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Modulation by flavonoids of DNA damage induced by estrogen-like compounds.
- Source :
-
Environmental and molecular mutagenesis [Environ Mol Mutagen] 2004; Vol. 44 (5), pp. 420-6. - Publication Year :
- 2004
-
Abstract
- Reactive oxygen species (ROS) are produced by a wide variety of exogenous chemicals and metabolic processes and cause a broad spectrum of damage to biological systems. As a consequence, ROS react with DNA, among many other biological targets, disrupting its structure and functionality. Estrogen-like compounds mediate DNA damage by ROS generation, implying that their effects can be modulated by antioxidants such as catalase, superoxide dismutase, and vitamin C. We examined DNA damage in human lymphocytes and sperm after treatment with four estrogen-like compounds (beta-estradiol, diethylstilbestrol, daidzein, and genistein) and its modulation by flavonoids (quercetin and kaempferol) using the Comet assay. The results indicated that quercetin and kaempferol reduced the DNA damage produced in sperm and lymphocytes by the four estrogenic compounds. The flavonoids also reduced the DNA damage induced by hydrogen peroxide, which was used as a positive control. Our results demonstrate that the antioxidant properties of flavonoids can protect the integrity of human sperm and lymphocyte DNA from ROS induced by estrogenic compounds.
- Subjects :
- Carcinogens adverse effects
Diethylstilbestrol adverse effects
Estradiol adverse effects
Genistein adverse effects
Humans
Isoflavones adverse effects
Kaempferols therapeutic use
Lymphocytes drug effects
Male
Phytoestrogens adverse effects
Quercetin therapeutic use
Reactive Oxygen Species metabolism
Spermatozoa drug effects
Antineoplastic Agents adverse effects
Antioxidants therapeutic use
DNA Damage drug effects
Subjects
Details
- Language :
- English
- ISSN :
- 0893-6692
- Volume :
- 44
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Environmental and molecular mutagenesis
- Publication Type :
- Academic Journal
- Accession number :
- 15540192
- Full Text :
- https://doi.org/10.1002/em.20071