Triclosan (TCS) and its two derivatives (2,4-dichlorophenol and 2,4,6-trichlorophenol) are priority pollutants that coexist in aquatic environments. Joint exposure of TCS, 2,4-dichlorophenol and 2,4,6-trichlorophenol, hereafter referred to as TCS-DT, contributes severe toxicity to aquatic organisms. There is currently a paucity of data regarding TCS-DT molecular toxicity, especially on cardiac diseases. We used zebrafish (Danio rerio) as a model organism, and evaluated the molecular-level cardiotoxicity induced by TCS-DT from embryonic to adult stages. TCS-DT exposure prominently led to phenotypic malformations, such as pericardial cysts, cardiac bleeding, increased SV-BA distance, decreased heart rate and reduced ejection fraction, as well as abnormal swimming behavior. Analyses of the GO and KEGG pathways revealed enrichment pathways related to cardiac development and screened for significantly down-regulated adrenaline signaling in cardiomyocytes. The cardiac marker genes (amhc, cmlc2, vmhc, and nkx2.5) were obtained through protein-protein interaction (PPI) networks, and expressed as down-regulation by WISH. After chronic exposure to TCS-DT from 30 to 90-dpf, both body mass and heart indexes prominently increased, showing myocardial hypertrophy, abnormal heart rate and histopathological injury. Heart tissue damage included disordered and ruptured myocardial fibers, broken and dissolved myofilaments, nuclear pyknosis, mitochondrial injury and inflammatory cell infiltration. Further, abnormal changes in a series of cardiac functions-related biomarkers, including superoxide dismutase, triglyceride, lactate dehydrogenase and creatinine kinase MB, provided evidence for cardiac pathological responses. These results highlight the molecular mechanisms involving TCS-DT induced cardiac toxicity, and provide theoretical data to guide prevention and treatment of pollutant-induced cardiac diseases.

Acrylamide (ACR), an environmental toxin though being investigated for decades, remains an enigma with respect to its mechanism/site of actions. We aim to explicate the changes in cerebral ganglions and giant fibers along with the behavior of worms on ACR intoxication (3.5–17.5 mg/mL of medium/7 days). Neurotransmitter analysis revealed increased levels of excitatory glutamate and inhibitory gamma amino butyrate with reduced levels of dopamine, serotonin, melatonin, and epinephrine (p < 0.001). Scanning electron microscopy showed architectural changes in cerebral ganglions at 3.5 mg/mL/ACR. The learning behavior as evidenced by Pavlovian and maze tests was also altered well at 3.5 mg/mL of ACR. Electrophysiological assessment showed a reduction in conduction velocity of the medial and lateral giant nerve fibers. We speculate that the observed dose/time-dependent changes in neurotransmission, neurosecretion, and conduction velocity on ACR intoxication at 17.5 mg/ml, possibly, could be due to its effect on nerve fibers governing motor functions. The bioaccumulation factor in the range of 0.38–0.99 mg/g of ACR causes a detrimental impact on giant fibers affecting behavior of worm. The observations made using the simple invertebrate model implicate that the cerebral ganglionic variations in the worms may be useful to appreciate the pathology of the neurological diseases which involve motor neuron dysfunction, esp where the availability of brain samples from the victims are scarce.

The aim of the present study was to verify if cocaine, at environmental concentrations, influences the endocrine system of the European eel. Silver eels (a stage of the eel life cycle preparing the fish for the oceanic reproductive migration) were exposed to a nominal cocaine concentration of 20 ng/l during 30 days; at the same time, control, carrier, and postexposure recovery groups were made. The effects of cocaine were observed in (1) brain dopamine content, (2) plasma catecholamine levels (dopamine, norepinephrine, and epinephrine), (3) pituitary–adrenal axis activity [plasma adrenocorticotropic hormone (ACTH), corticosterone, cortisol, and aldosterone levels], and (4) pituitary–thyroid axis activity [plasma thyroid-stimulating hormone (TSH), triiodothyronine, and thyroxine levels]. In the treated group, brain dopamine, plasma catecholamines, cortisol, and TSH levels were higher, whereas ACTH, corticosterone, and triiodothyronine levels were lower than controls. In the postexposure recovery group, brain dopamine, plasma dopamine and epinephrine, and thyroxine levels further increased, whereas plasma norepinephrine, cortisol, and corticosterone levels were similar to treated values. Finally, ACTH and TSH were similar, whereas triiodothyronine levels were lower than controls. Aldosterone levels were unaffected by cocaine exposure. The results of the present study show that cocaine, at environmental concentrations, behaves like an endocrine disruptor changing brain dopamine and plasma catecholamine levels and the activity of pituitary–adrenal/thyroid axes. Since the endocrine system plays a key role in the metabolic and reproductive processes of the eel, our results suggest that environmental cocaine could be considered another cause for the decline in the European eel.

Bisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present study, isolated rat adipocytes were exposed for 2 h to 1 and 10 nM BPA. Insulin-induced glucose conversion to lipids along with glucose transport was significantly increased in the presence of BPA. However, basal glucose conversion to lipids, glucose oxidation, and formation of lipids from acetate were unchanged in adipocytes incubated with BPA. It was also shown that BPA significantly increases lipolytic response of adipocytes to epinephrine. However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Moreover, BPA did not influence leptin and adiponectin secretion from adipocytes. Our new results show that BPA is capable of disturbing processes related to lipid accumulation in isolated rat adipocytes. This is associated with the potentiation of insulin and epinephrine action. The effects of BPA appear already after short-term exposure to low doses of this compound. However, BPA fails to change adipokine secretion.