The Genotoxic and Pro-Apoptotic Activities of Advanced Glycation End-Products (MAGE) Measured with Micronuclei Assay Are Inhibited by Their Low Molecular Mass Counterparts.

An association between the cancer invasive activities of cells and their exposure to advanced glycation end-products (AGEs) was described early in some reports. An incubation of cells with BSA-AGE (bovine serum albumin-AGE), BSA-carboxymethyllysine and BSA-methylglyoxal (BSA-MG) resulted in a significant increase in DNA damage. We examined the genotoxic activity of new products synthesized under nonaqueous conditions.

Can high dose rates used in cancer radiotherapy change therapeutic effectiveness?

Current cancer radiotherapy relies on increasingly high dose rates of ionising radiation (100-2400 cGy/min). It is possible that changing dose rates is not paralleled by treatment effectiveness. Irradiating cancer cells is assumed to induce molecular alterations that ultimately lead to apoptotic death.

Antioxidant activity and protective effects against oxidative damage of human cells induced by X-radiation of phenolic glycosides isolated from pepper fruits Capsicum annuum L.

The antioxidant and radioprotective effects of the phenolic glycosides from Capsicum annuum L. were examined. There were: sinapoyl-E-glucoside, quercetin-3-O-rhamnoside-7-O-glucoside, quercetin-3-O-rhamnoside and luteolin-7-O-(2-apiosyl)-glucoside.

VDR gene single nucleotide polymorphisms and their association with risk of oral cavity carcinoma.

Vitamin D3 (1,25(OH)2D3 (1,25-dihydroxyvitamin D3)) is a hormone playing a crucial role in numerous biological processes in the human body, including induction and control of cell proliferation and differentiation. Numerous data relate the vitamin D3 level with various types of cancer. It has been suggested that SNPs in the vitamin D3 receptor (VDR) gene might influence both the risk of cancer occurrence and cancer progression.

Bystander effects induced by direct and scattered radiation generated during penetration of medium inside a water phantom.

Background: The biological effects of ionizing radiation have long been thought to results from direct targeting of the nucleus leading to DNA damage. Over the years, a number of non-targeted or epigenetic effects of radiation exposure have been reported where genetic damage occurs in cells that are not directly irradiated but respond to signals transmitted from irradiated cells, a phenomenon termed the "bystander effects".

Aim: We compared the direct and bystander responses of human A 549, BEAS-2-B and NHDF cell lines exposed to both photon (6 MV) and electron (22 MeV) radiation inside a water phantom.

Bystander effects induced by medium from irradiated cells: similar transcriptome responses in irradiated and bystander K562 cells.

Purpose: Cells exposed to ionizing radiation release factors that induce deoxyribonucleic acid damage, chromosomal instability, apoptosis, and changes in the proliferation rate of neighboring unexposed cells, phenomena known as bystander effects. This work analyzes and compares changes in global transcript levels induced by direct irradiation and by bystander effects in K562 (human erythroleukemia) cells.

Methods And Materials: Cells were X-irradiated with 4 Gy or transferred into culture medium collected from cells 1 h after irradiation (irradiation-conditioned medium).

Modulation of cellular defense processes in human lymphocytes in vitro by a 1,4-dihydropyridine derivative.

The aim of this pilot study was to assess whether a compound of the beta-carbonyl-1,4-dihydropyridine series (AV-153 or sodium 3,5-bis-ethoxycarbonyl-2,6-dimethyl-1,4-dihydropyridine-4-carboxylate), which has high efficiency in stimulating DNA repair, can simultaneously modulate apoptosis in human cells. Peripheral blood lymphocytes of healthy donors were used in this study. DNA strand-break rejoining was assessed with the alkaline comet assay after a 3-h incubation of lymphocytes in the presence of a wide range of concentrations of AV-153 (10(-10)-10(-5) M).

The cytotoxic and genotoxic effects of conjugated trans-2-nonenal (T2N), an off-flavor compound in beer and heat processed food arising from lipid oxidation.

This study investigates the toxic effect of E(2)nonenal (trans-2-nonenal, T2N) and its conjugate with horse muscle myoglobin (Mb) tested on murine cell line L929 and human cell line A549, as well as the genotoxic effect of these compounds assayed by measuring of micronuclei in human cells K562. It is an aldehyde, which is occurring as the substance responsible for an off flavour in aged beers, but originates also from lipid oxidation in heat processed food. T2N is an aldehyde formed from linoleic acid as a secondary oxidation product.

The bystander effect-induced formation of micronucleated cells is inhibited by antioxidants, but the parallel induction of apoptosis and loss of viability are not affected.

X-rays induce various DNA damages including strand breaks that lead to formation of micronuclei and chromosomal aberrations as well as increased number of apoptotic cells. Similar effects appear when non-irradiated cells are treated with medium collected from cultures of irradiated cells (irradiation conditioned medium - ICM). This phenomenon was termed "bystander effect".

[Role of vitamin C in oxidative DNA damage].

Vitamin C (ascorbic acid) has considerable antioxidant activity: it scavenges reactive oxygen species and may, thereby, prevent oxidative damage to important biological macromolecules, such as DNA, proteins, and lipids. Data concerning the influence of vitamin C on oxidative DNA damage are conflicting and some of the discrepancies can be explained by the different experimental methodologies employed. Data using biomarkers of oxidative damage of DNA bases in human lymphocytes in vitro have provided no compelling evidence to conclude that vitamin C supplementation can decrease the level of oxidative DNA damage.

Thiamine prevents X-ray induction of genetic changes in human lymphocytes in vitro.

The effects of thiamine (vitamin B1) on the level of spontaneous or radiation-induced genetic changes in human lymphocytes in vitro were studied. Cultured lymphocytes were exposed to increasing concentrations of thiamine (0-500 microg/ml) and irradiated with X-rays. The DNA damage was estimated as the frequency of micronuclei and apoptotic or necrotic morphological changes in fixed cells.

Inhibitory effect of ascorbic acid post-treatment on radiation-induced chromosomal damage in human lymphocytes in vitro.

In the present study, the effect of exposure to ascorbic acid (vitamin C) after gamma-ray-induced chromosomal damage in cultured human lymphocytes was examined to explore the mechanism by which this antioxidant vitamin protects irradiated cells Non-irradiated lymphocytes were exposed to increasing concentrations of ascorbic acid (1-100 micro g/ml) and DNA damage was estimated using chromosomal aberration analysis and the comet assay. The results showed that ascorbic acid did not influence the frequency of chromosomal aberrations in non-irradiated cells, except at the highest concentration (20 micro g/ml), which induced breakage-type chromosomal aberrations. Vitamin C at the concentration of 50 micro g/ml caused DNA damage detected by the comet assay.