Reflux esophagitis in humans is mediated by oxygen-derived free radicals

Wetscher, Gerold J.; Hinder, Ronald A.; Bagchi, Debasis; Hinder, Paul R.; Bagchi, Manashi; Perdikis, Galen; McGinn, Thomas R.

doi:10.1016/s0002-9610(99)80014-2

Cited by 122 publications

(81 citation statements)

References 21 publications

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“…In recent studies, it has been shown that reflux esophagitis is mediated by oxygen-derived free radicals [12][13][14]. Administration of various free radical scavengers has been founded to prevent esophageal mucosal damage.…”

Section: Introductionmentioning

confidence: 99%

Involvement of oxidative stress in experimentally induced reflux esophagitis and Barrett’s esophagus: clue for the chemoprevention of esophageal carcinoma by antioxidants

Lee

Ahn

et al. 2001

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Section: Introductionmentioning

confidence: 99%

Involvement of oxidative stress in experimentally induced reflux esophagitis and Barrett’s esophagus: clue for the chemoprevention of esophageal carcinoma by antioxidants

Lee

Ahn

et al. 2001

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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“…Several lines of evidence suggest that reflux of gastric acid into the distal esophagus causes increased oxidative stress, which may play a critical role in the pathogenesis of reflux esophagitis and development of Barrett's esophagus (Wetscher, 1995;Chen, 2000;Sihvo, 2002). Wetscher et al (1995) assessed oxidative stress by measuring chemiluminescence, lipid peroxidation and superoxide dismutase (SOD) in the esophageal biopsy samples of GERD patients and controls.…”

Section: Discussionmentioning

confidence: 99%

“…Wetscher et al (1995) assessed oxidative stress by measuring chemiluminescence, lipid peroxidation and superoxide dismutase (SOD) in the esophageal biopsy samples of GERD patients and controls. These investigators observed that highest levels of free radicals and lipid peroxidation, and the lowest levels of SOD were present in patients with Barrett's esophagus.…”

Section: Discussionmentioning

confidence: 99%

Barrett's Esophagus and β-carotene Therapy: Symptomatic Improvement in GERD and Enhanced HSP70 Expression in Esophageal Mucosa

Dutta

Agrawal

Girotra

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Introduction: Epidemiological studies suggest a protective role for β-carotene with several malignancies. Esophageal adenocarcinoma frequently arises from Barrett's esophagus (BE). We postulated that β-carotene therapy maybe protective in BE. Materials and Method: We conducted a prospective study in which 25 mg of β-carotene was administered daily for six-months to six patients. Each patient underwent upper endoscopy before and after therapy and multiple mucosal biopsies were obtained. Additionally, patients completed a gastroesophageal reflux disease (GERD) symptoms questionnaire before and after therapy and severity score was calculated. To study the effect of β-carotene at molecular level, tissue extracts of the esophageal mucosal biopsy were subjected to assessment of heat-shock protein 70 (HSP70). Results: A significant (p<0.05) reduction in mean GERD symptoms severity score from 7.0±2.4 to 2.7±1.7 following β-carotene therapy was noted. Measurement of Barrett's segment also revealed a significant reduction in mean length after therapy. In fact, two patients had complete disappearance of intestinal metaplasia. Furthermore, marked enhancement of HSP70 expression was demonstrated in biopsy specimens from Barrett's epithelium in four cases that were tested. Conclusions: Longterm β-carotene therapy realizes amelioration of GERD symptoms along with restitution of the histological and molecular changes in esophageal mucosa of patients with BE, associated with concurrent increase in mucosal HSP70 expression.

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“…Oxidative damage appears to play a role in this process in humans (Olyaee et al 1995;Wetscher et al 1995) as well as in a rodent model of esophageal adenocarcinoma (Chen et al 2000). In a rat model of the regulatory mechanism of acid secretion in the stomach after damage with the bile acid taurocholate, endogenous nitric oxide was found to down-regulate acid production (Takeuchi et al 2000).…”

Section: Adenocarcinoma Of the Esophagusmentioning

confidence: 99%