Oxidative damage and genotoxicity biomarkers in transfused and untransfused thalassemic subjects

Ferro, Elisa; Visalli, Giuseppa; Civa, Rosa; Rosa, Maria Angela La; Papa, Gaetano Randazzo; Baluce, Barbara; D’Ascola, Domenico Giuseppe; Piraino, Beth; Salpietro, Carmelo; Pietro, Angela Di

doi:10.1016/j.freeradbiomed.2012.08.592

Cited by 43 publications

(41 citation statements)

References 46 publications

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“…These results are in agreement with those of Ferro et al [21], who found a positive association between 8-OHdG and ferritin in thalassemic patients.…”

Section: Discussionsupporting

confidence: 94%

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Oxidative DNA damage in β-thalassemic children

El-Gindi

Hassanin

Mostafa³

et al. 2015

Medical Research Journal

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Objective The aim of the present study was to assess DNA oxidative damage by detection of 8-hydroxydeoxyguanosine (8-OHdG), lipid peroxidation, and antioxidant status in thalassemic patients.Materials and methods Blood samples were collected from 94 participants (64 b-thalassemic patients and 30 healthy controls) in the range of ages 4-15 years.Results It was clear that markers of free oxygen radical injury in blood (i.e. 8-OHdG) were significantly elevated in b-thalassemia major (P < 0.001) and b-thalassemia intermediate (P < 0.001) compared with normal controls, and lipid peroxide was also significantly higher in both types of thalassemia compared with controls (P < 0.001). In contrast, mean catalase levels and glutathione-Stransferase were decreased (P < 0.001). There were highly significant changes in the values of 8-OHdG between the thalassemia major and thalassemia intermedia groups (P = 0.000), and it was significantly correlated with serum ferritin in thalassemic children (r = 0.5, P = 0.006).Conclusion b-Thalassemic children are at higher risk for tissue injury and DNA oxidative damage due to a state of enhanced oxidative stress.

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“…These results are in agreement with those of Ferro et al [21], who found a positive association between 8-OHdG and ferritin in thalassemic patients.…”

Section: Discussionsupporting

confidence: 94%

“…Combined antioxidant therapy with iron chelator in b-thalassemia major patients may improve the antioxidant status by neutralizing the free-radical formation. It also facilitates to trim down the hemolytic rate and recover the hepatic status by decreasing both the liver iron concentration and the degree of liver fibrosis [21].…”

Section: Discussionmentioning

confidence: 99%

Oxidative DNA damage in β-thalassemic children

El-Gindi

Hassanin

Mostafa³

et al. 2015

Medical Research Journal

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“…Mitochondrial damage was found to be induced by non-transferrin-bound Fe, resulting in decreased ΔΨ [100]. The observation of lower-than-normal levels of l-carnitine also might be related to MDF [101].…”

Section: Genetic Diseasesmentioning

confidence: 99%

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Pagano

Talamanca

Castello

et al. 2014

Oxidative Medicine and Cellular Longevity

117

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Beyond the disorders recognized as mitochondrial diseases, abnormalities in function and/or ultrastructure of mitochondria have been reported in several unrelated pathologies. These encompass ageing, malformations, and a number of genetic or acquired diseases, as diabetes and cardiologic, haematologic, organ-specific (e.g., eye or liver), neurologic and psychiatric, autoimmune, and dermatologic disorders. The mechanistic grounds for mitochondrial dysfunction (MDF) along with the occurrence of oxidative stress (OS) have been investigated within the pathogenesis of individual disorders or in groups of interrelated disorders. We attempt to review broad-ranging pathologies that involve mitochondrial-specific deficiencies or rely on cytosol-derived prooxidant states or on autoimmune-induced mitochondrial damage. The established knowledge in these subjects warrants studies aimed at elucidating several open questions that are highlighted in the present review. The relevance of OS and MDF in different pathologies may establish the grounds for chemoprevention trials aimed at compensating OS/MDF by means of antioxidants and mitochondrial nutrients.

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“…The first step is caused by insulin resistance, promoting steatosis, and an increased lipid peroxidation (3). Additional hits are oxidative stress (from antioxidants and glutathione depletion, mitochondrial dysfunction, hormonal imbalance, hypoxia (11)), lipotoxicity, inflammatory mediators as adipocytokines, and gut microbiota-derived lipopolysaccharide (LPS) leading to hepatocyte injury, inflammation, apoptosis and fibrosis. Therefore, it has been evalueted the possibility of multiple parallel hits (12).…”

Section: Resultsmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease/Non-Alcoholic Steatohepatitis in Childhood: Endocrine-Metabolic “Mal-Programming”

et al. 2014

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Context:Nonalcoholic Fatty Liver Disease (NAFLD) is the major chronic liver disease in the pediatric population. NAFLD includes a broad spectrum of abnormalities (inflammation, fibrosis and cirrhosis), ranging from accumulation of fat (also known as steatosis) towards non-alcoholic steatohepatitis (NASH). The development of NAFLD in children is significantly increased.Evidence Acquisition:A literature search of electronic databases was undertaken for the major studies published from 1998 to today. The databases searched were: PubMed, EMBASE, Orphanet, Midline and Cochrane Library. We used the key words: "non-alcoholic fatty liver disease, children, non-alcoholic steatohepatitis and fatty liver".Results:NAFLD/NASH is probably promoted by “multiple parallel hits”: environmental and genetic factors, systemic immunological disorders (oxidative stress, persistent-low grade of inflammation) as well as obesity and metabolic alterations (insulin resistance and metabolic syndrome). However its exact cause still underdiagnosed and unknown.Conclusions:Pediatric NAFLD/NASH is emerging problem. Longitudinal follow-up studies, unfortunately still insufficient, are needed to better understand the natural history and outcome of NAFLD in children. This review focuses on the current knowledge regarding the epidemiology, pathogenesis, environmental, genetic and metabolic factors of disease. The review also highlights the importance of studying the underlying mechanisms of pediatric NAFLD and the need for complete and personalized approach in the management of NAFLD/NASH.

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Oxidative damage and genotoxicity biomarkers in transfused and untransfused thalassemic subjects

Cited by 43 publications

References 46 publications

Oxidative DNA damage in β-thalassemic children

Oxidative DNA damage in β-thalassemic children

Oxidative Stress and Mitochondrial Dysfunction across Broad-Ranging Pathologies: Toward Mitochondria-Targeted Clinical Strategies

Nonalcoholic Fatty Liver Disease/Non-Alcoholic Steatohepatitis in Childhood: Endocrine-Metabolic “Mal-Programming”

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