Cytotoxicity and metabolic stress induced by acetaldehyde in human intestinal LS174T goblet-like cells

2014 ◽  
Vol 307 (3) ◽  
pp. G286-G294 ◽  
Author(s):  
Elhaseen Elamin ◽  
Ad Masclee ◽  
Freddy Troost ◽  
Jan Dekker ◽  
Daisy Jonkers
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
Membrane Integrity ◽  
Reactive Oxygen Species Generation ◽  
Intestinal Barrier ◽  
Atp Depletion ◽  
Intestinal Barrier Function ◽  
Double Labeling ◽  
Ldh Release ◽  
Negative Controls

There is compelling evidence indicating that ethanol and its oxidative metabolite acetaldehyde can disrupt intestinal barrier function. Apart from the tight junctions, mucins secreted by goblet cells provide an effective barrier. Ethanol has been shown to induce goblet cell injury associated with alterations in mucin glycosylation. However, effects of its most injurious metabolite acetaldehyde remain largely unknown. This study aimed to assess short-term effects of acetaldehyde (0, 25, 50, 75, 100 μM) on functional characteristics of intestinal goblet-like cells (LS174T). Oxidative stress, mitochondrial function, ATP, and intramitochondrial calcium (Ca2+) were assessed by dichlorofluorescein, methyltetrazolium, and bioluminescence, MitoTracker green and rhod-2 double-labeling. Membrane integrity and apoptosis were evaluated by measuring lactate dehydrogenase (LDH), caspase 3/7, and cleavage of cytokeratin 18 (CK18). Expression of mucin 2 (MUC2) was determined by cell-based ELISA. Acetaldehyde significantly increased reactive oxygen species generation and decreased mitochondrial function compared with negative controls ( P < 0.05). In addition, acetaldehyde dose-dependently decreased ATP levels and induced intramitochondrial Ca2+ accumulation compared with negative controls ( P < 0.05). Furthermore, acetaldehyde induced LDH release and increased caspase3/7 activity and percentage of cells expressing cleaved CK18 and increased MUC2 protein expression compared with negative controls ( P < 0.0001). ATP depletion and LDH release could be largely prevented by the antioxidant N-acetylcysteine, suggesting a pivotal role for oxidative stress. Our data demonstrate that acetaldehyde has distinct oxidant-dependent metabolic and cytotoxic effects on LS174T cells that can lead to induction of cellular apoptosis. These effects may contribute to acetaldehyde-induced intestinal barrier dysfunction and subsequently to liver injury.

scholarly journals L-Tryptophan Enhances Intestinal Integrity in Diquat-Challenged Piglets Associated with Improvement of Redox Status and Mitochondrial Function

Animals ◽  
2019 ◽  
Vol 9 (5) ◽  
pp. 266 ◽  
Author(s):  
Jingbo Liu ◽  
Yong Zhang ◽  
Yan Li ◽  
Honglin Yan ◽  
Hongfu Zhang
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Growth Performance ◽  
Mitochondrial Function ◽  
Intestinal Barrier ◽  
Dietary Supplementation ◽  
Fluorescein Isothiocyanate ◽  
Redox Status ◽  
Intestinal Barrier Function ◽  
Intestinal Integrity

Tryptophan (Trp) supplementation has been shown to improve growth performance and enhance intestinal integrity in piglets. However, the effects of dietary Trp supplementation on the intestinal barrier function in piglets exposed to oxidative stress remain unknown. This study was conducted to evaluate whether dietary Trp supplementation can attenuate intestinal injury, oxidative stress, and mitochondrial dysfunction of piglets caused by diquat injection. Thirty-two piglets at 25 days of age were randomly allocated to four groups: (1) the non-challenged control; (2) diquat-challenged control; (3) 0.15% Trp-supplemented diet + diquat; (4) 0.30% Trp supplemented diet + diquat. On day seven, the piglets were injected intraperitoneally with sterilized saline or diquat (10 mg/kg body weight). The experiment lasted 21 days. Dietary supplementation with 0.15% Trp improved growth performance of diquat-challenged piglets from day 7 to 21. Diquat induced an increased intestinal permeability, impaired antioxidant capacity, and mitochondrial dysfunction. Although dietary supplementation with 0.15% Trp ameliorated these negative effects induced by diquat challenge that showed decreasing permeability of 4 kDa fluorescein isothiocyanate dextran, increasing antioxidant indexes, and enhancing mitochondrial biogenesis. Results indicated that dietary supplementation with 0.15% Trp enhanced intestinal integrity, restored the redox status, and improved the mitochondrial function of piglets challenged with diquat.

Resveratrol improves intestinal barrier function, alleviates mitochondrial dysfunction and induces mitophagy in diquat challenged piglets1

2019 ◽  
Vol 10 (1) ◽  
pp. 344-354 ◽  
Author(s):  
Shuting Cao ◽  
Zhuojun Shen ◽  
Chunchun Wang ◽  
Qianhui Zhang ◽  
Qihua Hong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Injury ◽  
Intestinal Barrier Function

This study evaluated whether resveratrol can alleviate intestinal injury and enhance the mitochondrial function and the mitophagy level in diquat induced oxidative stress of piglets.

scholarly journals LPS from P. gingivalis Negatively Alters Gingival Cell Mitochondrial Bioenergetics

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Kiran Napa ◽  
Andrea C. Baeder ◽  
Jeffrey E. Witt ◽  
Sarah T. Rayburn ◽  
Madison G. Miller ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Human Gingival Fibroblast ◽  
Gingival Fibroblast ◽  
Oxygen Species ◽  
Atp Production ◽  
Lps Treatment

Objective. Oral inflammatory pathologies are linked to increased oxidative stress, thereby partly explaining their relevance in the etiology of systemic disorders. The purpose of this work was to determine the degree to which LPS from Porphyromonas gingivalis, the primary pathogen related to oral inflammation, altered gingival mitochondrial function and reactive oxygen species generation. Methods. Human gingival fibroblast (HGF-1) cells were treated with lipopolysaccharide of P. gingivalis. Mitochondrial function was determined via high-resolution respirometry. Results. LPS-treated HGF-1 cells had significantly higher mitochondrial complex IV and higher rates of mitochondrial respiration. However, this failed to translate into greater ATP production, as ATP production was paradoxically diminished with LPS treatment. Nevertheless, production of the reactive H2O2 was elevated with LPS treatment. Conclusions. LPS elicits an increase in gingival cell mitochondria content, with a subsequent increase in reactive oxygen species production (i.e., H2O2), despite a paradoxical reduction in ATP generation. These findings provide an insight into the nature of oxidative stress in oral inflammatory pathologies.

scholarly journals Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 82 ◽  
Author(s):  
Enrique Gabandé-Rodríguez ◽  
Manuel M. Gómez de las Heras ◽  
María Mittelbrunn
Keyword(s):  
Calorie Restriction ◽  
Mitochondrial Function ◽  
Intestinal Barrier ◽  
Mitochondrial Metabolism ◽  
Intestinal Barrier Function ◽  
Autophagic Flux ◽  
Inflammatory Cascade ◽  
Beneficial Effects ◽  
Cellular Processes ◽  
Inflammatory Processes

Mitochondrial metabolism and autophagy are two of the most metabolically active cellular processes, playing a crucial role in regulating organism longevity. In fact, both mitochondrial dysfunction or autophagy decline compromise cellular homeostasis and induce inflammation. Calorie restriction (CR) is the oldest strategy known to promote healthspan, and a plethora of CR mimetics have been used to emulate its beneficial effects. Herein, we discuss how CR and CR mimetics, by modulating mitochondrial metabolism or autophagic flux, prevent inflammatory processes, protect the intestinal barrier function, and dampen both inflammaging and neuroinflammation. We outline the effects of some compounds classically known as modulators of autophagy and mitochondrial function, such as NAD+ precursors, metformin, spermidine, rapamycin, and resveratrol, on the control of the inflammatory cascade and how these anti-inflammatory properties could be involved in their ability to increase resilience to age-associated diseases.

Exposure to oxidized soybean oil induces mammary mitochondrial injury in lactating rats and alters the intestinal barrier function of progeny

2021 ◽  
Vol 12 (8) ◽  
pp. 3705-3719
Author(s):  
Chuanqi Wang ◽  
Feng Gao ◽  
Xin Guan ◽  
Xinxin Yao ◽  
Baoming Shi ◽  
...  
Keyword(s):  
Soybean Oil ◽  
Mitochondrial Function ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Mitochondrial Injury

The ingestion of OSO promoted the expression of mitochondrial function-related genes, such as Sirt3 and PRDX3, and these genes contributed to the elimination of oxidative production in mitochondria.

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