Effects of triclosan on Japanese medaka (Oryzias latipes) during embryo development, early life stage and reproduction

Abstract

Triclosan has been shown to have endocrine-disrupting effects in aquatic organisms. In 2016, the US Food and Drug Administration banned the use of triclosan in consumer soaps. Before the ban, triclosan was reported at low concentrations in the aquatic environment, although the effect of triclosan on reproduction in teleost fish species is yet to be clarified. Here we investigated the effects of triclosan on embryo development and reproduction, and during the early life stage, in Japanese medaka (Oryzias latipes) by using Organisation for Economic Co-operation and Development tests 229, 212 and 210, with minor modifications. In adult medaka, exposure to 345.7 μg l suppressed fecundity and increased mortality but had no effect on fertility. Exposure to 174.1 or 345.7 μg l increased liver vitellogenin concentration in females but decreased liver vitellogenin concentration in males. With triclosan exposure, mortality was increased dose dependently during the embryonic and early larval stages, and a particularly steep increase in mortality was observed soon after hatching. The lowest observed effect concentrations of triclosan in Japanese medaka obtained in the present study (mortality [embryonic and larval stages, 276.3 μg l ; early life stage, 134.4 μg l ; adult stage, 174.1 μg l ], growth [134.4 μg l ], vitellogenin [174.1 μg l ], fecundity [345.7 μg l ] and fertility [>345.7 μg l ]) were at least 55 times (compared with the USA) and up to 13 400 times (compared with Germany) greater than the detected triclosan levels in the aquatic environment. These results suggest that triclosan may not be affecting fish populations in the aquatic environment.

The non‐steroidal anti‐inflammatory drug diclofenac sodium induces abnormal embryogenesis and delayed lethal effects in early life stage zebrafish (Danio rerio)

“…This study suggests that it is necessary to investigate not only the embryo stage (when various organs and tissue are formed) but also the influence after hatching (when all organs and biological functions are working normally), to evaluate accurately the influence of diclofenac. In addition, it has been previously demonstrated that the embryonic and larval stages of zebrafish have different sensitivities to toxic chemicals (Horie, Yamagishi, Koshio, et al, ; Horie, Yamagishi, Takahashi, et al, ; Mu et al, ; Yang et al, ). Furthermore, we revealed that triclosan exposure also negatively affects with a particularly steep increase in mortality soon after hatching in O. latipes (Horie, Yamagishi, Takahashi, Shintaku, et al, ).…”

“…Recently, toxicity testing using zebrafish embryos has been recommended from the point of view of animal welfare (EU, ). Ecotoxicological assays using zebrafish are increasingly used to clarify whether environmental chemicals induce abnormal embryogenesis because this effect is often induced at exposures lower than those are that cause lethal effects (Horie, Yamagishi, Koshio, et al, ; Horie, Yamagishi, Takahashi, et al, ). Indeed, there are reports that diclofenac induces abnormal embryogenesis in zebrafish (Chen et al, ; Horie, Yamagishi, Koshio, et al, ; Ribeiro et al, ).…”

“…Previously, we demonstrated that the embryonic and larval stages of zebrafish have different sensitivities to toxic chemicals,i.e., a particularly steep increase in mortality after hatching (Horie, Yamagishi, Koshio, et al, ; Horie, Yamagishi, Takahashi, et al, ), possibly because the chorion blocks the transport of certain chemical compounds into eggs (Kim & Tanguay, ; Olivares, Field, Simonich, Tanguay, & Sierra‐Alvarez, ). Morphological abnormalities at the embryo stage have been shown to be induced by various chemicals in zebrafish, and these abnormalities can lead to delayed development or mortality (Almond & Trombetta, ; Bonventre, White, & Cooper, ; Di Paolo et al, ; Horie, Yamagishi, Koshio, et al, ; Horie, Yamagishi, Takahashi, et al, ; Melo et al, ; Mu et al, ; Vergauwen et al, ; Yang et al, ). This suggests that morphological abnormalities at the embryo stage may be suitable endpoints for predicting the lethal effects of environmental chemicals after hatching.…”

Assessment of triclosan impact on enzymatic biomarkers in an Indian major carp, Catla catla

“…Earlier findings have indicated that the TCS is highly toxic to aquatic organisms. It was reported that TCS cause developmental anomalies with embryotoxicity and biochemical changes, bioaccumulation, endocrine disruption, and reproductive effects in Japanese medaka (Foran, Bennett, & Benson, 2000;Horie, Yamagishi, Takahashi, Iguchi, & Tatarazako, 2017;Ishibashi et al, 2004) and zebrafish (Falisse, Voisin, & Silvestre, 2017;Oliveira, Domingues, Grisolia, & Soares, 2009). In male medaka (Foran et al, 2000), triclosan has been shown to exhibit changes in fin length and sex ratios, suggesting that triclosan has a weak androgenic effect.…”

Physiological and biochemical effects of triclocarban stress on freshwater algae

“…Due to the persistence and toxicity of TCC, its aquatic ecotoxicity has attracted wide attention [4]. In recent years, its toxic effects, such as inhibitory effects on growth and development, endocrine disruption, and reproductive toxicity, have caused great concerns [5][6][7][8][9][10][11]. Several studies provided evidence that TCC interferes with biological receptors in vitro, including a stably transfected aryl hydrocarbon receptor (AhR)-, androgen receptor (AR)-, or estrogen receptor (ER)responsive firefly luciferase reporter gene that responds to chemicals that can bind to and/or activate the respective receptor [12].…”