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DIVERTICULAR DISEASE AND OXIDATIVE STRESS: THE LINK WITH MITOCHONDRIA ALTERATIONS IN THE DIFFERENT CLINICAL PHENOTYPES

Martina Cappelletti 1, Rosa Vona 2, Lidia Castagneto Gissey 3, Mariarita Tarallo 3, Annalinda Pisano 4, Paola Matarrese 2, Ivan Tattoli 5, Lucia Pallotta 6, Carla Giordano 4, Carola Severi 7

Affiliations

1 University "sapienza Universita' Di Roma", Perugia, Italy

2 Center for Gender-Specific Medicine, Italian National Institute of Health, Roma, Italy

3 Department of Surgical Science, Sapienza University of Rome, Roma, Italy

4 Department of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome, Roma, Italy

5 University Hospital Careggi, Florence, Italy

6 University Sapienza of Rome, Roma, Italy

7 University Sapienza Of Rome, Roma, Italy

Summary

AI Generated

A laboratory study of surgical specimens from diverticular disease patients demonstrates mitochondrial dysfunction and oxidative stress in longitudinal smooth muscle, with severity correlating to disease stage and partial reversal by polyphenol treatment in vitro.

Oxidized protein content was elevated in both uncomplicated diverticula (5.0-fold) and complicated stenotic diverticular disease (2.6-fold) compared to controls, with progressive loss of antioxidant thioredoxin (70.9% and 83.3% decrease respectively).
Mitochondrial complex II succinate dehydrogenase decreased by 43.4% in uncomplicated and 67.9% in complicated disease, while compensatory increases in complex IV cytochrome c oxidase and mitochondrial mass occurred, most prominently in complicated disease.
Cellular glutathione content progressively decreased (51.9% in uncomplicated, 72.2% in complicated disease), associated with impaired smooth muscle contraction (approximately 51-52% reduction) and relaxation (approximately 35-38% reduction) in both phenotypes.
Twenty-four hour incubation with 14mM polyphenols restored glutathione content and relaxation function in cells from both disease phenotypes.
This material would interest researchers investigating diverticular disease pathophysiology and potential antioxidant therapeutic strategies.

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This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

Abstract

Introduction

A transmural oxidative imbalance, mainly affecting longitudinal muscle, has been reported in the different clinical phenotypes of Diverticular Disease (DD) (Pallotta L,2022; Cappelletti M,2022) but the genesis of the oxidative stress remains to be defined. Since the central role of the mitochondria for the cell metabolism and radicals production, aim of the study is to elucidate the involvement of mitochondria alterations in the different DD clinical phenotypes in order to improve the knowledge of the DD natural history and management.

Aims & Methods

Longitudinal smooth muscle tissues and cells were isolated separately from surgical specimens of complicated stenotic DD (cDD n=5), up-stream non-occlusive colon cancer with diverticula (DIV n=5) and without diverticula (controls n=5). Oxidized proteins, thioredoxin and, succinate deidrogenase (complex II) and complex IV (cytochrome c oxidase) of mitochondrial respiratory chain were evaluated on tissues by Western Blot. Mitochondrial mass, mitochondrial ROS, mitochondrial membrane potential and glutathione (GSH) were evaluated in cells by FACS. Functional cells activity was tested by image micrometry assessing maximal contraction to acetylcholine and relaxation to VIP, before and after 24h-incubation with 14mM polyphenols (Phenolea Active Complex L). Data (mean±SE) were expressed as fold variations or % decrease from controls, *p value<0.05 considered significant.

Results

In respect to control, oxidized proteins content in longitudinal muscle was increased both in DIV (5.0*±1.1) and cDD (2.6±0.6), associated to a progressive loss of the antioxidant thioredoxin molecule (DIV:70.9%±9.2;cDD:83.3%±3.4). The oxidative status resulted associated to a loss of the mitochondrial complex II succinate deidrogenase codified by nuclear DNA (DIV:43.4%±19.7;cDD:67.9%±10.3) suggestive of the electron respiratory chain impairement. Compensatory stress mechanisms likely occurred with an increase of the complex IV cytochrome c oxidase codified by mitochondrial DNA in muscle tissue (DIV:1.1±0.77;cDD:2.3±1.7) and mitochondrial mass increase (DIV:2.4±1.2;cDD:3.7*±1.3) in cells. Radicals over production was observed mainly in cDD with a cellular increase in mitochondrial ROS (cDD:1.50±0.57) and mitochondrial membrane potential (cDD:1.4±0.3). Antioxidant GSH cellular content progressively decreased from DIV (51.9%*±9.5) to cDD (72.2%*±1.5). These oxidative alterations were associated to an impairment of functional cellular activity with a reduction of contraction (DIV:51.3%*±4.5;cDD:52.5%*±8.5) and relaxation (DIV:34.9%*±14.3;cDD:37.6%*±10.6). The prominent role of oxidative stress in these functional alterations was confirmed by the ability of a 24/h polyphenols treatment to restore GSH content (DIV:1.1±0.06;cDD:1.4±0.3) and relaxation, in both DD phenotypes.

Conclusion

Oxidative stress-driven alterations are present in longitudinal muscle in DD, independently from the clinical stage. In accordance to the severity of the pathology, mitochondrial imbalance resulted more prevalent in complicated diverticular disease. The beneficial effects of the antioxidant treatment could open new tailored-therapeutic and prevention strategies still not tested in this disease.

Disclosure

No disclosure

Conference

UEG Week Copenhagen 2023

Topics

Colorectal

Submission format

Abstract

Session

All about disorders of gut-brain interaction (Posters)

Citation

United European Gastroenterology Journal 2023; 11 (Supplement 8)

Published

2023

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THE PEPPER TRIAL: WHAT TO EXPECT WHEN STOPPING CHRONIC PROTON PUMP INHIBITOR THERAPY IN PRIMARY CARE PATIENTS

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