Health & Environmental Research Online (HERO)


Print Feedback Export to File
746847 
Journal Article 
Genotoxicity of Di(2-ethylhexyl) phthalate and mono(2-ethylhexyl) phthalate and prevention by selenium compounds in prostatic cell lines 
Erkekoglu, P; Rachidi, W; Giray, B; Hincal, F 
2009 
1 
Toxicology Letters
ISSN: 0378-4274
EISSN: 1879-3169 
189 
Supplement 
S146 
English 
WOS:000269778800428 
Selenium is an essential trace element which is present in trace amount in foods (Brazil nuts, oysters, tuna fish). Glutathione peroxidase and thioredoxin reductase, which have important antioxidant and detoxification functions, are selenoenzymes. Selenium's role in fertility is likely to be maintaining the oxidant–antioxidant balance in testis. Phthalates are ubiquitous environmental contaminants that target the fetal and pubertal testis and lead to alterations in endocrine and spermatogenic function. Phthalates such as di(2-ethylhexyl) phthalate (DEHP) add flexibility to plastics. DEHP's main metabolite is mono(2-ethylhexyl) phthalate (MEHP) and it is even more toxic than the parent compound. Taking into account the widespread availability of inadequate selenium intakes, the essentiality of selenium in antioxidant system and high DEHP exposure of humans, this study was aimed to investigate the genotoxic effect of DEHP and MEHP and to examine the possible preventive effects of selenium supplementation in prostatic LnCAP cells using alkaline Comet assay. We determined that DEHP (3 mM) and MEHP (3 μM) increased the tail intensity up to 250% and both sodium selenite (SS, 30 nM) and selenomethionine (SM, 10 μM) pretreatment for 72 h were able to reduce the tail intensity in DEHP and MEHP-treated cells. We can postulate that reprotoxicity of both MEHP and DEHP could be related to their genotoxicity. Finally, we demonstrated that SS and SM pretreatments were successful in the prevention of genotoxicity of these compounds. 
Toxicology Abstracts; Selenium compounds; Phthalic acid; Genotoxicity; X 24360:Metals