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Journal Article 2008; 29(5): 644-648 PubMed PMID: 18987600 Citation  Keywords:  Animals, Antioxidants, Apoptosis:drug effects, Cell Count, Cell Death, Cell Separation, Chitin:analogs & derivatives, Comet Assay, DNA:drug effects, DNA Damage:drug effects, Female, Glucans:pharmacology, Hepatocytes:drug effects, Hydrogen Peroxide:toxicit.   

OBJECTIVES: Utilizing primary rat hepatocytes we investigated the potential antimutagenic and anti-cytotoxic effects of carboxymethyl chitin-glucan (CM-CG) with respect to oxidative stress induced by the model free-radical-generating compounds hydrogen peroxide (H2O2) or 2,3-dimethoxy-1,4-naphthoquinone (DMNQ). Different kinds of CM-CG action were studied by two different treatment protocols: a. pre-incubation of freshly isolated hepatocytes with the potential anti-mutagen followed by exposure to the oxidant or b. simultaneous treatment of hepatocytes with the potential anti-mutagen and the oxidant.

METHODS: As a measure of genotoxicity, the percentages of DNA in tails of comets by single cell gel electrophoresis were evaluated. The cytotoxicological endpoints analysed were the cell density (number of cells/cm2), and the percentages of apoptotic and necrotic cells.

RESULTS: H2O2 and DMNQ, causing DNA single-strand breaks via the formation of *OH radicals, have been demostrated to induce both genotoxic and cytotoxic effects in primary rat hepatocytes resulting in increased percentages of DNA in tails of comets, and increased frequencies of apoptotic and necrotic cells accompanied by a decreased cell density. Further investigations were therefore focussed on possible modifications of these parameters by CM-CG. The results obtained clearly demonstrate that CM-CG (applied before and during treatment) protects primary rat hepatocytes against the genotoxic and cytotoxic effects of oxidative stress (H2O2 or DMNQ), whereas CM-CG itself has no effect on the endpoints of genotoxicity and cytotoxicity studied.

CONCLUSION: Our results indicate that carboxymethyl chitin-glucan represents a natural fungal polysaccharide that can inhibit the genotoxicity and cytotoxicity of experimentally induced oxidative stress in primary rat hepatocytes....

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Journal Article 2018; 39(4): 294-298 PubMed PMID: 30531698 Citation  Keywords:  Benzhydryl Compounds:toxicity, Comet Assay, DNA:drug effects, DNA Breaks, Double-Stranded:drug effects, DNA Damage:drug effects, Endocrine Disruptors:toxicity, Environmental Pollutants:toxicity, Estrogens, Non-Steroidal:toxicity, Free Radical Scavengers:t.   

OBJECTIVES: Bisphenol A (BPA) is an endocrine disruptor which has been shown to be a harmful compound for living organisms. It is the main component of the most commonly used plastic products such as plastic bottles, food cans and containers or dental fillings, and other medical aids. Recently, it has become a new environmental pollutant. The current knowledge about the BPA effects (including genotoxic one) on different cells is in many cases contradictory. Thus, the aim of the paper is to study the potential genotoxic effect of BPA. METHODS: An observation of the genotoxic activity of BPA on human lymphocytes was evaluated by using the alkaline comet assay and a modified comet assay with bacterial DNA repair enzyme Fpg. The potential DNA-protective effect of BPA was tested by using the DNA-topology assay. RESULTS: The results show that rising concentrations of BPA increase the risk of DNA double-strand breaks and modified purines in human lymphocytes. Interestingly, BPA shows an ability to protect plasmid DNA from the damage of iron ions in cell-free system. CONCLUSIONS: BPA itself does not induce genotoxic effect to DNA. However, BPA treatment of human lymphocytes leads to the induction of DNA damage. The proposed mechanism of BPA action in the human lymphocytes could be mediated by cell metabolism that induces an oxidative stress and ROS formation. ROS subsequently attack DNA and thus induce DNA damage. According to our results, BPA can be included in the group of substances with dual effects involving genotoxic and DNA-protective activity....

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