Accumulation of Organotins in Seafood Leads to PCOS Features, Abnormal Placental Function and Transgenerational Inheritance of Increased Body Weight, Hepatic Oxidative Stress and Fat Depot in Rats

Presentation Number: SAT 262
Date of Presentation: April 1st, 2017

Priscila Lang Podratz*1, Eduardo Merlo1, Julia F P Araújo1, Leandro C Freitas-Lima1, Mercia B Costa1, Leandro Miranda-Alves2, Ian Victor Silva1 and Jones B Graceli3
1Federal University of Espirito Santo, Vitoria, Brazil, 2Federal University of Rio de Janeiro, Rio de Janeiro, BRAZIL, 3Federal University of Espirito Santo, Vitoria, BRAZIL

Abstract

Organotins (OT) are xenobiotic used as biocides in antifouling paints that have been shown to be endocrine disrupters. OTs are able to accumulate in the seafood in the food chain. However, the effects of OT accumulated in seafood on the endocrine health or whether these effects were heritable are particularly sparse. Here, we describe the reproductive characterization as result of seafood-contaminated with OT (SF-OT) exposure, as well the metabolic characterization of F1 generation from female (F0) SF-OT-treated rat mated with male control rat. To study F0 reproductive and F1 metabolic function, we administered vehicle (CON, distilled water), seafood without OT contamination (SF, 600mg/day) and SF-OT (600mg/day) in the Wistar female rat for 15 days via gavage. SF-OT rats displayed a higher serum tin levels (CON:4.0±1.0 vs SF:7.0±2.0 vs SF-OT: 37.0±2.0 ng. g−1; p≤0.05; n=6) and abnormal estrous cyclicity (p≤0.01; n=8-10). SF-OT rats had higher serum testosterone (CON:0.15±0.01 vs SF: 0.17±0.04 vs SF-OT:0.20±0.02 ng/mL; p≤0.01), estrogen (CON:9.9±1.5 vs SF:7.8±0.6 vs SF-OT:33.4±1.7 pg/mL; p≤0.01; n=7-9) and fasting glucose levels (CON:104.0±5.1 vs SF:100.7±2.8 vs SF-OT:126.3±2.2 mg/dL; p≤0.01; n=5-6). Further, impaired fertility was noted with dysfunctional ovarian folliculogenesis in the SF-OT rats (p≤0.05; n=6). Ovary and uterus fibrosis was observed in the SF-OT rats, as well the uterine inflammation (p≤0.01; n=5-8). Abnormal placental function was noted in the SF-OT rats, such as an increase in the placental weight (CON:0.85±0.01 vs SF:0.82±0.03 vs SF-OT:0.93±0.03 g; p≤0.01; n=12-32) and inflammation (p≤0.01; n=8-10). Placental triglyceride (TG) (CON:203.2±6.9 vs SF:195.6±13.2 vs SF-OT:248.0±12.2mg/dL; p≤0.01) and cholesterol (Chol) (CON:58.1±5.1 vs SF:64.2±3.2 vs SF-OTs:74.8±1.2mg/dL; p≤0.01; n=5-8) levels were raised in the SF-OT rats but with similar GSH activity and TBARS levels (p≥0.05; n=8-10). Caesarean sections were performed on the gestational day 20, showing a higher body and liver weights in both gender of SF-OT-exposure F1 pups (p≤0.05; n=12-32). Hepatic TG (CON:204.6±21.5 vs SF:232.4±51.8 vs SFOT: 397.0±21.7 mg/dL; p≤0.01) and Chol (CON:44.0±2.1 vs SF:38.0±6.2 vs SF-OT:62.5±7.0 mg/dL; p≤0.01; n=5-8) levels were raised in the ST-OT-exposed F1 female pups. However, an higher in the hepatic TG levels was observed in the ST-OT-exposed F1 male pups (CON:245.9±30.4 vs SF:252.4±19.2 vs SF-OT: 386.1±29.1 mg/dL; p≤0.01; n=5-8). Both gender of ST-OT-exposed pups, a lower GSH activity and higher TBARS levels was observed in the liver (p≤0.05; n=8-10). Thus, ST-OT exposure disrupted the reproductive tract proper functioning leading to PCOS features, as well as placental dysfunction in F0 generation. This work supports the hypothesis that ST-OT produced transgenerational effects on the body weight, hepatic oxidative stress and fat depot in F1 generation.

 

Nothing to Disclose: PLP, EM, JFPA, LCF, MBC, LM, IVS, JBG