent potentiation of field-stimulated [3H]NE release with the following rank order of potency: cuOOH > H2O2 > buOOH. Furthermore, the free radical scavenger, melatonin (2 mM), prevented the enhancement of evoked [3H]NE overflow elicited by H2O2 and cuOOH. At equimolar concentrations, H2O2 (1 mM) increased stimulated [3H]NE release from rabbit, human (mean age, 29.7; range, 15 to 48 years), and Fischer 344 rat (4 months old) iris-ciliary bodies by 98%, 50%, and 40%, respectively. However, H2O2 (1 mM) caused a 9% increase in evoked [3H]NE release in tissues from aged Fischer 344 rats (30 months old) and a 5% decrease in neurotransmitter release in tissues from old human donors (mean age, 72.3 years; range, 69 to 74 years). Conclusions. Peroxides such as H2O2 can potentiate sympathetic neurotransmission in the anterior uvea of several mammalian species. In bovine irides, H2O2 induced enhancement of neurotransmitter release can be mimicked by synthetic peroxides and may involve the generation of reactive oxygen species.

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