Effect of Benzophenone-3 to Acetylcholinesterase and Antioxidant System in Zebrafish (Danio rerio) Embryos (original) (raw)
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Ecotoxicology and Environmental Safety, 2015
Personal care products have been detected in superficial waters, representing an environmental risk to the biota. Some studies indicated that 3-benzophenone (3BP) alters hormones, inducing vitellogenesis and having adverse effects on fish reproduction. Other studies have reported generation of free radicals and changes in antioxidant enzymes. Therefore, the aim of the present study was to test acute exposure to 3BP at concentrations within and beyond that found environmentally to provide important toxicological information regarding this chemical. We evaluated the effect of 3BP on vitellogenin 1 (VTG1) gene expression and the transcription of the enzymes catalase (CAT), superoxide dismutase (SOD) or glutathione peroxidase (GPx), which are involved in cellular redox balance. Zebrafish eluthero-embryos (168 hpf) were exposed to 1,10, 100, 1000 mg/L 3BP, in addition to a negative control and a 0.1% ethanol control for 48 h. The results of our study indicated a positive significant correlation between exposure concentrations and VTG1 expression (r ¼0.986, p¼0.0028) but only 1000 mg/L 3BP produced a significant increase from control. Acute exposure showed no significant differences in transcription levels of CAT, SOD or GPx at the tested conditions. Nevertheless, a trend toward increase in GPx expression was observed as a positive significant correlation (r¼ 0.928, p¼ 0.017) was noted.
Environmental Toxicology and Chemistry, 2011
Bisphenol A (BPA) and nonylphenol (NP) are well-known endocrine-disrupting chemicals (EDCs) present in the aquatic environment, but little is known about their oxidative stress effects on fish embryos. In the present study, we examined the oxidative stress indices and antioxidant parameters of zebrafish embryos after a short-term exposure to various concentrations of BPA, NP, and their mixture (BPA-NP) for 4 h postfertilization (hpf) to 168 hpf. Exposure to the chemicals was found to enhance the production of hydroxyl radicals and lipid peroxidation in a concentration-dependent manner. The content of total glutathione (TG), reduced glutathione (GSH), and oxidized glutathione (GSSH), as well as the activity of antioxidant enzymes including catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase were all significantly inhibited after exposure to BPA, NP, and BPA-NP, indicating the occurrence of oxidative stress. Coexposure to BPA-NP resulted in an additive effect on some antioxidant parameters. In addition, the alkaline phosphatase activity was also significantly inhibited after exposure to BPA, NP, and their mixtures. Our results demonstrated that BPA, NP, and BPA-NP in aquatic systems can affect antioxidant responses in zebrafish embryos. Environ. Toxicol. Chem. 2011;30:233530: -234130: . # 2011
The Embryotoxicity of Some Phenol Derivatives on Zebrafish, Danio rerio
caspian journal of environmental sciences, 2019
The existence of toxicants in ecosystems has been increased dramatically in recent years, especially in aquatic environments. Phenols and chlorinated phenol derivatives are toxic industrial compounds. Phenols and derivatives are known to be environmental contaminants. In the present study, 2,4-Dichlorophenol, 2-Chlorophenol and substituted phenol were tested for embryotoxicity and mortality in a four-day period using zebrafish, Danio rerio embryos. Tested phenol derivatives caused teratogenicity and embryo mortality in the embryos. The semi static 48-h LC50 (median lethal concentration) value for Substituted-phenol was 13.850 mg L-1; the corresponding values for 2-Chlorophenol and 2,4-Dichlorophenol were 8.378 mg L-1 and 6.558 mg L-1, respectively. The endpoints are incomplete eyes, head and tail, heart and chorda deformity, yolk sac edema, tail curvature, shrunken eyes, lordosis, delayed hatching, weak pigmentation, heart edema and non-pigmentation after exposure to the compounds. ...
Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology, 2015
Organophosphate pesticides cause irreversible inhibition of AChE which leads to neuronal overstimulation and death. Thus, dogma indicates that the target of OP pesticides is AChE, but many authors postulate that these compounds also disturb cellular redox processes, and change the activities of antioxidant enzymes. Interestingly, it has also been reported that oxidative stress plays also a role in the regulation and activity of AChE. The aims of this study were to determine the effects of the antioxidant, vitamin C (VC), the oxidant, t-butyl hydroperoxide (tBOOH) and the organophosphate Chlorpyrifos (CPF), on AChE gene transcription and activity in zebrafish embryos after 72 h exposure. In addition, oxidative stress was evaluated by measuring antioxidant enzymes activities and transcription, and quantification of total glutathione. Apical effects on the development of zebrafish embryos were also measured. With the exception of AChE inhibition and enhanced gene expression, limited effects of CPF on oxidative stress and apical endpoints were found at this developmental stage. Addition of VC had little effect on oxidative stress or AChE, but increased pericardial area and heartbeat rate through an unknown mechanism. TBOOH diminished AChE gene expression and activity, and caused oxidative stress when administered alone. However, in combination with CPF, only reductions in AChE activity were observed with no significant changes in oxidative stress suggesting the adverse apical endpoints in the embryos may have been due to AChE inhibition by CPF rather than oxidative stress. These results give additional evidence to support the role of prooxidants in AChE activity and expression.
"GenX" [ammonium perfluoro (2-methyl-3-oxahexanoate] was developed as a replacement chemical for toxic perfluorinated compounds to be used in product manufacturing. Here, we assessed developmental, mitochondrial, and behavioral toxicity endpoints in zebrafish embryos/larvae exposed to GenX. GenX exerted low toxicity to zebrafish embryos/larvae up to 20 mg/L. GenX did not affect mitochondrial oxidative phosphorylation nor ATP levels. ROS levels were reduced in larvae fish exposed to 10 and 100 µg/L, indicative of an antioxidant defense; however, ROS levels were elevated in fish exposed to 1000 µg/L. Increased expression of cox1 and sod2 in Gen-X exposed 7-day larvae was noted. GenX (0.1 or 1 µg/L) altered transcripts associated with neurotoxicity (elavl3, gfap, gap43, manf, and tubb). Locomotor activity of larvae was reduced by 100 µg/L GenX, but only in light periods. Anxiety-related behaviors in larvae were not observed with GenX exposure. These data inform risk assessments for long-lived perfluorinated chemicals of concern.
Biochemical and biophysical research communications, 2018
Sodium benzoate (SB) is a common food preservative. Its FDA described safety limit is 1000 ppm. Lately, increased use of SB has prompted investigations regarding its effects on biological systems. Data regarding toxicity of SB is divergent and controversial with studies reporting both harmful and beneficial effects. Therefore, we did a systematic dose dependent toxicity study of SB using zebrafish vertebrate animal model. We also investigated oxidative stress and anxiety-like behaviour in zebrafish larva treated with SB. Our results indicate that SB induced developmental (delayed hatching), morphological (pericardial edema, yolk sac edema and tail bending), biochemical (oxidative stress) and behavioural (anxiety-like behaviour) abnormalities in developing zebrafish larva. LC of SB induced toxicity was approximately 400 ppm after 48 h of SB exposure. Our study strongly supports its harmful effects on vertebrates at increasing doses. Thus, we suggest caution in the excessive use of th...
Journal of Biochemical and Molecular Toxicology, 2018
To assess the developmental toxicity of trichloroacetate (TCA), zebrafish embryos were exposed to 8 to 48 mM of TCA and evaluated for developmental milestones from 8-to 144-hour postfertilization (hpf). All developmental toxicities are reported in this paper. Embryos were found to have developed edema in response to 16 to 48 mM of TCA exposure at 32-to 80-hpf, experienced delay in hatching success in response to 24 to 48 mM at 80-hpf. Lordosis was observed in developing embryos exposed to 40 to 48 mM at 55-to 144-hpf. The observed toxic effects of TCA exposure were found to be concentration and exposure period independent. Effects were found to be associated with increases in superoxide anion production, but these increases were also found to be concentration and time independent. TCA resulted in concentration-dependent increases in embryonic lethality at 144-hpf, with an LC 50 determined to be 29.7 mM.
Human & Experimental Toxicology, 2020
Cancer continues to be a major cause of mortality globally. Zebrafish present suitable models for studying the mechanisms of genotoxic carcinogens. The aim of this study was to investigate the interaction between oxidant–antioxidant status, apoptosis and immunity in zebrafish that were exposed to three different genotoxic carcinogens methylnitrosourea, dimethylbenzanthracene, benzoapyrene and methylnitrosourea + dimethylbenzanthracene starting from early embryogenesis for 30 days. Lipid peroxidation, nitric oxide levels, superoxide dismutase and glutathione- S-transferase activities and mRNA levels of apoptosis genes p53, bax, casp3a, casp2 and immunity genes fas, tnfα and ifnγ1 were evaluated. The disruption of the oxidant–antioxidant balance accompanied by altered expressions of apoptotic and immunity related genes were observed in different levels according to the carcinogen applied. Noteworthy, ifnγ expressions decreased in all carcinogen-exposed groups. Our results will provide...
Antioxidant Responses and NRF2 in Synergistic Developmental Toxicity of PAHs in Zebrafish
Toxicological Sciences, 2009
Early piscine life stages are sensitive to polycyclic aromatic hydrocarbon (PAH) exposure, which can cause pericardial effusion and craniofacial malformations. We previously reported that certain combinations of PAHs cause synergistic developmental toxicity, as observed with coexposure to the aryl hydrocarbon receptor agonist b-naphthoflavone (BNF) and cytochrome P4501A inhibitor a-naphthoflavone (ANF). Herein, we hypothesized that oxidative stress is a component of this toxicity. We examined induction of antioxidant genes in zebrafish embryos (Danio rerio) exposed to BNF or ANF individually, a BNF 1 ANF combination, and a prooxidant positive control, tert-butylhydroperoxide (tBOOH). We measured total glutathione (GSH) and attempted to modulate deformities using the GSH synthesis inhibitor L-buthionine (S,R)-sulfoximine (BSO) and increase GSH pools with N-acetyl cysteine (NAC). In addition, we used a morpholino to knockdown expression of the antioxidant response element transcription factor NRF2 to determine if this would alter gene expression or increase deformity severity. BNF 1 ANF coexposure significantly increased expressions of superoxide dismutase 1 and 2, glutathione peroxidase 1, pi class glutathione-s-transferase, and glutamate cysteine-ligase to a greater extent than tBOOH, BNF, or ANF alone. BSO pretreatment decreased some GSH levels, but did not worsen deformities, nor did NAC diminish toxicity. Knockdown of NRF2 increased mortality following tBOOH challenge, prevented significant upregulation of antioxidant genes following both tBOOH and BNF 1 ANF exposures, and exacerbated BNF 1 ANF-related deformities. Collectively, these findings demonstrate that antioxidant responses are a component of PAH synergistic developmental toxicity and that NRF2 is protective against prooxidant and PAH challenges during development.
2012
Organic UV filters including benzophenone-3 (BP-3) are widely used to protect humans and materials from damage by UV irradiation. Despite the environmental occurrence of BP-3 in the aquatic environment, little is known about its effects and modes of action. In the present study we assess molecular and physiological effects of BP-3 in adult male zebrafish (Danio rerio) and in eleuthero-embryos by a targeted gene expression approach focusing on the sex hormone system. Fish and embryos are exposed for 14 days and 120 hours post fertilization, respectively, to 2.4-312 μg/L and 8.2-438 μg/L BP-3. Chemical analysis of water and fish demonstrates that BP-3 is partly transformed to benzophenone-1 (BP-1) and both compounds are accumulated in adult fish. Biotransformation to BP-1 is absent in eleuthero-embryos. BP-3 exposure leads to similar alterations of gene expression in both adult fish and eleuthero-embryos. In the brain of adult males esr1, ar and cyp19b are down-regulated at 84 μg/L BP-3. There is no induction of vitellogenin expression by BP-3, both at the transcriptional and protein level. An overall down-regulation of the hsd3b, hsd17b3, hsd11b2 and cyp11b2 transcripts is observed in the testes, suggesting an antiandrogenic activity. No histological changes were observed in the testes after BP-3 treatment. The study leads to the conclusion that low concentrations of BP-3 exhibit similar multiple hormonal activities at the transcription level in two different life stages of zebrafish. Forthcoming studies should show whether this translates to additional physiological effects.