Excessive production of reactive oxygen metabolites by inflamed colon: Analysis by chemiluminescence probe

Keshavarzian, Ali; Sedghi, Shahriar; Kanofsky, Jefferey; List, Troy J.; Robinson, C.D.; Ibrahim, Christine; Winship, Daniel H.

doi:10.1016/0016-5085(92)91111-g

Cited by 248 publications

(163 citation statements)

References 32 publications

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“…Oxidative stress is accelerated by a combination of ROS generation and impaired antioxidant capacity (Kankuri et al 2003;Keshavarzian et al 1992;Osburn et al 2006). Previous pharmacological studies have shown that EGCG is metabolized through methylation, glucuronidation, and sulfation under normal physiological conditions, and then subsequently excreted in urine (Okushio et al 1999;Li et al 2001).…”

Section: Discussionmentioning

confidence: 99%

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

Inoue

Akiyama

Maeda‐Yamamoto

et al. 2011

Cell Stress and Chaperones

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Previously, we reported that oral feeding of 1% green tea polyphenols (GTPs) aggravated the dextran sulfate sodium (DSS)-induced colitis in mice. In the present study, we assessed the toxicity of 1% GTPs in several organs from normal and DSS-exposed mice. Sixty-two male ICR mice were initially divided into four groups. Nontreated group (group 1, n=15) was given standard diet and water, GTPs (group 2, n=15) received 1% GTPs in diet and water, DSS (group 3, n=15) received diet and 5% DSS in water, and GTPs + DSS group (group 4, n=17) received 1% GTPs in diet and 5% DSS in water. We found that group 4 significantly increased (P<0.05) kidney weight, the levels of serum creatinine and thiobarbituric acid-reactive substances in both kidney and liver, as compared with those in group 3. The mRNA expression levels of antioxidant enzymes and heat-shock proteins (HSPs) in group 4 were lower than those of group 3. For instance, heme oxygenase-1 (HO-1), HSP27, and 90 mRNA in the kidney of group 4 were dramatically down-regulated as compared with those of group 3. Furthermore, 1% GTPs diet decreased the expression of HO-1, NAD(P)H:quinone oxidoreductase 1 (NQO1) and HSP90 in kidney and liver of non-treated mice. Taken together, our results indicate that high-dose GTPs diet disrupts kidney functions through the reduction of antioxidant enzymes and heat-shock protein expressions in not only colitis but also non-treated ICR mice.

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Section: Discussionmentioning

confidence: 99%

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

Inoue

Akiyama

Maeda‐Yamamoto

et al. 2011

Cell Stress and Chaperones

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“…Specifically, upregulation of iNOS and the formation of RNMs (e.g., NO, ONOO Ϫ ) under conditions of oxidative stress appears to be essential in the promotion of an inflammatory response in non-GI as well as GI models (e.g., 34,37,40,50,55). Furthermore, we and others have shown that upregulation of iNOS and RNMs is found in the intestinal mucosa of patients with ulcerative colitis and Crohn's disease (17,37,50,55), in which high levels of oxidants (e.g., H 2 O 2 ) as well as loss of mucosal barrier integrity have been reported (17,30,31,37,39,43). In these studies, tissue nitration was associated with the inflamed human mucosa of IBD (37,50,55) and was linked with the upregulation of iNOS (37,55).…”

Section: Discussionmentioning

confidence: 73%

“…However, the pathophysiology of mucosal barrier disruption in IBD remains poorly understood. Nonetheless, several studies have shown that chronic gut inflammation in IBD is associated with excessive amounts of oxidants (e.g., H 2 O 2 ) and that a high level of these oxidants appears to be a key contributor to mucosal injury (2,10,17,18,37,39,40,43). Oxidant-induced disruption is of substantial clinical and biological value not only because oxidants are common in inflammation (e.g., they are elaborated by neutrophils that infiltrate the mucosa during inflammation) but also because they can lead to mucosal barrier dysfunction and, in turn, to the initiation and/or continuation of mucosal inflammation and injury (29-31, 38, 39, 60).…”

mentioning

confidence: 99%

“…Indeed, overproduction and uncontrolled generation of iNOS-derived reactive nitrogen metabolites (e.g., NO, ONOO Ϫ ) have been proposed to be an important factor in tissue damage during inflammation, including in IBD (17,34,37,39,40,55). For example, we have shown that a number of these oxidative reactions, including cytoskeletal nitration and oxidation, also occur in intestinal mucosa from patients with IBD (17,37) as well as in intestinal cell monolayers in culture (9,10).…”

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confidence: 99%

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Key role of PLC-γ in EGF protection of epithelial barrier against iNOS upregulation and F-actin nitration and disassembly

Banan

Zhang

Shaikh

et al. 2003

American Journal of Physiology-Cell Physiology

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Upregulation of inducible nitric oxide synthase (iNOS) is key to oxidant-induced disruption of intestinal (Caco-2) monolayer barrier, and EGF protects against this disruption by stabilizing the cytoskeleton. PLC-␥ appears to be essential for monolayer integrity. We thus hypothesized that PLC-␥ activation is essential in EGF protection against iNOS upregulation and the consequent cytoskeletal oxidation and disarray and monolayer disruption. Intestinal cells were transfected to stably overexpress PLC-␥ or to inhibit its activation and were then pretreated with EGF Ϯ oxidant (H 2O2). Wild-type (WT) intestinal cells were treated similarly. Relative to WT monolayers exposed to oxidant, pretreatment with EGF protected monolayers by: increasing native PLC-␥ activity; decreasing six iNOS-related variables (iNOS activity/protein, NO levels, oxidative stress, actin oxidation/nitration); increasing stable F-actin; maintaining actin stability; and enhancing barrier integrity. Relative to WT cells exposed to oxidant, transfected monolayers overexpressing PLC-␥ (ϩ2.3-fold) were protected, as indicated by decreases in all measures of iNOS-driven pathway and enhanced actin and barrier integrity. Overexpression-induced inhibition of iNOS was potentiated by low doses of EGF. Stable inhibition of PLC-␥ prevented all measures of EGF protection against iNOS upregulation. We conclude that 1) EGF protects against oxidative stress disruption of intestinal barrier by stabilizing F-Actin, largely through the activation of PLC-␥ and downregulation of iNOS pathway; 2) activation of PLC-␥ is by itself essential for cellular protection against oxidative stress of iNOS; and 3) the ability to suppress iNOS-driven reactions and cytoskeletal oxidation and disassembly is a novel mechanism not previously attributed to the PLC family of isoforms. actin cytoskeleton; gut barrier; growth factors; oxidative stress; nitration and carbonylation; reactive nitrogen metabolites; phospholipase C isoform; inflammatory bowel disease; Caco-2 cells THE EPITHELIUM of gastrointestinal (GI) mucosa is a highly selective permeability barrier that normally excludes the passage of harmful proinflammatory molecules (e.g., bacterial endotoxin, immunoreactive antigens) but allows the absorption from the lumen of nutrients and water into the mucosa and the systemic circulation.

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“…Growing evidence demonstrated the significance of oxidative stress both in the clinical and experimental studies of UC. Excessive production of reactive oxygen species (ROS) in mucosal cells induced inflammatory and immune responses which could directly or indirectly cause damage of intestinal epithelial cells, subsequently influence mucosal integrity or initiate an inflammatory signaling cascade and lead to severe impairment in experimental colitis 6 .…”

Section: Introductionmentioning

confidence: 99%

Prophylactic and curative anti-ulcerative colitis activity and the possible mechanisms of action of some desert plants

El‐Meligy

Awaad

Soliman

et al. 2014

Journal of Enzyme Inhibition and Medicinal Chemistry

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The aim of the present study was to evaluate both prophylactic and curative anti-ulcerative colitis activity and the possible mechanism of action of seven desert plant extracts. (Asclepiadaceae) were separately evaluated at three doses (125, 250, and 500 mg/kg) using the acetic acid-induced colitis model. The investigated extracts possessed prophylactic and curative anti-ulcerative colitis activities in a dose-dependent manner, where Salvia lanigera (87.9) and Solenostemma arghel (89.2) were the most effective extracts whereas the dexamesathone produced 68%. These extracts were further investigated for estimation of their mechanism of action. The in vitro potential radical (DPPH) scavenging activities of the investigated extracts were well supported with the reduction of colonic MDA content for both extracts. Suppression of the inflammatory mediator TNF-a and inhibition of both PLA2 and protease enzymes may play an important role in the anti-ulcerative colitis activities. The investigated extracts were safe for use up to 5 g/kg and the total alcohol extracts of Salvia lanigera and Solenostemma arghel (400 mg/kg for 35 d) showed no alteration on liver and kidney functions. Phytochemical screening of the investigated extracts revealed the presence of flavonoids, tannins, unsaturated sterols, and proteins which could be responsible for the activities.

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Excessive production of reactive oxygen metabolites by inflamed colon: Analysis by chemiluminescence probe

Cited by 248 publications

References 32 publications

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

High-dose green tea polyphenols induce nephrotoxicity in dextran sulfate sodium-induced colitis mice by down-regulation of antioxidant enzymes and heat-shock protein expressions

Key role of PLC-γ in EGF protection of epithelial barrier against iNOS upregulation and F-actin nitration and disassembly

Prophylactic and curative anti-ulcerative colitis activity and the possible mechanisms of action of some desert plants

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