Tributyltin chloride disrupts aortic vascular reactivity and increases reactive oxygen species production in female rats

• Published in: Environmental science and pollution research international 2017-11, Vol.24 (31), p.24509-24520
• Main Authors: Ximenes, Carolina Falcão, Rodrigues, Samya Mere Lima, Podratz, Priscila Lang, Merlo, Eduardo, de Araújo, Julia Fernandez Puñal, Rodrigues, Lívia Carla Melo, Coitinho, Juliana Barbosa, Vassallo, Dalton Valentim, Graceli, Jones Bernardes, Stefanon, Ivanita
• Format: Article
• Language: English
• Subjects: 17β-Estradiol; Acetylcholine; Allopurinol; Animals; Antifouling substances; Aorta; Aorta - drug effects; Aquatic Pollution; Arginine; Atmospheric Protection/Air Quality Control/Air Pollution; Atrophy; Bioaccumulation; Butyltin; Cardiovascular diseases; Cardiovascular system; Catalase; Chlorides; Collagen; Contaminants; Earth and Environmental Science; Ecotoxicology; Endothelium; Endothelium, Vascular - drug effects; Environment; Environmental Chemistry; Environmental Health; Environmental Pollutants - adverse effects; Environmental science; Exposure; Female; Females; Genotoxicity; Health risks; Immunotoxicity; Marine sediments; Neurotoxicity; NG-Nitroarginine methyl ester; Nitric oxide; Organotin compounds; Oxidative stress; Oxidative Stress - drug effects; Random Allocation; Rats; Rats, Wistar; Reactive oxygen species; Reactive Oxygen Species - metabolism; Reactivity; Research Article; Risk factors; Rodents; Sediments; Sex hormones; Superoxide dismutase; Teratogenicity; Trialkyltin Compounds - adverse effects; Tributyltin; Waste Water Technology; Water Management; Water Pollution Control
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-017-0061-8

Organotin compounds, such as tributyltin (TBT), are environment contaminants that induce bioaccumulation and have potential toxic effects on marine species and mammals. TBT have been banned by the International Maritime Organization in 2003. However, the assessment of butyltin and metal contents in marine sediments has demonstrated high residual levels of TBT in some cases exceeding 7000 ng Sn g −1 . The acceptable daily intake (ADI) level for TBT established by the World Health Organization is 0.5 μg/kg bw/day is based on genotoxicity, reproduction, teratogenicity, immunotoxicity, and mainly neurotoxicity. However, their effect on the cardiovascular system is not well understood. In this study, female rats were exposed to 0.5 μg/kg/day of TBT for 15 days with the goal of understanding the effect of TBT on vascular function. Female Wistar rats were treated daily by gavage and divided into control ( n  = 10) and TBT ( n  = 10) groups. The aortic rings were incubated with phenylephrine in both the presence and absence of endothelium. The phenylephrine concentration–response curves were generated by exposing endothelium-intact samples to N G -nitro- l -arginine methyl ester (L-NAME), apocynin, superoxide dismutase (SOD), catalase, tiron, and allopurinol. Acetylcholine (ACh) and sodium nitroprusside (SNP) were used to evaluate the relaxation response. Exposure to TBT reduced serum 17β-estradiol E 2 levels and increased vascular reactivity. After incubation with L-NAME, the vascular reactivity to phenylephrine was significantly higher. Apocynin, SOD, catalase, and tiron decreased the vascular reactivity to phenylephrine to a significantly greater extent in TBT-treated rats than in the control rat. The relaxation induced by ACh and SNP was significantly reduced in TBT rats. Exposure to TBT induced aortic wall atrophy and increased superoxide anion production and collagen deposition. These results provide evidence that exposing rats to the current ADI for TBT (0.5 μg/kg) for 15 days induced vascular dysfunction due to oxidative stress and morphological damage and should be considered an important cardiovascular risk factor.