Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport.

Karayalçın, Selim; Sturbaum, Christopher W.; Wachsman, J. T.; Ho, Jih; Powell, Don W.

doi:10.1172/jci114715

Cited by 90 publications

(61 citation statements)

References 36 publications

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“…Our experimental design generated ϳ30 M/min O 2 Ϫ ⅐ and 80 M H 2 O 2 (measured after 20 min of incubation). This concentration is similar to that of another study in which ROS altered colonic electrolyte transport in rats (16).…”

Section: Discussionsupporting

confidence: 89%

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Mechanism of dilation to reactive oxygen species in human coronary arterioles

Sato¹,

Sakuma²,

Gutterman³

2003

American Journal of Physiology-Heart and Circulatory Physiology

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We tested whether reactive oxygen species (ROS) generated from treatment with xanthine (XA) and xanthine oxidase (XO) alter vascular tone of human coronary arterioles (HCA). Fresh human coronary arterioles (HCA) from right atrial appendages were cannulated for video microscopy. ROS generated by XA (10–4 M) + XO (10 mU/ml) dilated HCA (99 ± 1%, 20 min after application of XA/XO). This dilation was not affected by denudation or superoxide dismutase (150 U/ml). Catalase (500 U/ml or 5,000 U/ml) attenuated the dilation early on, but a significant latent vasodilation appeared after 5 min peaking at 20 min (51 ± 1%, 20 min after application of XA/XO + 500 U/ml catalase, P < 0.01 vs. control). KCl (40 mM) reduced the early and sustained vasodilation to XA/XO in the absence of catalase but 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 × 10–5 M), diethyldithiocarbamate trihydrate (DDC, 10–2 M), and deferoxamine (DFX, 10–3 M) had no effect. In contrast, the catalase-resistant vasodilation was significantly attenuated by DDC, ODQ, and DFX as well as polyethylene-glycolated catalase (5,000 U/ml), but KCl had no effect. Confocal microscopy revealed that even in the presence of catalase, 2′,7′-dichlorodihydrofluoresein diacetate fluorescence was observed in the vascular smooth muscle, but this was abolished by DDC. These data indicate that the exogenously generated superoxide anion ([Formula: see text]) by XA/XO is spontaneously converted to H2O2, which dilates HCA through vascular smooth muscle hyperpolarization. [Formula: see text] is also converted to H2O2 likely by superoxide dismustase within vascular cells and dilates HCA through a different pathway involving the activation of guanylate cyclase. These findings suggest that exogenously and endogenously produced H2O2 may elicit vasodilation by different mechanisms.

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Section: Discussionsupporting

confidence: 89%

“…The combination of XA (10 Ϫ4 M) and XO (10 mU/ml) that we used in our study produces O 2 Ϫ ⅐ (22), which spontaneously dismutates to H 2 O 2 (16). We confirmed generation of both ROS species by using cytochrome c and TMB, respectively.…”

Section: Discussionsupporting

confidence: 62%

Mechanism of dilation to reactive oxygen species in human coronary arterioles

Sato¹,

Sakuma²,

Gutterman³

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…ROS also stimulate a cytoprotective response that includes an increase in the production of PGE 2 , which in turn generates scavengers of free radicals such as SOD and catalase. Furthermore, by increasing the synthesis of PGE 2 , H 2 O 2 causes muscle contraction through the activation of PKC and MAPK (15,18,24,27,31). The mechanisms whereby ROS stimulate the cPLA 2 -PGE 2 pathway are unknown.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Xiao

Andrada²,

Biancani

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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The level of lipid peroxidation as well as the PGE2 content was significantly increased after H2O2 pretreatment. Unlike superoxide dismutase, the free radical scavenger catalase prevented the H2O2 induced contraction, and its inhibition of the CCK-8 induced contraction. It is concluded that ROS cause damage to the plasma membrane of the gallbladder muscle and contraction through the generation of PGE2 induced by cPLA2-cyclooxygenase and probably mediated by the PKC-MAPK pathway. lipid peroxidation; prostaglandin E2 content; smooth muscle REACTIVE OXYGEN SPECIES (ROS) such as superoxide radical anion, hypochlorous acid, and hydrogen peroxide (H 2 O 2 ) are by-products of oxidative metabolism, in which energy activation and electron reduction are involved. Inflammatory processes enhance their production, which could affect cell functions (20). The mechanisms whereby ROS act at the cellular level are not fully understood. Their pathogenic role on cell membranes and signal-transduction pathways may explain the early events that are associated with cell dysfunction caused by inflammation. Therefore, the understanding of these mechanisms is important for developing therapeutic strategies at cellular sites of dysfunction.Acute cholecystitis is characterized by an inflammatory process that involves the gallbladder wall with polymorphonuclear cells (23). ROS play a major role in mediating cell injury during inflammatory processes. Disorders of gallbladder motility caused or aggravated by inflammatory processes may be due to the actions of ROS. They may also contribute to the inhibition of agonist-induced contraction (25, 37). The actions of ROS are mediated in part by cyclooxygenase by-products that are important participants in the inflammatory process (16). The contraction of tracheal and ileal muscle strips induced by ROS in vitro appear to be mediated by prostaglandins (24,29).Prostaglandins have varied effects on gastrointestinal motility (5,12,17,32). Muscle strips from various segments of guinea pig stomach exhibited different responses to PGE 1 , PGE 2 , and PGF 2␣ (22). In rat stomach, PGE 2 caused a contraction in the longitudinal preparation but had no effect on the circular muscle (35). PGE 1 , PGE 2 , and PGF 2␣ potentiated the contractile responses of guinea pig gallbladder to transmural stimulation and ACh (28). Prostaglandins may also be involved in muscle cytoprotection since PGE 2 and other prostaglandins appear to participate in the pathway responsible for increased formation of scavengers of free radicals (2). These studies therefore were aimed at examining the effects of ROS on gallbladder muscle function utilizing H 2 O 2 on enzymatic digested single muscle cells from normal guinea pig gallbladders. MATERIALS AND METHODSAnimals. Adult male guinea pigs were purchased from Elm Hill Breeding Laboratory (Chelmsford, MA). The Animal Welfare Committee of Rhode Island Hospital approved their use. Animals were housed in thermoregulated rooms and had free access to food and water. After an overnight fast, th...

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“…Superoxide produced by X/XO spontaneously dismutates to hydrogen peroxide in the presence of endogenous SOD (9). Hydrogen peroxide hyperpolarizes (8) and relaxes (6) smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K⁺ channels

Ohashi¹,

Faraci²,

Heistad³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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Ohashi, Masuo, Frank Faraci, and Donald Heistad. Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K ϩ channels. Am J Physiol Heart Circ Physiol 289: H2244 -H2250, 2005; doi:10.1152/ajpheart.00254.2005.-The goal of this study was to determine the effects of peroxynitrite (ONOO Ϫ ) on smooth muscle membrane potential and vasomotor function in rabbit carotid arteries. ONOO Ϫ is known to affect vascular tone by several mechanisms, including effects on K ϩ channels. Xanthine (X, 0.1 mM), xanthine oxidase (XO, 0.01 U/ml), and a low concentration of sodium nitroprusside (SNP, 10 nM) were used to generate ONOO Ϫ . In the common carotid artery, X and XO (X/XO) in the presence of SNP tended to increase tension. In contrast, in the internal carotid artery, X/XO in the presence of SNP transiently hyperpolarized the membrane (Ϫ8.5 Ϯ 1.8 mV, mean Ϯ SE) and decreased tension (by 85 Ϯ 5.6%). In internal carotid arteries, in the absence of SNP, X/XO did not hyperpolarize the membrane and produced much less relaxation (by 23 Ϯ 5.6%) than X/XO and SNP. Ebselen (50 M) inhibited both hyperpolarization and relaxation to X/XO and SNP, and uric acid (100 M) inhibited relaxation. Glibenclamide (1 M) abolished hyperpolarization and inhibited relaxation during X/XO and SNP. Charybdotoxin (100 nM) or tetraethylammonium (1 mM) did not affect hyperpolarization or relaxation, respectively. These results suggest that ONOO Ϫ hyperpolarizes and relaxes smooth muscle in rabbit internal carotid artery but not in common carotid artery through activation of K ATP channels.hyperpolarization; membrane potential; vasomotor function; reactive oxygen species REACTIVE OXYGEN SPECIES (ROS) and nitrogen species play an important role in the maintenance of vascular homeostasis and after injury. Pathophysiological conditions such as ischemia and reperfusion increase production of both nitric oxide (NO) and superoxide (28). Superoxide reacts with NO and forms peroxynitrite (ONOO Ϫ

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Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport.

Cited by 90 publications

References 36 publications

Mechanism of dilation to reactive oxygen species in human coronary arterioles

Mechanism of dilation to reactive oxygen species in human coronary arterioles

Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K⁺ channels

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Hydrogen peroxide stimulates rat colonic prostaglandin production and alters electrolyte transport.

Cited by 90 publications

References 36 publications

Mechanism of dilation to reactive oxygen species in human coronary arterioles

Mechanism of dilation to reactive oxygen species in human coronary arterioles

Reactive oxygen species (H2O2): effects on the gallbladder muscle of guinea pigs

Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K+ channels

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Product

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Reactive oxygen species (H₂O₂): effects on the gallbladder muscle of guinea pigs

Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K⁺ channels