Metabolism of arsenic in <i>Drosophila melanogaster</i> and the genotoxicity of dimethylarsinic acid in the Drosophila wing spot test

Rizki, M. T. M.; Kossatz, Elk; Velázquez, Antonia; Creus, A.; Farina, Massimo; Fortaner, Salvador; Sabbioni, E.; Marcos, Ricard

doi:10.1002/em.20178

Cited by 32 publications

(16 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2 Methylene arsenic compounds have been shown to be genotoxic. 3 The consumption of agricultural products irrigated through natural water having arsenic can reach people as it is accumulated in the food chain. 4 More than 80% of arsenic compounds which are toxic and tasteless, as additives in metal alloys and glass are used for products such as semiconductors and dyes.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

et al. 2015

View full text Add to dashboard Cite

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

show abstract

Section: Introductionmentioning

confidence: 99%

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Previous studies with Drosophila as well as with bacterial and mammalian cell mutation assays have shown that arsenic alone fails to behave as a point mutagen and thus it was classified largely as an epigenetic carcinogen (24)(25)(26). However, in another recent study, evidence was reported on the chromosomal aberrations in bone marrow cells of arsenic exposed rats (13).…”

Section: Discussionmentioning

confidence: 99%

Genetic and epigenetic changes induced by chronic low dose exposure to arsenic of mouse testicular Leydig cells

Singh¹,

DuMond²

2007

Int J Oncol

View full text Add to dashboard Cite

Abstract. Arsenic is an important environmental carcinogen that affects millions of people worldwide through contaminated water supplies. Genotoxicity of arsenic has been a topic of controversy. Both genetic alterations (mutations) and epigenetic changes (methylation) have been shown to play a crucial role in environmental carcinogenesis. Chronic exposure to arsenic has been shown to induce malignant transformation of mammalian cells. However, the genetic aberrations induced by arsenic in this process are unclear. The purpose of this study was to determine if both lower (1 pg/ml) and higher concentrations (100 ng/ml) of arsenic induces either mutations or methylation changes that could lead to the development of genomic instability in TM3 cells, immortalized Leydig cells derived from normal mouse testis. Two independent exposure times were used in this study which resulted in cells of 33 and 100 generations in age. Arsenic-induced genetic and epigenetic changes were screened at a genome-wide level by random amplified polymorphic DNA (RAPD), also known as AP-PCR method with undigested DNA as well as DNA digested by the methylation sensitive isosizomeric restriction enzymes MSPI and HpaII and untreated controls. Changes in the DNA fingerprint of both, the restriction enzyme digested DNA (indicating methylation changes) as well as undigested DNA (indicating mutations) from arsenic-treated (low as well as high dose) samples were observed as compared to their controls. Thus, this study provides the first evidence at DNA sequence level for mutagenic potential of arsenic. Further characterization of these altered genomic regions is underway. The understanding of these genetic and epigenetic changes in arsenic-induced carcinogenesis will provide a basis for better interventional approaches in both the treatment and prevention of arsenicinduced cancer.

show abstract

“…Exposure to arsenic has been observed to cause prostate cancer in humans and liver cancer in mice [18,19]. Mutation caused by arsenic has not been evident till date, but epigenetic changes by altering methylation of promoter of genes are superfluous in the literature [20][21][22]. Arsenic has also been shown to cause hypermethylation of tumor suppressor genes [18].…”

Section: Resultsmentioning

confidence: 99%

Hypomethylation of Deoxyribonucleic Acid in Testicular Tissue Due to Arsenic Exposure in Mice

Anshu¹,

Nath²,

Priyanka³

et al. 2016

Asian J Pharm Clin Res

View full text Add to dashboard Cite

Objective: Among various environmental carcinogens, arsenic is highly sensitive and possesses potential to cause several diseases including cancer. Nevertheless, arsenic has not been observed to induce mutation directly but is involved in epigenetic changes. Hypomethylation of oncogenes and hypermethylation of tumor suppressor genes are reported to be associated with accumulation of arsenic. The present investigation demonstrates a direct correlation arsenic and deoxyribonucleic acid (DNA) methylation. Methods:Swiss albino mice were grouped as control and arsenic treated for 12 weeks. Arsenic concentration in blood and testes was analyzed by atomic absorption spectrometer. Furthermore, DNA was extracted from the testes of mice by DNA purification kit and used for determining global methylation in mice genome with the help of MethylFlash Methylated DNA Quantification Kit.Results: Arsenic concentration in arsenic-treated mice was significantly higher than the control group in both blood and testes. Interestingly, arsenic concentration in blood was recorded to be higher than testes in the arsenic-treated group with significance (p<0.0001). Moreover, a lower percentage of cytosine of mice genome was found to be methylated in arsenic-treated mice group than control group (p<0.0001). Conclusion:Greater concentration of arsenic in mice leads to hypomethylation of mice genome globally. Arsenic fosters deregulation of gene expression by modifying methylation of CpG island of the promoter region. Epigenetic study is of prime importance in the field of oncology. Drug development for repressing alteration of DNA methylation is imperative for cancer treatment.

show abstract

Metabolism of arsenic in Drosophila melanogaster and the genotoxicity of dimethylarsinic acid in the Drosophila wing spot test

Cited by 32 publications

References 42 publications

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

Genetic and epigenetic changes induced by chronic low dose exposure to arsenic of mouse testicular Leydig cells

Hypomethylation of Deoxyribonucleic Acid in Testicular Tissue Due to Arsenic Exposure in Mice

Contact Info

Product

Resources

About