Impact of selenium status on Aroclor 1254-induced DNA damage in sperm and different tissues of rats. (4th May 2018)

• Record Type: Journal Article
• Authors: Aydin, Sevtap; Erkekoglu, Pinar; Başaran, Nurşen; Kocer-Gumusel, Belma
• Is Part Of: Toxicology mechanisms and methods. Volume 28:Number 4(2018)
• Page Start: 252
• Page End: 261
• Publication Date: 2018-05-04
• Subjects: Aroclor 1254 -- Comet assay -- DNA damage -- genotoxicity -- polychlorinated biphenyls (PCBs) -- selenium; Analytical toxicology -- Periodicals; Toxicology -- Periodicals; Toxicology -- Methodology -- Periodicals; 615.907
• DOI: 10.1080/15376516.2017.1397234
• Languages: English
• ISSNs: 1537-6516

Abstract

Abstract: Aroclor 1254 is a commercial mixture of polychlorinated biphenyls (PCBs), which are widespread environmental pollutants. It is used as non-flammable heat transfer agent and plasticizer. Animal studies have reported that Aroclor 1254 exerted toxic effects in different organs and systems. Although the evidences are limited, it seems reasonable that Aroclor 1254 may have a potential for similar adverse effects in humans. Selenium (Se) is a trace element and an important component of cellular antioxidant defense. This study was designed to investigate the effects of different Se status on the genotoxicity of Aroclor 1254 in sperm and different organs of Sprague-Dawley rats using Comet assay. Se deficiency (SeD) was generated by feeding 3-week old Sprague-Dawley rats with <0.05 Se mg/kg diet for 5 weeks. Se supplementation groups (SeS) were fed with 1 mg Se/kg diet. Aroclor 1254-treated rats received 10 mg/kg dose by gavage during the last 15 d of feeding period. SeD increased DNA damage in all of the organs as well as in lymphocytes and sperm. Aroclor 1254 treatment caused pronounced changes in liver, kidney and brain cells along with marked increases in lymphocytes and sperm. Se supplementation provided full or partial protection decreases in Aroclor 1254-induced DNA damage in sperm and all of tissues. Se deficiency aggravated the toxicity by increasing DNA damage caused by Aroclor 1254. Further studies should be performed to clarify the mechanism(s) underlying the protective role of Se status against Aroclor 1254 genotoxicity.