DNA damage in peripheral blood lymphocytes of patients with cirrhosis related to alcohol abuse or to hepatitis B and C viruses

Grossi, Sarah; Sumberaz, Alessandro; Gosmar, Marzia; Mattioli, Francesca; Testino, Gianni; Martelli, Antonietta

doi:10.1097/meg.0b013e3282f163fe

Cited by 24 publications

(18 citation statements)

References 22 publications

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“…The occurrence of DNA fragmentation in peripheral blood lymphocytes reflects a direct genotoxic effect of alcohol, HBV, and/or HCV, and suggests that the same genotoxic effect may operate in the liver and contribute to hepatocarcinogenesis [75] .…”

Section: Induced Oxidative Stressmentioning

confidence: 99%

Oxidative stress and antioxidants in hepatic pathogenesis

Shin²,

Feitelson³

et al. 2010

WJG

203

137

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Long term hepatitis B virus (HBV) infection is a major risk factor in pathogenesis of chronic liver diseases, including hepatocellular carcinoma (HCC). The HBV encoded proteins, hepatitis B virus X protein and preS, appear to contribute importantly to the pathogenesis of HCC. Both are associated with oxidative stress, which can damage cellular molecules like lipids, proteins, and DNA during chronic infection. Chronic alcohol use is another important factor that contributes to oxidative stress in the liver. Previous studies reported that treatment with antioxidants, such as curcumin, silymarin, green tea, and vitamins C and E, can protect DNA from damage and regulate liver pathogenesis-related cascades by reducing reactive oxygen species. This review summarizes some of the relationships between oxidative stress and liver pathogenesis, focusing upon HBV and alcohol, and suggests antioxidant therapeutic approaches.

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Section: Induced Oxidative Stressmentioning

confidence: 99%

Oxidative stress and antioxidants in hepatic pathogenesis

Shin²,

Feitelson³

et al. 2010

WJG

203

137

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show abstract

“…It has been known for more than four decades that members of different virus families can induce chromosome damage in infected cells in vitro [15] , and chromosome breakages have been observed in leukocytes isolated from patients experiencing systemic viral active infections [16,17] . In recent years evidence has accumulated indicating the ability of different viruses to induce aberrant mitosis, genetic instability and interfere with cellular DNA repair pathways, which has confirmed early reports [18][19][20][21] .…”

Section: Instability?mentioning

confidence: 99%

How virus persistence can initiate the tumorigenesis process

Avanzi

Alvisi²,

Ripalti³

2013

WJV

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Human oncogenic viruses are defined as necessary but not sufficient to initiate cancer. Experimental evidence suggests that the oncogenic potential of a virus is effective in cells that have already accumulated a number of genetic mutations leading to cell cycle deregulation. Current models for viral driven oncogenesis cannot explain why tumor development in carriers of tumorigenic viruses is a very rare event, occurring decades after virus infection. Considering that viruses are mutagenic agents per se and human oncogenic viruses additionally establish latent and persistent infections, we attempt here to provide a general mechanism of tumor initiation both for RNA and DNA viruses, suggesting viruses could be both necessary and sufficient in triggering human tumorigenesis initiation. Upon reviewing emerging evidence on the ability of viruses to induce DNA damage while subverting the DNA damage response and inducing epigenetic disturbance in the infected cell, we hypothesize a general, albeit inefficient hit and rest mechanism by which viruses may produce a limited reservoir of cells harboring permanent damage that would be initiated when the virus first hits the cell, before latency is established. Cells surviving virus generated damage would consequently become more sensitive to further damage mediated by the otherwise insufficient transforming activity of virus products expressed in latency, or upon episodic reactivations (viral persistence). Cells with a combination of genetic and epigenetic damage leading to a cancerous phenotype would emerge very rarely, as the probability of such an occurrence would be dependent on severity and frequency of consecutive hit and rest cycles due to viral reinfections and reactivations

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“…It shows both its early (initiation) and late effects (promotion/progression). We have recently evaluated the possible mechanism of initiation in patients affected by chronic alcoholic liver disease (ALD) [12].…”

mentioning

confidence: 99%