Methylation pattern of THBS1, GATA-4, and HIC1 in pediatric and adult patients infected with Helicobacter pylori.

Background: Helicobacter pylori infection is usually acquired in childhood and persists into adulthood if untreated. The bacterium induces a chronic inflammatory response, which is associated with epigenetic alterations in oncogenes, tumor-suppressor genes, cell-cycle regulators, and cell-adhesion molecules.

Aim: The aim of this study was to analyze the effect of H.

Influence of diet on oxidative DNA damage, uracil misincorporation and DNA repair capability.

The contribution of diet to cancer ranges from 10 to 80%. The low ingestion of antioxidants and enzymatic cofactors involved in DNA repair and methylation reactions and the high ingestion of chemical additives present in the modern diet, associated with genetic factors, could lead to genomic instability and the hypomethylation of proto-oncogenes, thus contributing to development of genetic-related diseases such as cancer. The present study evaluated the influence of diet on the level of oxidative DNA damage, misincorporated uracil and DNA repair capability in peripheral blood lymphocytes from two groups of individuals with antagonist diets as follows: (i) 49 healthy individuals with a diet rich in organic products, whole grains, fruit and vegetables and poor in processed foods (Group I) and (ii) 56 healthy individuals with diet rich in processed foods and poor in fruit and vegetables (Group II).

Genotoxicity of cigarette smoking in maternal and newborn lymphocytes.

Tobacco smoke contains a large number of substances known to induce DNA damage and to be hazardous to human health. Several reviews and meta-analyses have reported an association between maternal or paternal smoking habits and genetic-related diseases, such as cancer, in children. The aim of the present study was to evaluate the level of DNA damage in lymphocytes of active- and passive-smoking mothers and in their newborns, using the comet assay.

Effects of Helicobacter pylori infection on the expressions of Bax and Bcl-2 in patients with chronic gastritis and gastric cancer.

The aim of the present study is to evaluate the influence of Helicobacter pylori on Bax and Bcl-2 mRNA and protein levels in patients with chronic gastritis and gastric cancer. The study included 217 patients, of which 26 were uninfected; 127 had chronic gastritis and were H. pylori-positive, and 64 had gastric cancer.

Relationship among oxidative DNA damage, gastric mucosal density and the relevance of cagA, vacA and iceA genotypes of Helicobacter pylori.

The aim of this study was to evaluate the relationship among oxidative DNA damage, density of Helicobacter pylori and the relevance of cagA, vacA and iceA genotypes of H. pylori. Gastric epithelial cells were isolated from 24 uninfected patients, 42 H.

Tomato-oleoresin supplement prevents doxorubicin-induced cardiac myocyte oxidative DNA damage in rats.

Doxorubicin (DOX) is an efficient chemotherapeutic agent used against several types of tumors; however, its use is limited due to severe cardiotoxicity. Since it is accepted that reactive oxygen species are involved in DOX-induced cardiotoxicity, antioxidant agents have been used to attenuate its side effects. To determine tomato-oleoresin protection against cardiac oxidative DNA damage induced by DOX, we distributed Wistar male rats in control (C), lycopene (L), DOX (D) and DOX+lycopene (DL) groups.

Use of Comet assay to assess DNA damage in patients infected by Helicobacter pylori: comparisons between visual and image analyses.

Studies of DNA damage in gastric epithelial cells of Helicobacter pylori (H. pylori)-infected patients are conflicting, possibly due to different methods used for scoring DNA damage by Comet assay. Therefore, we compared the sensitivity of visual microscopic analysis (arbitrary units-scores and comets%) and image analysis system (tail moment), in the gastric epithelial cells from the antrum and corpus of 122 H.

Relationships between cagA, vacA, and iceA genotypes of Helicobacter pylori and DNA damage in the gastric mucosa.

Helicobacter pylori (H. pylori) is believed to predispose carriers to gastric cancer by inducing chronic inflammation. The inflammatory processes may result in the generation of reactive oxygen and nitrogen species that damage DNA.

DNA damage in patients infected by Helicobacter pylori.

Helicobacter pylori (H. pylori) is considered to predispose carriers to gastric cancer but its role on gastric carcinogenesis is still unknown. The aim of this study was to investigate DNA damage by the comet assay in gastric epithelial cells from antrum and corpus in H.