Role of catalase in pre- and postjunctional responses of mammalian irides to hydrogen peroxide.
Role of catalase in pre- and postjunctional responses of mammalian irides to hydrogen peroxide.
复制标题
过氧化氢酶在哺乳动物虹膜对过氧化氢的结前和结后反应中的作用。
DOI：
10.1089/jop.2000.16.429
复制
发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Ohia,SE
中科院分区：
文献类型：
--
作者：
Matutte,B;Awe,SO;Ameh,FA;Leday,AM;Rice,JC;Opere,CA;Ohia,SE
在本研究中，我们研究了过氧化氢酶抑制剂3-氨基三唑（3-AT）对过氧化氢（H2 O2）诱导的牛虹膜交感神经传递增强的影响，以及这种氧化剂对人虹膜释放去甲肾上腺素（NE）的抑制作用。此外，我们研究了3-AT对H2 O2诱导的牛离体虹膜对卡巴胆碱收缩反应的衰减的影响。分离的哺乳动物虹膜制备的研究[3 H]NE释放使用灌流方法和收缩研究使用离体器官浴。当H2 O2浓度小于100 μM时，H2 O2对场刺激牛或人虹膜释放[3 H]NE无显著影响。在牛虹膜中，3-AT引起H_2O_2（10-300 μM）浓度-反应曲线显著（P<0.001）的显著性位移。3-AT还增加H2 O2引起的人离体虹膜[3 H]NE释放的衰减。低浓度H2 O2（<100 μM）对卡巴胆碱收缩无影响。然而，3-AT揭示了低浓度H2 O2（3-100 μM）对卡巴胆碱诱导的收缩的抑制作用。我们的结论是，过氧化氢酶的抑制导致前和postjunctional反应的孤立的哺乳动物虹膜更容易受到氧化应激诱导的H2 O2。
In the present study, we examined the effect of inhibition of catalase with 3-aminotriazole (3-AT) on hydrogen peroxide (H202)-induced enhancement of sympathetic neuro-transmission in bovine irides and on the inhibitory effect of this oxidant on norepinephrine (NE) release from human irides,in vitro. Furthermore, we investigated the effect of 3-AT on H2O2-induced attenuation of contractile responses to carbachol in the bovine isolated irides. Isolated mammalian irides were prepared for studies of [3H]NE release using the superfusion method and for contractile studies using isolated organ baths. At concentrations less than 100 μM, H2O2had no significant effect on field-stimulated [3H]NE release from bovine or human irides. In bovine irides, 3-AT caused significant (P<0.001) leftward shifts of concentration-response curves to H2O2(10-300 μM). 3-AT also increased H2O2-induced attenuation of evoked [3H]NE release from human isolated irides. Low concentrations of H2O2(<100 μM) had no effect on carbachol contractions. However, 3-AT unmasked an inhibitory effect of low concentrations of H2O2(3-100 μM) on carbachol-induced contractions. We conclude that inhibition of catalase causes both pre- and postjunctional responses of isolated mammalian irides to be more susceptible to oxidative stress induced by H2O2.