ABSTRACT
Las células cuentan con mecanismos complejos que vigilan la integridad del ADN, activando mecanismos de reparación cuando hay deficiencias o errores durante la replicación. Una consecuencia potencial de los daños son las alteraciones permanentes en la estructura del ADN que pueden generar mutaciones, transformación carcinogénica y muerte celular. Estos son atribuidos a diferentes agentes endógenos como los radicales libres de oxígeno (RLO) provenientes de la respiración, los cuales son considerados el centro de la carcinogénesis y el envejecimiento por daño genómico; agentes exógenos como la luz ultravioleta que inducen dímeros de pirimidina y la radiación ionizante que produce una gran variedad de daños sobre las bases, muchos de ellos por efecto indirecto. También se encuentran las genotoxinas presentes en los alimentos, humo de tabaco y agentes quimioterapéuticos, con grandes cualidades para alterar la estructura de la molécula ADN e interferir con su expresión. De esta manera, cerca de 10(5) lesiones espontáneas por día son inducidas en nuestros genes, en donde los mecanismos de reparación detectan daños y perturbaciones durante el crecimiento y división celular. Esto es posible gracias a las funciones específicas de reconocimiento, corrección o eliminación de daños que asegura la integridad del genoma. En este artículo se presentan los principales mecanismos de reparación del ADN, su relación y activación de acuerdo al tipo de daño.
Cells have complex mechanisms that monitor DNA integrity that activate repair mechanisms when there are deficiencies or errors during replication. A potential result of the damage is a permanent alteration in DNA structure that can generate mutations, carcinogenic transformation and cell death. These are attributed to different endogenous agents such as oxygen free radicals (OFR) from respiration, which are considered the center of carcinogenesis and aging process due to genomic damage; exogenous agents, such as ultraviolet light, induce pyrimidine dimers and ionizing radiation that produce a variety of damage on the bases, many by indirect effect. Genotoxins present in food, tobacco and chemotherapeutic agents are also found with high potential in altering the DNA molecule structure and interfering with its expression. Thus, around 10(5) spontaneous lesions are induced per day in our genes, where the repair mechanisms can detect damages and disturbances during cell growth and division. This is possible thanks to the specific recognition, correction or elimination of damage functions, ensuring the integrity of the genome. In this article the main mechanisms of DNA repair, as well as their relationship and activation according to the type of damage, are presented.
ABSTRACT
An aqueous extract of Rhizophora mangle L. bark is used as raw material in pottery making in the State of Espirito Santo, Brazil. This extract presents large quantities of tannins, compounds possessing antioxidant properties. Tannin antioxidant activity, as a plant chemical defense mechanism in the process of stabilizing free radicals, has been an incentive to studies on anti-mutagenicity. The present work aimed to evaluate possible antimutagenic activity of a R. mangle aqueous extract, using the Allium cepa test-system and micronuclear (MN) assay with blockage of cytokinesis in Chinese hamster ovary cells (CHO-K1). The Allium cepa test-system indicated antimutagenic activity against the damage induced by the mutagenic agent methyl methanesulfonate. A reduction in both MN cell frequency and chromosome breaks occurred in both the pre and post-treatment protocols. The MN testing of CHO-K1 cells revealed anti-mutagenic activity of the R. mangle extract against methyl methanesulfonate and doxorubicin in pre, simultaneous and post-treatment protocols. These results suggest the presence of phyto-constituents in the extract presenting demutagenic and bio-antimutagenic activities. Since the chemical constitution of Rhizophora mangle species presents elevated tannin content, it is highly probable that these compounds are the antimutagenic promoters themselves.
ABSTRACT
Cytotoxicity of metals is important because some metals are potential mutagens able to induce tumors in humans and experimental animals. Chromium can damage DNA in several ways, including DNA double strand breaks (DSBs) which generate chromosomal aberrations, micronucleus formation, sister chromatid exchange, formation of DNA adducts and alterations in DNA replication and transcription. In our study, water samples from three sites in the Córrego dos Bagres stream in the Franca municipality of the Brazilian state of São Paulo were subjected to the comet assay and micronucleus test using erythrocytes from the fish Oreochromis niloticus. Nuclear abnormalities of the erythrocytes included blebbed, notched and lobed nuclei, probably due to genotoxic chromium compounds. The greatest comet assay damage occurred with water from a chromium-containing tannery effluent discharge site, supporting the hypothesis that chromium residues can be genotoxic. The mutagenicity of the water samples was assessed using the onion root-tip cell assay, the most frequent chromosomal abnormalities observed being: c-metaphases, stick chromosome, chromosome breaks and losses, bridged anaphases, multipolar anaphases, and micronucleated and binucleated cells. Onion root-tip cell mutagenicity was highest for water samples containing the highest levels of chromium.