Abstract

Bisphenol A is a widely used compound found in large amount of consumer products. As concerns have been raised about its toxicological and public health effect, the use of alternatives to bisphenol A are now increasing. Bisphenol S is one of the analogues being used as a replacement for bisphenol A despite the fact that little is known about the effects of bisphenol S on living organisms. In this study, we investigated the potential endocrine and genotoxic effects of bisphenol A and bisphenol S in juvenile brown trout (Salmo trutta). The fish were exposed to the compounds for either 2 weeks or 8 weeks via sustained-release cholesterol implants containing doses of 2 mg/kg fish or 20 mg/kg fish of the substances. The effects on the thyroid hormone levels and the estrogenic disrupting marker vitellogenin were evaluated, along with the genotoxic markers micronucleated cells and erythrocyte nuclear abnormalities. An increase in plasma vitellogenin was observed in fish exposed to the high dose of bisphenol A for 2 weeks. At this experimental time the level of the thyroid hormone triiodothyronine (T3) in plasma was elevated after bisphenol S exposure at the high concentration, and paralleled by an increase of micronucleated cells. Moreover, bisphenol A induced an increase of micronuclei frequency in fish erythrocytes after the exposure at the lowest dose tested. Taken together the results indicate that both bisphenol A and its alternative bisphenol S cause endocrine disrupting and genotoxic effects in brown trout, although suggesting two different mechanisms of damage underlying bisphenol A and bisphenol S activity.

Highlights

  • Chemicals released into the environment can mimic natural hormones affecting endocrine functions of animals and humans [1], acting as endocrine disrupting chemicals (EDCs)

  • The concentrations of bisphenol A (BPA) and Bisphenol S (BPS) detected in fish liver tissues from both 2 and 8 weeks sampling were a magnitude of more than 2,500 times higher in BPA/BPS-exposed fish compared with controls, which had very low levels, confirming that the sustainedrelease implants were active during the whole experimental period (Table 2)

  • We compared biological effects of BPA and BPS in brown trout exposed to these compounds for 2 and 8 weeks using slow-release implants to attain a chronic exposure to these chemicals

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Summary

Introduction

Chemicals released into the environment can mimic natural hormones affecting endocrine functions of animals and humans [1], acting as endocrine disrupting chemicals (EDCs). Such EDCs may represent a major toxicological and public health issue [2]. The release of BPA from polycarbonates is accelerated by UV light, aging, heating, and contact with acidic or basic compounds [5, 6]. It can leach from plastic products, food and drink packaging contaminating canned food [5, 7, 8]. A large amount of studies, mainly laboratory studies, have demonstrated a long range of biological effects following BPA exposure

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