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Daniel Araki Ribeiro - One of the best experts on this subject based on the ideXlab platform.

  • Acute crack cocaine exposure induces Genetic Damage in multiple organs of rats
    Environmental Science and Pollution Research, 2016
    Co-Authors: Eduardo Gregolin Moretti, Veronica Quispe Yujra, Samuel Rangel Claudio, Marcelo Jose Dias Silva, Wagner Vilegas, Camilo Dias Seabra Pereira, Flavia De Oliveira, Daniel Araki Ribeiro
    Abstract:

    Crack cocaine is a very toxic product derived from cocaine. The aim of this study was to evaluate Genetic Damage in multiple organs of rats following acute exposure to crack cocaine. A total of 20 Wistar rats were distributed into four groups ( n  = 5), as follows: 0, 4.5, 9, and 18 mg/kg body weight (b.w.) of crack cocaine administered by intraperitoneal route (i.p.). All animals were killed 24 h after intraperitoneal (i.p.) injection. The results showed that crack cocaine increased the number of micronucleated cells in bone marrow cells exposed to 18 mg/kg crack cocaine ( p  

  • Gum acacia mitigates Genetic Damage in adenine-induced chronic renal failure in rats.
    European journal of clinical investigation, 2015
    Co-Authors: Badreldin H. Ali, K A Al Balushi, I. Al-husseini, P. Mandel, Abderrahim Nemmar, Nicole Schupp, Daniel Araki Ribeiro
    Abstract:

    Background Subjects with chronic renal failure (CRF) exhibit oxidative genome Damage, which may predispose to carcinogenesis, and Gum acacia (GumA) ameliorates this condition in humans and animals. We evaluated here renal DNA Damage and urinary excretion of four nucleic acid oxidation adducts namely 8-oxoguanine (8-oxoGua), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), 8-oxoguanosine (8-oxoGuo) and 8-hydroxy-2-deoxyguanisone (8-OHdg) in rats with adenine (ADE)-induced CRF with and without GumA treatment. Materials and methods Twenty-four rats were divided into four equal groups and treated for 4 weeks. The first group was given normal food and water (control). The second group was given normal food and GumA (15% w/v) in drinking water. The third group was fed powder diet containing adenine (ADE) (0·75% w/w in feed). The fourth group was fed like in the third group, plus GumA in drinking water (15%, w/v). Results ADE feeding induced CRF (as measured by several physiological, biochemical and histological indices) and also caused a significant Genetic Damage and significant decreases in urinary 8-oxo Gua and 8-oxoGuo, but not in the other nucleic acids. However, concomitant GumA treatment reduced the level of Genetic Damage in kidney cells as detected by Comet assay and significantly reversed the effect of adenine on urinary 8-oxoGuo. Conclusions Treatment with GumA is able to mitigate Genetic Damage in renal tissues of rats with ADE-induced CRF.

  • Limb compression induces multi-system Genetic Damage in rats
    Pathophysiology : the official journal of the International Society for Pathophysiology, 2013
    Co-Authors: Nicola Jorge Carneiro Neto, Carolina Foot Gomes De Moura, Mauricio Wanderley Moral Sgarbi, Gustavo Protasio Pacheco De Jesus, Daniel Araki Ribeiro
    Abstract:

    Abstract Muscle crush injury is a common trauma in the modern society after as a result of mass disasters after penetration into muscle by high-velocity projectiles, blunt external trauma, or by gravity during prolonged immobilization in comatose patients after head trauma, alcoholic or drug overdose. However, the underlying mechanisms linking these alterations are still not fully understood, especially in acute phase. The aim of this study was to analyze genomic instability in multiple organs of rats after acute muscle injury by means of single cell gel (comet) assay. Rats were randomly distributed into three groups ( n =6 each group): control group and experimental groups: sacrificed 6h as 12h after muscle compression. These results indicate Genetic Damage in peripheral blood cells as depicted by tail moment results. DNA breakage was also detected in liver, lung and kidney cells after acute muscle injury for two times evaluated. Heart cells showed Genetic Damage after 12h following muscle compression. Taken together, our results suggest that acute muscle injury induces genomic Damage in multiple organs of Wistar rats. This novel finding offers new insights into the underlying mechanisms of the relationship between acute crush muscle injury and clinical manifestations that can occur during limb compression.

  • Nandrolone Decanoate Induces Genetic Damage in Multiple Organs of Rats
    Archives of environmental contamination and toxicology, 2012
    Co-Authors: Renan Pozzi, Kelly Rosseti Fernandes, Carolina Foot Gomes De Moura, Raquel Agnelli Mesquita Ferrari, Kristianne Porta Santos Fernandes, Ana Claudia Muniz Renno, Daniel Araki Ribeiro
    Abstract:

    To evaluate the impact potential of nandrolone decanoate on DNA Damage in multiple organs of Wistar rats by means of single-cell gel (comet) assay and micronucleus test. A total of 15 animals were distributed into three groups of five animals each as follows: control group = animal not exposed to nandrolone decanoate; experimental group = animals exposed to nandrolone decanoate for 24 h at 5 mg/kg subcutaneously; and experimental group = animals exposed to nandrolone decanoate for 24 h at 15 mg/kg subcutaneously. Significant statistical differences (p < 0.05) were noted in peripheral blood, liver, and heart cells exposed to nandrolone decanoate at the two doses evaluated. A clear dose–response relationship was observed between groups. Kidney cells showed Genetic Damage at only the highest dose (15 mg/kg) used. However, micronucleus data did not show remarkable differences among groups. In conclusion, the present study indicates that nandrolone decanoate induces Genetic Damage in rat blood, liver, heart, and kidney cells as shown by single-cell gel (comet) assay results.

  • Genetic Damage in multiple organs of acutely exercised rats.
    Cell biochemistry and function, 2010
    Co-Authors: Renan Pozzi, José C. Rosa, Ricardo Eguchi, Cláudia M. Oller Do Nascimento, Lila Missae Oyama, Odair Aguiar, Marcelo Donizetti Chaves, Daniel Araki Ribeiro
    Abstract:

    The aim of this study was to investigate the effects of acute exercise on genomic Damage in an animal model. Male adult Wistar rats were divided into the following groups: control and acute exercised (experimental). For this purpose, 15 animals were accustomed to running on a rodent treadmill for 15 min per day for 5 days (10–20 m min−1; 08 grade). After 4 days at rest, active animals ran on the treadmill (22 m min−1, 58 grade) till exhaustion. Cells from peripheral blood, liver, heart, and brain were collected after 0, 2, and 6 h after exercise. The results showed that acute exercise was able to induce Genetic Damage in peripheral blood cells after 2 and 6 h of exercise, whereas liver pointed out Genetic Damage for all periods evaluated. No Genetic Damage was induced either in brain or in heart cells. In conclusion, our results suggest that acute exercise could contribute to the Genetic Damage in peripheral blood and liver cells. It seems that liver is a sensitive organ to the genotoxic insult after acute exercise. Copyright © 2010 John Wiley & Sons, Ltd.

Guang Jia - One of the best experts on this subject based on the ideXlab platform.

  • cr vi induced methylation and down regulation of dna repair genes and its association with markers of Genetic Damage in workers and 16hbe cells
    Environmental Pollution, 2018
    Co-Authors: Xiaoxing Cui, Jing Wang, Zuchang Zhao, Ji Zhang, Xinxiao Zhai, Shichuan Tang, Guang Jia
    Abstract:

    Abstract To examine the mechanism of hexavalent chromium [Cr(VI)]-induced carcinogenesis, a cross-sectional study in workers with or without exposure to Cr(VI) as well as in vitro administration of Cr(VI) in 16HBE cells was conducted. We explored the associations between Cr(VI) exposure, methylation modification of DNA repair genes and their expression levels, and Genetic Damage. Results showed that hypermethylation of CpG sites were observed in both occupationally exposed workers and 16HBE cells administrated Cr(VI). DNA Damage markers including 8-hydroxydeoxyguanosine (8-OHdG) and micronucleus frequency in Cr(VI)-exposed workers were significantly higher than the control group. Among workers, blood Cr concentration was positively correlaed with the methylation level of CpG sites in DNA repair genes including CpG6,7, CpG8, CpG9,10,11 of MGMT, CpG11 of HOGG1; CpG15,16,17, CpG19 of RAD51, and Genetic Damage markers including 8-OHdG and micronucleus frequency. Significant negative association between methylation levels of CpG sites in DNA repair genes and corresponding mRNA was also observed in 16HBE cells. This indicated that Cr(VI) exposure can down-regulate DNA repair gene expression by hypermethylation, which leads to enhanced Genetic Damage. The methylation level of these CpG sites of DNA repair genes can be potential epiGenetic markers for Cr(VI)-induced DNA Damage.

  • miR-3940-5p associated with Genetic Damage in workers exposed to hexavalent chromium
    Toxicology letters, 2014
    Co-Authors: Ji Zhang, Tiancheng Wang, Guang Jia
    Abstract:

    To understand the regulation of Genetic Damage by epiGenetics at the early stage of carcinogenesis after hexavalent chromium (Cr(VI)) and assessed Genetic Damage to explore their association with DNA repair genes mediated by differently expressed miRNA. Genetic Damages were evaluated using cytokinesis-block micronucleus assay (CBMN) and serum 8-hydroxyguanine (8-OHdG) ELISA assay. Blood Cr level showed significant association with plasma miR-3940-5p level (r=-0.33, P=0.001) and non-linear relationship with micronuclei frequency in CBMN and serum 8-OHdG level (β(std)=0.29, P=0.039; β(std)=0.35, P=0.001), with micronuclei frequency not increasing apparently under high Cr exposure. In contrast, no significant association was found between plasma miR-3940-5p level and the two Genetic indicators. However, plasma miR-3940-5p level was linked to micronuclei frequency under high blood Cr level (β(std)=0.18, P=0.015). To explore the effect of miR-3940-5p on Genetic Damage under high Cr exposure, the protein expression levels of miR-3940-5p-mediated DNA repair genes in leukocytes were quantified using enzyme-linked immunosorbent assay for subjects with high blood Cr level. The results showed that XRCC2 and BRCC3 protein levels were statistically associated with miR-3940-5p level respectively (β(std)=-0.31, P=0.010; β(std)=-0.24, P=0.037). Meanwhile, a weak but statistically negative association between XRCC2 level and micronuclei frequency was found (β(std)=-0.15, P=0.027). These data suggests that high Cr(VI) does not always aggravate Genetic Damage after reaching a high Cr(VI) exposure in real situation, which may be due to the regulation of miRNA on DNA repair genes responsive to high Cr(VI) exposure.

Zhou Jian-hua - One of the best experts on this subject based on the ideXlab platform.

  • Study on the effect of Genetic Damage in workers occupationally exposed to lead
    China Occupational Medicine, 2010
    Co-Authors: Zhou Jian-hua
    Abstract:

    Objective To study the effect of Genetic Damage in workers occupationally exposed to lead.Methods 187 lead exposed workers from three storage battery factories were taken as exposed group.Simultaneously 179 villagers from other town who were not exposed to lead or other occupational hazardous agents were used as control group.Comet assay and micronucleus assay were applied to both groups.Results Statistically significant increases in the rate of comet and the tail length and the rate of micronucleus cell were observed in the exposed group when compared with the controls(P0.001).There was an increasing trend of the rate of comet with the increase of blood lead or urinary lead.When blood lead 1.45 μmol/L or urinary lead 0.58 μmol/L,the rate of micronucleus cell significantly increased when compared with the control (P0.001).Conclusion Occupational lead exposure may result in Genetic Damage.Comet assay can be used to detect the effect of Genetic Damage in workers occupationally exposed to lead.

Ricard Marcos - One of the best experts on this subject based on the ideXlab platform.

  • Time in hemodialysis modulates the levels of Genetic Damage in hemodialysis patients
    Environmental and molecular mutagenesis, 2014
    Co-Authors: Lara Rodríguez-ribera, Elitsa Stoyanova, Zuray Corredor, Elisabet Coll, Irene Silva, Juan M. Sánchez Díaz, José Ballarín, Ricard Marcos, Susana Pastor
    Abstract:

    It is assumed that hemodialysis treatment can diminish the levels of Genetic Damage in circulating lymphocytes by cleaning the blood of uremic toxins that cause oxidative stress. However, the hemodialysis process by itself may also induce genomic Damage by producing reactive oxygen species (ROS). We conducted a follow-up study in a group of 70 hemodialysis patients followed for a mean time of 15 months. We investigated the effect of exposure time in hemodialysis on the levels of Genetic Damage in peripheral blood lymphocytes using the micronucleus assay. In addition, Genetic Damage after in vitro irradiation with 0.5 Gy was also analyzed to evaluate changes in radiosensitivity. Our results showed that, at the end of the study, there was a decrease in both the basal levels of Genetic Damage (9.9 ± 1.0 vs. 7.6 ± 0.7) and radiosensitivity values (38.5 ± 3.0 vs. 27.6 ± 2.4). We conclude that hemodialysis procedures may act as an ameliorating factor reducing the Genetic Damage present in chronic kidney disease patients. Environ. Mol. Mutagen. 55:363–368, 2014. © 2014 Wiley Periodicals, Inc.

  • Genetic Damage in chronic renal failure patients is associated with the glomerular filtration rate index
    Mutagenesis, 2010
    Co-Authors: Silvia Berenice Sandoval, Elitsa Stoyanova, Elisabet Coll, José Ballarín, Susana Pastor, Joselyn Reyes, Enrique Andrés, Noel Xamena, Ricard Marcos
    Abstract:

    Chronic renal failure (CRF) patients are considered to present genomic instability and, as a consequence, elevated levels of Genetic Damage. An open question is whether this Damage is related to the stage of the pathology. To determine the background levels of Genetic Damage, a large population of 258 Caucasian adults (201 CRF patients and 57 controls) was analysed using the micronucleus (MN) assay. The frequency of MN in CRF patients was significantly higher than in controls and correlated with the progression of the disease, according to the glomerular filtration rate. In addition, a significant association was observed between Genetic Damage and serum creatinine levels. Genetic Damage, measured as frequency of MN, increases when renal function decreases. The fact that an increased level of MN is already observed in patients' Stage 2 seems to indicate a Genetic predisposition on these patients. Nevertheless, part of the observed Damage can be attributed to the uraemic state itself.

Tiancheng Wang - One of the best experts on this subject based on the ideXlab platform.

  • Circulating lead modifies hexavalent chromium-induced Genetic Damage in a chromate-exposed population: An epidemiological study
    The Science of the total environment, 2020
    Co-Authors: Changmao Long, Tian Chen, Xiaoyin Gao, Yali Zhang, Pai Zheng, Li Wang, Tiancheng Wang
    Abstract:

    Abstract Chromium (Cr) can coexist with other heavy metals in the blood of chronically chromate-exposed individuals. However, few studies have explored the health impacts of other hazardous metals after exposure to hexavalent chromium [Cr(VI)]. This study aimed to assess the modification effects of blood lead (Pb) on the Genetic Damage induced by Cr(VI). During 2010–2019, 1000 blood samples were collected from 455 workers exposed to chromate and 545 workers not exposed to chromate from the same factory with similar labor intensity. The levels of Cr and Pb were measured in whole blood samples. Micronucleus frequency (MNF) and urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured to reflect different types of Genetic Damage. Multivariate linear regression analyses were performed to evaluate the associations between hazardous metals and the modification effects of Pb on Genetic Damage. The geometric mean levels of Cr and Pb in the exposure group were significantly higher than those in the control group [Cr: 6.42 (6.08– 6.79) vs. 1.29 (1.22– 1.36) μg/L; Pb: 38.82 (37.22– 40.50) vs. 34.47 (33.15– 35.85) μg/L]. The geometric means of urinary 8-OHdG and MNF in exposure group were 4.00 (3.64– 4.40) μg/g and 5.40 (4.89– 5.97) ‰, respectively, significantly higher than the 3.20 (2.94– 3.48) μg/g and 4.57 (4.15– 5.03) ‰, respectively, in control group. log2Cr was independently and positively associated with urinary 8-OHdG (β-adjusted = 0.143, 95% CI: 0.082– 0.204) and MNF (β-adjusted = 0.303, 95%CI: 0.020– 0.587). With the change in circulating Pb levels, the types of Genetic Damage induced by Cr(VI) were different. At low levels of circulating Pb (

  • Modulation of homologous recombination repair gene polymorphisms on Genetic Damage in chromate exposed workers
    Environmental toxicology and pharmacology, 2019
    Co-Authors: Changmao Long, Jiaxing Liu, Huimin Feng, Di Zhou, Jing Wang, Xinxia Zhai, Zuchang Zhao, Tiancheng Wang
    Abstract:

    Hexavalent chromium [Cr(VI)] is one of the most common environmental carcinogens, which is associated with DNA Damage, Genetic instability and increase the risk of cancer development. However, the mechanisms of Genetic Damage induced by Cr(VI) remains to be thoroughly illustrated. A molecular epidemiological study was conducted on 120 chromate exposed workers and 97 controls. Results indicated that,the rs12432907 of XRCC3 carrying T allele, the rs144848 of BRCA2 with C allele and the rs1805800 of NBS1 with genotype(TT) of individuals were associated with lower Genetic Damage, while the rs2295152 of XRCC3 carrying T allele, the rs13312986 (CC and CT genotypes) and the rs2697679 of NBS1 with A allele were associated with higher Genetic Damage in workers exposed to chromate. The interaction of chromate exposure with rs2295152 of XRCC3 had a significant effect on micronuclei frequency (MNF). The gene polymorphisms in homologous recombination repair pathway could modulate chromate-induced Genetic Damage.

  • miR-3940-5p associated with Genetic Damage in workers exposed to hexavalent chromium
    Toxicology letters, 2014
    Co-Authors: Ji Zhang, Tiancheng Wang, Guang Jia
    Abstract:

    To understand the regulation of Genetic Damage by epiGenetics at the early stage of carcinogenesis after hexavalent chromium (Cr(VI)) and assessed Genetic Damage to explore their association with DNA repair genes mediated by differently expressed miRNA. Genetic Damages were evaluated using cytokinesis-block micronucleus assay (CBMN) and serum 8-hydroxyguanine (8-OHdG) ELISA assay. Blood Cr level showed significant association with plasma miR-3940-5p level (r=-0.33, P=0.001) and non-linear relationship with micronuclei frequency in CBMN and serum 8-OHdG level (β(std)=0.29, P=0.039; β(std)=0.35, P=0.001), with micronuclei frequency not increasing apparently under high Cr exposure. In contrast, no significant association was found between plasma miR-3940-5p level and the two Genetic indicators. However, plasma miR-3940-5p level was linked to micronuclei frequency under high blood Cr level (β(std)=0.18, P=0.015). To explore the effect of miR-3940-5p on Genetic Damage under high Cr exposure, the protein expression levels of miR-3940-5p-mediated DNA repair genes in leukocytes were quantified using enzyme-linked immunosorbent assay for subjects with high blood Cr level. The results showed that XRCC2 and BRCC3 protein levels were statistically associated with miR-3940-5p level respectively (β(std)=-0.31, P=0.010; β(std)=-0.24, P=0.037). Meanwhile, a weak but statistically negative association between XRCC2 level and micronuclei frequency was found (β(std)=-0.15, P=0.027). These data suggests that high Cr(VI) does not always aggravate Genetic Damage after reaching a high Cr(VI) exposure in real situation, which may be due to the regulation of miRNA on DNA repair genes responsive to high Cr(VI) exposure.