Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion

Li, Yan; Wo, John M.; Su, Ruifeng; Ray, Mukunda B.; Martin, Robert C.G.

doi:10.1016/j.surg.2006.07.042

Cited by 16 publications

(19 citation statements)

References 30 publications

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“…On the other hand, one of the most important adaptive responses to cell loss in reflux esophagitis is an increase of the proliferation Research. A progressive increase of MnSOD is found after EDA 3 and 6 months, which is corresponding to our previous observation (13,26). The increased MnSOD levels in the esophageal epithelium of EDA rat may reflect an adaptive process and the reasons could be as follows: (a) MnSOD is an inducible antioxidant and it can be induced to a high level by several stimuli, including oxidative stress and inflammatory (32), or (b) a compensatory mechanism against the decreased MnSOD enzymatic activity (14).…”

Section: Discussionsupporting

confidence: 91%

“…We have also shown that, in an esophagoduodenal anastomosis (EDA) rat model, the relationship between oxidative damage and the transition from chronic inflammation to adenocarcinoma remains consistent. Loss of MnSOD protective enzymatic activity was also found at a very early stage, and alteration of MnSOD protein level was closely related to the progression from esophagitis to metaplasia to EAC in EDA rats (13).…”

mentioning

confidence: 85%

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Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Martin¹,

Liu²,

Wo³

et al. 2007

Clinical Cancer Research

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Purpose: Oxidative stress is related to the carcinogenic pathway of reflux esophagitis to Barrett's metaplasia to esophageal adenocarcinoma (EAC). Recent studies have shown that a decreased manganese superoxide dismutase (MnSOD) level is associated with the increased incidences of Barrett's esophagus (BE) and EAC. The aim of this study was to investigate MnSOD supplementation as a chemopreventive agent to prevent oxidative injury and subsequent BE and EAC formation. Experimental Design: Our esophagoduodenal anastomotic (EDA) model was done on rats according to our established procedure and treated with Mn(III)tetrakis(4-benzoic acid) porphyrin (MnTBAP; 10 mg/kg, i.p. every 3 days). Histologic changes were determined after the EDA model at 1, 3, and 6 months. Lipid peroxidation and 8-hydroxy-deoxyguanosine for DNA oxidative damage were determined by thiobarbituric acid^reactive substance assay and immunohistochemical staining. Enzymatic activities of MnSOD and Cu/ZnSOD were evaluated, and the rate of proliferation was determined by proliferating cell nuclear antigen staining. Results: Severe esophagitis was seen in 100% of the EDA rats, and morphologic transformation within the esophageal epithelium was observed with intestinal metaplasia (40% of animals) and cancer (40% of animals) identified after 3 months. Decreased oxidative damage, along with the decreased degree of esophagitis and incidence of BE (20%) and EAC (0%), was found in MnTBAP-treated EDA rats comparing with the saline-treated EDA control. Decreased proliferation (46%) and increased SOD enzymatic activities (25%) were also found in the EDA rats treated with MnTBAP. Conclusion: MnTBAP protected rat esophageal epithelium from oxidative injury induced by EDA, and it could prevent the transformation of esophageal epithelial cell to BE to EAC by preservation of antioxidants.Esophageal adenocarcinoma (EAC) has received considerable attention because of the dramatically increased incidence in the past 2 decades and the poor prognoses with a 5-year survival rate of 10% to 20% (1 -5). Currently, it is widely accepted that a cause-effect relationship exists between gastroesophageal reflux disease and EAC. Oxidative stress has been proposed to be closely related to the carcinogenic progression of reflux esophagitis, Barrett's metaplasia, and EAC. It has been shown that reactive oxygen species increase with the grade of reflux esophagitis and are highest in Barrett's esophagus (BE) in clinical patients (6). Several studies have also shown that reactive oxygen species cause DNA injury, such as strand breakage, alterations in guanine and thymine bases, and DNA cross-linkage (7,8). Therefore, oxidative DNA damage may contribute to the accumulation of genetic damage, and the accumulation of genetic and epigenetic aberrations produces one or more clones with metaplastic and/or malignant potential (9).In our previous studies using an external esophageal perfusion rat model (10 -13), we have shown significant increased levels of lipid peroxidation and 8-hydr...

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Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 85%

Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Martin¹,

Liu²,

Wo³

et al. 2007

Clinical Cancer Research

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“…The loss of MnSOD function was previously shown to be associated with increased incidence of BE (37). Furthermore, a recent study by Li et al (35) suggests that exposure to hydrophobic bile acids decreases MnSOD activity.…”

Section: G299 Resistance To Bile Acids and Acid In Esophageal Cellsmentioning

confidence: 93%

Characterization of squamous esophageal cells resistant to bile acids at acidic pH: implication for Barrett's esophagus pathogenesis

Goldman

Chen²,

Roesly³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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Barrett's esophagus (BE) is a premalignant condition, where normal squamous epithelium is replaced by intestinal epithelium. BE is associated with an increased risk of developing esophageal adenocarcinoma (EAC). However, the BE cell of origin is not clear. We hypothesize that BE tissue originates from esophageal squamous cells, which can differentiate to columnar cells as a result of repeated exposure to gastric acid and bile acids, two components of refluxate implicated in BE pathology. To test this hypothesis, we repeatedly exposed squamous esophageal HET1A cells to 0.2 mM bile acid (BA) cocktail at pH 5.5 and developed an HET1AR-resistant cell line. These cells are able to survive and proliferate after repeated 2-h treatments with BA at pH 5.5. HET1AR cells are resistant to acidification and express markers of columnar differentiation, villin, CDX2, and cytokeratin 8/18. HET1AR cells have increased amounts of reactive oxygen species, concomitant with a decreased level and activity of manganese superoxide dismutase compared with parental cells. Furthermore, HET1AR cells express proteins and activate signaling pathways associated with inflammation, cell survival, and tumorigenesis that are thought to contribute to BE and EAC development. These include STAT3, NF-κB, epidermal growth factor receptor (EGFR), cyclooxygenase-2, interleukin-6, phosphorylated mammalian target of rapamycin (p-mTOR), and Mcl-1. The expression of prosurvival and inflammatory proteins and resistance to cell death could be partially modified by inhibition of STAT3 signaling. In summary, our study shows that long-term exposure of squamous cells to BA at acidic pH causes the cells to display the same characteristics and markers as BE.

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“…28,29 We have demonstrated that the EDA model is consistent with the clinically relevant pathological changes of esophageal cancer. 30,31 The EDA surgical procedure was performed as described previously.…”

Section: Eda Model To Induce Esophageal Cancermentioning

confidence: 66%

Infrared light-absorbing gold/gold sulfide nanoparticles induce cell death in esophageal adenocarcinoma

Li¹,

Gobin²,

Dryden³

et al. 2013

IJN

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Gold nanoparticles and near infrared-absorbing light are each innocuous to tissue but when combined can destroy malignant tissue while leaving healthy tissue unharmed. This study investigated the feasibility of photothermal ablation therapy for esophageal adenocarcinoma using chitosan-coated gold/gold sulfide (CS-GGS) nanoparticles. A rat esophagoduodenal anastomosis model was used for the in vivo ablation study, and three human esophageal cell lines were used to study the response of cancer cells and benign cells to near infrared light after treatment with CS-GGS. The results indicate that both cancerous tissue and cancer cells took up more gold nanoparticles and were completely ablated after exposure to near infrared light. The benign tissue and noncancerous cells showed less uptake of these nanoparticles, and remained viable after exposure to near infrared light. CS-GGS nanoparticles could provide an optimal endoluminal therapeutic option for near infrared light ablation of esophageal cancer.

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Loss of manganese superoxide dismutase expression and activity in rat esophagus with external esophageal perfusion

Cited by 16 publications

References 30 publications

Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Chemoprevention of Carcinogenic Progression to Esophageal Adenocarcinoma by the Manganese Superoxide Dismutase Supplementation

Characterization of squamous esophageal cells resistant to bile acids at acidic pH: implication for Barrett's esophagus pathogenesis

Infrared light-absorbing gold/gold sulfide nanoparticles induce cell death in esophageal adenocarcinoma

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