DNA damage induced by industrial solid waste leachates inDrosophila melanogaster: A mechanistic approach
| Autor: | Daya K. Saxena, Alok Dhawan, Hifzur R. Siddique, Anurag Sharma, Debapratim Kar Chowdhuri, Ramesh C. Murthy, Subash C. Gupta |
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| Rok vydání: | 2008 |
| Předmět: |
DNA Repair
Epidemiology DNA damage DNA repair Health Toxicology and Mutagenesis Industrial Waste Mutagen Biology medicine.disease_cause Arsenic chemistry.chemical_compound Metals Heavy medicine Postreplication repair Animals Coloring Agents Genetics (clinical) Genetics fungi Tanning Double Strand Break Repair DNA-Binding Proteins Gastrointestinal Tract Comet assay Drosophila melanogaster chemistry Biochemistry Larva Ganglia Comet Assay Water Pollutants Chemical DNA DNA Damage Nucleotide excision repair |
| Zdroj: | Environmental and Molecular Mutagenesis. 49:206-216 |
| ISSN: | 1098-2280 0893-6692 |
| Popis: | Genomic stability requires that error-free genetic information be transmitted from generation to generation, a process that is dependent upon efficient DNA repair. Industrial leachates which contain mixtures of diverse chemicals are a major environmental concern. The interaction between these chemicals may have synergistic, antagonistic, or simply additive effects on biological systems. In the present study, the Comet assay was used to measure the DNA damage produced by leachates of solid wastes from flashlight battery, pigment, and tanning factories in the midgut cells and brain ganglia of Drosophila melanogaster mutants deficient in DNA repair proteins. Larvae were allowed to feed for 48 or 72 hr on diets containing 0.1, 0.5, and 2.0% (v/v) of the leachates. Physicochemical analysis run on the solid wastes, leachates, and treated larvae detected elevated levels of heavy metals. Leachates produced significantly greater levels of DNA damage in mutant strains mei41 (deficient in cell cycle check point protein), mus201 (deficient in excision repair protein), mus308 (deficient in postreplication repair protein), and rad54 (deficient in double strand break repair protein) than in the OregonR+ wild-type strain. Larvae of the ligaseIV mutant (deficient in double strand break repair protein) were hypersensitive only to the pigment plant waste leachate. Conversely, the dnase2 mutant (deficient in protein responsible for degrading fragmented DNA) was more sensitive to DNA damage induction from the flashlight battery and tannery waste leachates. Our data demonstrate that repair of DNA damage in organisms exposed to leachates is dependent upon several DNA repair proteins, indicative of the involvement of multiple overlapping repair pathways. The study further suggests the usefulness of the Comet assay for studying the mechanisms of DNA repair in Drosophila. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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