Oxidative Stress and Mitochondrial Functions in the Intestinal Caco-2/15 Cell Line
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Post-publication record
- Nature
- Retraction
- Reason
- Concerns/Issues about Data;Concerns/Issues about Image;Duplication of/in Image;Investigation by Journal/Publisher;Objections by Third Party;Original Data and/or Images not Provided and/or not Available;
- Date
- 4/14/2022 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
BACKGROUND: Although mitochondrial dysfunction and oxidative stress are central mechanisms in various pathological conditions, they have not been extensively studied in the gastrointestinal tract, which is known to be constantly exposed to luminal oxidants from ingested foods. Key among these is the simultaneous consumption of iron salts and ascorbic acid, which can cause oxidative damage to biomolecules. METHODOLOGY/PRINCIPAL FINDINGS: The objective of the present work was to evaluate how iron-ascorbate (FE/ASC)-mediated lipid peroxidation affects mitochondrion functioning in Caco-2/15 cells. Our results show that treatment of Caco-2/15 cells with FE/ASC (0.2 mM/2 mM) (1) increased malondialdehyde levels assessed by HPLC; (2) reduced ATP production noted by luminescence assay; (3) provoked dysregulation of mitochondrial calcium homeostasis as evidenced by confocal fluorescence microscopy; (4) upregulated the protein expression of cytochrome C and apoptotic inducing factor, indicating exaggerated apoptosis; (5) affected mitochondrial respiratory chain complexes I, II, III and IV; (6) elicited mtDNA lesions as illustrated by the raised levels of 8-OHdG; (7) lowered DNA glycosylase, one of the first lines of defense against 8-OHdG mutagenicity; and (8) altered the gene expression and protein mass of mitochondrial transcription factors (mtTFA, mtTFB1, mtTFB2) without any effects on RNA Polymerase. The presence of the powerful antioxidant BHT (50 microM) prevented the occurrence of oxidative stress and most of the mitochondrial abnormalities. CONCLUSIONS/SIGNIFICANCE: Collectively, our findings indicate that acute exposure of Caco-2/15 cells to FE/ASC-catalyzed peroxidation produces harmful effects on mitochondrial functions and DNA integrity, which are abrogated by the powerful exogenous BHT antioxidant. Functional derangements of mitochondria may have implications in oxidative stress-related disorders such as inflammatory bowel diseases.
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The record
- Venue
- PLoS ONE
- Topic
- Vitamin C and Antioxidants Research
- Field
- Nursing
- Canadian institutions
- McGill UniversityCanadian Institutes of Health ResearchUniversité de SherbrookeUniversité de MontréalCentre Hospitalier Universitaire Sainte-Justine
- Funders
- Fonds de Recherche du Québec - SantéCanadian Institutes of Health Research
- Keywords
- Oxidative stressMitochondrionTFAMLipid peroxidationOxidative phosphorylationReactive oxygen speciesBiologyMitochondrial DNAAscorbic acidBiochemistryChemistryCell biologyMolecular biologyMitochondrial biogenesisGene
- Has abstract in OpenAlex
- yes