The effects of di(2‐ethylhexyl)phthalate on rat liver in relation to selenium status

Abstract

This study was performed to determine the hepatotoxicity of di(2-ethylhexyl)phthalate (DEHP) in relation to selenium status. In 3-week-old Sprague-Dawley rats, selenium deficiency was induced by a ≤0.05 selenium mg/kg. A selenium supplementation group was given 1 mg selenium/kg diet for 5 weeks. Di(2-ethylhexyl)phthalate-treated groups received 1000 mg/kg dose by gavage during the last 10 days of the experiment. Histopathology, peroxisome proliferation, catalase (CAT) immunoreactivity and activity and apoptosis were assessed. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR1)], superoxide dismutase (SOD), and glutathione S-transferase (GST); aminotransferase, total glutathione (tGSH), and lipid peroxidation (LP) levels were measured. Di(2-ethylhexyl)phthalate caused cellular disorganization while necrosis and inflammatory cell infiltration were observed in Se-deficient DEHP group (DEHP/SeD). Catalase activity and immunoreactivity were increased in all DEHP-treated groups. Glutathione peroxidase 1 and GPx4 activities decreased significantly in DEHP and DEHP/SeD groups, while GST activities decreased in all DEHP-exposed groups. Thioredoxin reductase activity increased in DEHP and DEHP/SeS, while total SOD activities increased in all DEHP-treated groups. Lipid peroxidation levels increased significantly in SeD (26%), DEHP (38%) and DEHP/SeD (71%) groups. Selenium supplementation partially ameliorated DEHP-induced hepatotoxicity; while in DEHP/SeD group, drastic changes in hepatic histopathology and oxidative stress parameters were observed.

Protective Effects of Combined Selenium and Punica granatum Treatment on Some Inflammatory and Oxidative Stress Markers in Arsenic-Induced Hepatotoxicity in Rats

“…The decline in TAC and TrxR observed herein was in accordance with Erkekoglu et al [37], who d e m o n s t r a t e d t h a t i n h i b i t i o n o f Tr x R i n d i ( 2 -ethylhexyl)phthalate-induced hepatotoxicity leads to decreased activity of enzymes dependent on thioredoxin and reduced scavenging ability of ROS leading to oxidative stress, apoptosis, and necrosis. However, treatment with selenium or P. granatum increased the activities of anti-oxidant enzymes and TAC.…”

Effect of diethylhexyl phthalate on sperm motility parameters in bull

“…Dietilheksil fitalatın spermatozoon motilitesi üzerindeki etkileriyle ilgili olası bir diğer mekanizma ise oksidatif stres kaynaklı olabilir. Çünkü DEHP'in testis dokusu dahil çeşitli hücre tiplerinde oksidatif strese neden olduğu bilinmektedir (12,13,32,33). Her ne kadar düşük düzeydeki reaktif oksijen türleri spermatozoon hareketliliği ve kapasitasyonu için gerekli olsa da, artan reaktif oksijen türleri ve membran lipit peroksidasyon miktarı spertmatozoon hareketliliğinde düşüşe hatta ilerleyen süreçte hücre ölümüne neden olabilmektedir (19).…”

The adjuvant effect induced by di-(2-ethylhexyl) phthalate (DEHP) is mediated through oxidative stress in a mouse model of asthma

“…For example, 1000 mg/kg DEHP exposure by gavage can cause lipid peroxidation in the liver of rats (Erkekoglu et al, 2014). In order to block the effect of oxidative stress, vitamin E (Vit E) has typically been used to scavenge excess ROS, and for adults the recommended dietary allowance of Vit E is 15 mg (or 22.4 IU of the natural form; 33.3 IU for the synthetic forms) (Nakamura and Omaye, 2009).…”