Mitochondrial DNA damage associated with lipid peroxidation of the mitochondrial membrane induced by Fe2+-citrate

Almeida, Aparecida Marques de; Bertoncini, Clélia Rejane Antônio; Borecký, Jiřı́; Souza-Pinto, Nadja C.; Vercesi, Anı́bal E.

doi:10.1590/s0001-37652006000300010

Cited by 45 publications

(30 citation statements)

References 43 publications

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“…(32) Iron imbalance/accumulation has been implicated in oxidative injury associated with many diseases, including β-thalassemia, via multiple mechanisms. (33) …”

Section: Resultsmentioning

confidence: 99%

Lack of correlation between non-labile iron parameters, total carbonyl and malondialdehyde in major thalassemia

Al‐Hakeim

Auda

Ali

2014

J. Clin. Biochem. Nutr.

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Thalassemia patients are at high risk of iron-induced toxicity and oxidative stress consequences. The present cross-sectional study is conducted to determine whether or not lipid peroxidation or protein oxidation is correlated with iron parameters in patients with thalassemia major. To prove this hypothesis, malondialdehyde and total carbonyl were correlated with the degree of excess iron concentration in the patients. A total of 118 Arabic Iraqi patients and 30 healthy children were participated in the present study. Results showed a significant increase (p<0.05) in serum total carbonyls, malondialdehyde and the iron indices of patients as compared with the control group. Total iron binding capacity and transferrin concentrations decreased significantly (p<0.05) in patients with thalassemia compared with the control group. The results also showed a lack of a significant correlation between each serum malondialdehyde and total carbonyl with each component of iron status. In conclusion, total carbonyls and malondialdehyde were increased in thalassemia patients indicating the vulnerability of these patients to tissue injury caused by oxidative stress. The formation of total carbonyl and malondialdehyde are independent of excess non-labile iron concentration, indicating that different mechanisms are involved in injury caused by the labile iron and in the formation of oxidation end products.

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“…(32) Iron imbalance/accumulation has been implicated in oxidative injury associated with many diseases, including β-thalassemia, via multiple mechanisms. (33) …”

Section: Resultsmentioning

confidence: 99%

Lack of correlation between non-labile iron parameters, total carbonyl and malondialdehyde in major thalassemia

Al‐Hakeim

Auda

Ali

2014

J. Clin. Biochem. Nutr.

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“…Lipid peroxidation is known to cross-link and polymerise membrane components resulting in modification of membrane lipids and altered membrane activity such as release of mitochondrial calcium. The released Ca2+ can potentiate ROS formation, which in turn leads to production of oxidised lipids and cross-linked proteins, culminating in membrane permeability [60][61][62][63]. As cadmium is seen to induce a 12.5-fold increase of Ca2+ after 2 h of intoxication in osteosarcoma cells, cadmium intoxication may be involved in mitochondrial membrane transition via lipid peroxidation and calcium release [64].…”

Section: Pm-induced Changes In Mitochondrial Membrane Potentialmentioning

confidence: 99%

Mitochondrial Function in Allergic Disease

Iyer

Mishra

Agrawal

2017

Curr Allergy Asthma Rep

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Recent research has shown allergy, asthma and metabolic syndrome to be linked to mitochondrial dysfunction. Environmental pollutants and allergens are observed to cause mitochondrial dysfunction, primarily by inducing oxidative stress and ROS production. Malfunctioning mitochondria change the bioenergetics of the cell and its metabolic profile to favour systemic inflammation, which drives all three types of morbidities. Given the existing experimental evidence, approaches targeting mitochondria (e.g. antioxidant therapy and mitochondrial replacement) are being conducted in relevant disease models-with some progressing towards clinical trials, making mitochondrial function the focus of translational therapy research in asthma, allergy and linked metabolic syndrome.

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“…For example, lung tissues from smokers are generally acknowledged to have a mitochondrial genome content with an increased density of mutations, at a higher copy number [74], than is observed in tissues of non-smokers [72, 73, 75–77]. The environmental toxins can preferentially generate oxidative damage and/or form adducts in the mitochondrial genome over the nuclear genome [50, 78–82]. …”

Section: Somatic Mitochondrial Mutationsmentioning

confidence: 99%

The awakening of an advanced malignant cancer: An insult to the mitochondrial genome

Cook

Higuchi

2012

Biochimica et Biophysica Acta (BBA) - General Subjects

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Background In only months-to-years a primary cancer can progress to an advanced phenotype that is metastatic and resistant to clinical treatments. As early as the 1900s, it was discovered that the progression of a cancer to the advanced phenotype is often associated with a shift in the metabolic profile of the disease from a state of respiration to anaerobic fermentation – a phenomenon denoted as the Warburg Effect. Scope of Review Reports in the literature strongly suggest that the Warburg Effect is generated as a response to a loss in the integrity of the sequence and/or copy number of the mitochondrial genome content within a cancer. Multiple studies regarding the progression of cancer indicate that mutation, and/or, a flux in the copy number, of the mitochondrial genome content can support the early development of a cancer, until; the mutational load and/or the reduction-to-depletion of the copy number of the mitochondrial genome content induces the progression of the disease to an advanced phenotype. General Significance Collectively, evidence has revealed that the human cell has incorporated the mitochondrial genome content into a cellular mechanism that, when pathologically actuated, can de (un)differentiate a cancer from the parental tissue of origin into an autonomous disease that disrupts the hierarchical structure-and-function of the human body.

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Mitochondrial DNA damage associated with lipid peroxidation of the mitochondrial membrane induced by Fe2+-citrate

Cited by 45 publications

References 43 publications

Lack of correlation between non-labile iron parameters, total carbonyl and malondialdehyde in major thalassemia

Lack of correlation between non-labile iron parameters, total carbonyl and malondialdehyde in major thalassemia

Mitochondrial Function in Allergic Disease

The awakening of an advanced malignant cancer: An insult to the mitochondrial genome

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