DNA damage and repair in haemolymph cells of golden mussel (Limnoperna fortunei) exposed to environmental contaminants

Villela, Izabel Vianna; Oliveira, Iuri Marques de; Silva, Juliana da; Henriques, João Antônio Pêgas

doi:10.1016/j.mrgentox.2006.02.006

Cited by 133 publications

(80 citation statements)

References 20 publications

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“…However, a recurring theme in discussions of copper toxicity has been the expectation that copper participates in Fenton-like reactions, generating hydroxyl radicals that might then damage DNA, lipids, and proteins. Indeed, exposure of mammalian cells to high doses of copper resulted in some indications of accelerated DNA damage (18,55,67). However, these experiments did not unam- COPPER DOES NOT CATALYZE OXIDATIVE DNA DAMAGE 1623 biguously imply the mechanism by which copper was acting, since in addition to providing a metal catalyst for hydroxyl radical formation, copper treatment may also have increased the rate of H 2 O 2 generation (3,19,37,41), which could have accelerated iron-mediated oxidative DNA damage.…”

Section: Discussionmentioning

confidence: 99%

Intracellular Copper Does Not Catalyze the Formation of Oxidative DNA Damage in Escherichia coli

2007

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Because copper catalyzes the conversion of H2O2 to hydroxyl radicals in vitro, it has been proposed that oxidative DNA damage may be an important component of copper toxicity. Elimination of the copper export genes, copA, cueO, and cusCFBA, rendered Escherichia coli sensitive to growth inhibition by copper and provided forcing circumstances in which this hypothesis could be tested. When the cells were grown in medium supplemented with copper, the intracellular copper content increased 20-fold. However, the copper-loaded mutants were actually less sensitive to killing by H2O2 than cells grown without copper supplementation. The kinetics of cell death showed that excessive intracellular copper eliminated iron-mediated oxidative killing without contributing a copper-mediated component. Measurements of mutagenesis and quantitative PCR analysis confirmed that copper decreased the rate at which H2O2 damaged DNA. Electron paramagnetic resonance (EPR) spin trapping showed that the copper-dependent H2O2 resistance was not caused by inhibition of the Fenton reaction, for copper-supplemented cells exhibited substantial hydroxyl radical formation. However, copper EPR spectroscopy suggested that the majority of H2O2-oxidizable copper is located in the periplasm; therefore, most of the copper-mediated hydroxyl radical formation occurs in this compartment and away from the DNA. Indeed, while E. coli responds to H2O2 stress by inducing iron sequestration proteins, H2O2-stressed cells do not induce proteins that control copper levels. These observations do not explain how copper suppresses iron-mediated damage. However, it is clear that copper does not catalyze significant oxidative DNA damage in vivo; therefore, copper toxicity must occur by a different mechanism.

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Section: Discussionmentioning

confidence: 99%

Intracellular Copper Does Not Catalyze the Formation of Oxidative DNA Damage in Escherichia coli

2007

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“…Micronuclei assay provide information as a simple bioindicator for chromosomal aberrations not available from other methods: (i) the consolidated effect of a variety of environmental stresses on the health of an organism, population, community, and ecosystem (ii) warning of harmful effects to human health based on the responses of wildlife to pollution, and (iii) the effectiveness of remediation efforts in decontaminating waterways [25]. Counting of micronuclei is faster and less demanding of technical than scoring of chromosomal aberrations, the micronuclei assay has been widely used for chemicals screening that cause these types of damage and also it demonstrate that micronuclei test in fish can be used for the genotoxicity assessment in environment [26].…”

Section: Micronuclei Assaymentioning

confidence: 99%

Assessing the Genotoxic Potentials of Methomyl-based Pesticide in Tilapia (Oreochromis niloticus) Using Micronucleus Assay

Islamy

Yanuhar

Hertika

2017

JELS

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Pesticides are recognized as serious pollutants in the aquatic environment with the potential to cause genotoxic on the aquatic organism, especially fish. The micronucleus (MN) assay has been used to evaluate genotoxicity of many compounds in polluted ecosystems such pesticides. im of this study to determine genotoxic effect of methomylbased pesticide on tilapia (Oreochromis niloticus). Fish were exposed to six different concentrations base on range finding test (0 ppm, 3.2 ppm, 4.2 ppm, 6.5 ppm, 8.7 ppm and 10 ppm) of methomyl-based pesticide. The micronucleus were collected from peripheral blood erythrocyte of fish after 96 h exposure. Peripheral blood samples smears were stained with Giemsa, MN frequencies were counted and statistically analyzed using one-way ANOVA. The result of this study showed after 96 hours exposed to methomyl-based pesticide, at concentration 0 ppm causes 0% mortality, at concentration to 3.2 ppm causes 30% mortality, at concentration 4.2 ppm causes 60% mortality, at concentration 6.5 ppm causes 70% mortality, at concentration 8.7 ppm causes 80% mortality, at concentration 10 ppm causes 100% mortality of fish test. Lethal Concentration 50 (LC50 -96 hours) of methomy-base pesticide towards tilapia (O. niloticus) is 4.015 ppm. Through micronuclei assay during 96 hour exposure of methomyl-based pesticide, the result shows that frequencies of micronuclei in erythrocyte of fish test at concentration at 0ppm is 12‰, 18‰ and 16‰; at concentration at 3.2ppm is 33‰, 26‰ and 29‰; at concentration at 4.2ppm is 41‰, 38‰ and 46‰; at concentration at 6.5ppm is 68‰, 81‰ and 82‰; at concentration 8.7ppm is 133‰, 130‰ and 137‰; at concentration 10ppm is 163‰, 166‰ and 156‰. It revealed that methomyl-based pesticide exposure induced after 96 h significantly (P<0.05) increased genotoxic potentials simultaneous with increased concentration.

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“…There is need to develop molecular bioassays which can remedy the detrimental effects of environment on living organisms. DNA damaging agents require continuous monitoring and detection (Villela et al, 2006). With increasing demand, the population of fish in different areas of the world has been reduced drastically due to pollution and overfishing (Baršienė et al, 2013;Pavlica et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Habitat induced mutational effects and fatty acid profile changes in bottom dweller <em>Cirrhinus mrigala</em> inhabitant of river Chenab

Hussain¹,

Sultana²,

Sultana³

et al. 2015

Grasas y Aceites

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SUMMARY:Fish from the river Chenab were analyzed for DNA damage by the Comet and Micronucleus assays. The fatty acid profile was determined by gas chromatography using a Flame Ionization Detector. Atomic absorption spectrophotometry showed significant (p<0.05) levels of contamination due to Cd, Hg, Cu, Mn, Zn, Pb, Cr, Sn and phenols in the fish habitat. The Comet assay revealed significant (p<0.05) DNA damage in Cirrhinus mrigala of 37.29±2.51%, 34.96±2.53% and 38.80±2.42% in the comet tail, in the tail moment of 23. 48±3.90, 19.78±4.26 and 14.30±1.82, in the olive moment of 16.22±2.04, 13.83±1.96 10.99±0.90, respectively, from three experimental sites. The micronucleus assay showed a high frequency of single micronucleus induction of 44.80±3.73, double induction of 06.20±0.97 and nuclear abnormalities of 09.60±1.72, as calculated in a thousand cells. C8:0, C12:0, C20:0, C16:1(n-7), C16:1(n-9), C20:1(n-9), C18:2(n-6), C18:4(n-3), C20:5(n-3), C22:4(n-6) fatty acids were found missing in the fish with a higher intensity of DNA damage but were found in optimal amounts both in farmed and wild fish from non polluted habitats. A highly significant (p<0.01) correlation was also found in saturated, unsaturated fatty acids and DNA damage and habitat. The present study revealed that the habitat of even lower intensity pollutions not only induce DNA damage but also confiscate essential fatty acids of the omega series and reduce the amount of unsaturated fatty acids for which fish is preferred over other animals.KEYWORDS: Cirrhinus; DNA damage; Fatty acids; Habitat; Niche; Pollution RESUMEN: Efectos inducidos por el hábitat sobre mutaciones y perfil de ácidos grasos en carpas mrigala que habitan en el fondo del río Chenab. Los daños en el ADN de los peces del río Chenab se analizaron mediante la técnica del "ensayo del cometa" y el ensayo de micronúcleos. El perfil de ácidos grasos se determinó mediante cromatografía de gases con detector de ionización de llama. La espectrofotometría de absorción atómica mostró diferencias significativas (p<0.05) de los niveles de contaminación por Cd, Hg, Cu, Mn, Zn, Pb, Cr, Sn y fenoles en el hábitat de los peces. El ensayo del cometa mostró daños significativos (p<0,05) en el ADN de las carpas mrigala de tres sitios experimentales: 37,29±2,51%, 34,96±2,53 y 38,80±2,42% del ADN en la cola del cometa, momento de la cola con 23,48±3,90, 19,78±4,26 y 14,30±1,82% y cola media con 16,22±2,04, 13,83±1,96 10,99±0,90. Los ensayos de micronúcleos mostraron una alta frecuencia de inducción de micronú-cleos como única 44,80±3,73, 06,20±0,97 y doble anomalías nucleares 09,60±1,72 calculados en miles de células. C8:0, C12:0, C20:0, C16:1(n-7), C16:1 (n-9), C20:1(n-9), C18:2(n-6), C18:4(n-3), C20:5(n-3) y C22:4(n-6) se mostraron como ácidos grasos que faltan en el pescado que tiene una mayor intensidad de daño en el ADN, aunque se encuentran en cantidades óptimas, tanto en los peces de piscifactoría como en los salvajes donde no hay hábitats contaminados. Se encontró una correlación altamente significa...

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DNA damage and repair in haemolymph cells of golden mussel (Limnoperna fortunei) exposed to environmental contaminants

Cited by 133 publications

References 20 publications

Intracellular Copper Does Not Catalyze the Formation of Oxidative DNA Damage in Escherichia coli

Intracellular Copper Does Not Catalyze the Formation of Oxidative DNA Damage in Escherichia coli

Assessing the Genotoxic Potentials of Methomyl-based Pesticide in Tilapia (Oreochromis niloticus) Using Micronucleus Assay

Habitat induced mutational effects and fatty acid profile changes in bottom dweller <em>Cirrhinus mrigala</em> inhabitant of river Chenab

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