Long term exposure to tris (2-chloroethyl) phosphate (TCEP) causes alterations in reproductive hormones, vitellogenin, antioxidant enzymes, and histology of gonads in zebrafish (Danio rerio): In vivo and computational analysis.

In aquatic milieus, tris (2-chloroethyl) phosphate (TCEP) was detected as an emerging environmental contaminant. In this study, in vivo experiment and in-silico docking was integrated systematically to explore the toxic mechanisms of TCEP using zebrafish (Danio rerio). Fish (mean weight of 0.24 ± 0.02 g) were exposed to 100 and 1500 µg L-1 concentrations of TCEP for 28 days under the static renewal method. During chronic exposure, plasma steroid hormones such as testosterone (T) and 17ß estradiol (E2), plasma vitellogenin (Vtg) and antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), and lipid peroxidation (LPO) in gonads were significantly (P < 0.05) altered in TCEP exposed group (1500 µg L-1) compared to the control group. However, the alterations of these parameters were not significant on the 14th day (except Vtg and GR in testis) in 100 µg L-1 of TCEP exposed groups. There were no significant differences (p > 0.05) in the growth parameters comparing TCEP exposed groups with the control group. The gonads of fish exposed to TCEP showed significant histopathological changes when compared to the control groups. A docking study observed that TCEP possessed binding affinity with the estrogen receptor (ERß) and androgen receptor (AR). These data indicate that TCEP at tested concentrations adversely affects the aquatic organisms.

Synthesis and characterization of palladium nanoparticles by chemical and green methods: A comparative study on hepatic toxicity using zebrafish as an animal model.

Nanoparticles synthesized by chemical methods are of a matter of concern, whereas, the green methods are said to be eco-friendly and environmentally safe. In this study, the toxicity of palladium nanoparticles (Pd NPs) synthesized through chemical co-precipitation and green route method using Annona squamosa seed kernels (As-Pd NPs) were evaluated using zebrafish as an animal model. The synthesized nanoparticles (NPs) were characterized using UV-Visible spectroscopy, Field Emission Scanning Electron Microscopy (FE-SEM), Energy Dispersive X-ray (EDX), Fourier Transform Infrared Spectroscopy (FTIR), Dynamic Light Scattering (DLS) and Zeta potential. Zebrafish (Danio rerio) were exposed to 0.4 ng/L of Pd NPs and As-Pd NPs for 96-h, further oxidative stress parameters and histological changes were evaluated. The superoxide dismutase (SOD), catalase (CAT) activity and the lipid peroxidation (LPO) levels were elevated in the Pd NPs groups. But in the As-Pd NPs group, the SOD activity showed a biphasic nature while the CAT activity gradually declined till the 96-h compared to the control and Pd NPs groups. The LPO levels in the As-Pd NPs groups showed a measurable increase till 72-h and sudden decline at the end of 96-h. Anomalies in the histological changes such as ruptured hepatocytes, sinusoidal congestion, vacuolation and accumulation of erythrocytes were observed in both the NPs treated groups but As-Pd NPs exhibited lesser lesions than the control and Pd NPs groups. However, our present study reveals the possible reliability of the nanoparticles and the mechanism of scavenging activity suggesting that the As-Pd NPs synthesized by green route are less toxic comparing to the chemically synthesized Pd NPs.

In vivo evaluation of Nano-palladium toxicity on larval stages and adult of zebrafish (Danio rerio).

The existence and usage of nano-sized palladium (nano-Pd) as catalytic promoters among industries and researchers have been laid a way to explore the release of nano-Pd particles into the aquatic environment, bio-accumulating in living organisms. However, the data on fate and toxicity in response to nano-Pd on aquatic organisms are very limited. Herein, we report the concentration-specific toxicity of nano-Pd in zebrafish (Danio rerio). Nano-Pd was synthesized and characterized by Field Emission Scanning Electron Microscopy (FE-SEM), Dynamic Light Scattering (DLS) and Zeta potential. To determine the in vivo toxicity of nano-Pd, the 96 hpf larvae and the adult zebrafish were treated with two (22 and 0.4 ng/L) environmental relevant concentrations. High doses of nano-Pd influenced the hatching rate, embryo survival, heartbeat and teratological anomalies in the 96 hpf larvae. Reactive oxygen species (ROS) and apoptosis were also influenced by nano-Pd exposure while the acetylcholinesterase (AChE) activity was declined in a dose dependent manner. In long-term exposure (42 days), the adult fish showed erratic movements in swimming pattern inhibiting the AChE activity in both the concentrations of brain and liver. The antioxidant enzyme activity such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR) and lipid peroxidation (LPO), showed a significant change (P < 0.05) indicating that oxidative stress was induced by nano-Pd. Similarly, nano-Pd also induced histopathological lesions in gill, liver and brain providing an insight of fate and toxicity of nano-Pd in the aquatic environment. Our study contributes a significant mechanism to understand the toxicity concern of nano-Pd in the aquatic environment.

Responses of Cirrhinus mrigala to second-generation fluoroquinolone (ciprofloxacin) toxicity: Assessment of antioxidants, tissue morphology, and inorganic ions.

Ciprofloxacin drugs are a second-generation fluoroquinolone highly prescribed medication against various bacterial infections in human and aquaculture practices. These drugs are chemically designed to persist in the body long enough to achieve target objectives. Extensive usage has resulted in ciprofloxacin becoming a ubiquitous contaminant in the environment. Unfortunately, the ecotoxicological profiles for ciprofloxacin are scanty. This study was aimed to assess the ecotoxicity of ciprofloxacin at environmentally relevant concentrations (1 µg/L, and 1.5 µg/L) to a cultivable fish Cirrhinus mrigala. Responses of antioxidant enzymes, histological anomalies, and inorganic ion levels were studied. SOD activity in gill, liver, and kidney tissues was elevated in ciprofloxacin-exposed groups when compared with the control group. CAT activity was predominantly decreased in ciprofloxacin treated groups relative to the control group. GST activity in the ciprofloxacin treated groups was increased (except kidney tissues [Treatment I (1 µg/L)], and gill tissues fifteenth day) significantly (p < .05). The LPO level was elevated in the ciprofloxacin treatment groups throughout the study period (except Treatment II (1.5 µg/L) tenth day in kidney tissues). A series of histological anomalies were noticed in the gill, liver, and kidney tissues of the ciprofloxacin treated groups. Ciprofloxacin exposure caused a significant decrease of sodium, potassium, and chloride levels in the plasma of C. mrigala. A parallel among an imbalanced oxidative defense system, tissue structural changes, and alterations of plasma inorganic ions could be considered as a reliable biomarker for antibiotic toxicity study. This study could be a primary platform for further toxicity studies to understand the potential molecular impacts and adverse effects of ciprofloxacin on aquatic organisms.

Biochemical responses of a freshwater fish Cirrhinus mrigala exposed to tris(2-chloroethyl) phosphate (TCEP).

Freshwater fish Cirrhinus mrigala were exposed to tris(2-chloroethyl) phosphate (TCEP) with three different concentrations (0.04, 0.2, and 1 mg/L) for a period of 21 days. During the study period, thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) levels were significantly (p < 0.05) inhibited. The superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and lipid peroxidation (LPO) levels were increased significantly (p < 0.05) in gills, liver, and kidney tissues, whereas glutathione (GSH) and glutathione peroxidase (GPx) (except liver tissue) activities were inhibited when compared to the control group. Likewise, exposure to TCEP significantly (p < 0.05) altered the biochemical (glucose and protein) and electrolyte (sodium, potassium, and chloride) levels of fish. Light microscopic studies exhibited series of histopathological anomalies in the gills, liver, and kidney tissues. The present study reveals that TCEP at tested concentrations causes adverse effects on fish and the studied biomarkers could be used for monitoring the ecotoxicity of organophosphate esters (OPEs).