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This study was designed to investigate the potential neuronal damage mechanism of the okadaic acid (OA) in the brain tissues of zebrafish embryos by evaluating in terms of immunofluorescence of Nf KB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG signaling pathways. We also evaluated body malformations. For this purpose, zebrafish embryos were exposed to 0.5 μg/ml, 1 μg/ml and 2.5 μg/ml of OA for 5 days. After application, FITC/GFP labeled protein-specific antibodies were used in immunofluorescence assay for NfKB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG respectively. The results indicated that OA caused immunofluorescence positivity of NfKB, TLR-4, caspase 3, ERK ½, c-FOS and 8-OHdG in a dose-dependent manner in the brain tissues of zebrafish embryos. Pericardial edema (PE), nutrient sac edema (YSE) and body malformations, tail malformation, short tail and head malformation (BM) were detected in zebrafish embryos. These results suggest that OA induces neuronal damage by affecting the modulation of DNA damage, apoptotic, and inflammatory activities in the brain tissues of zebrafish embryos. The increase in signaling pathways shows that OA can cause damage in the structure and function of brain nerve cells. Our results provide a new basis for the comprehensive assessment of the neural damage of OA and will offer enable us to better understand molecular the mechanisms underlying the pathophysiology of OA toxicity., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Water temperature is one of the most important environmental factors affecting the growth and survival of fish. Increased water temperature became a global problem and it is estimated that there will be an increase in water temperature due to global climate change. The physiological mechanism for the effects of high water temperature on the fish brain is not fully known. In the present study, fish were exposed to different temperatures (10 °C/15 °C/20 °C/25°) and brain tissues were sampled 2 h-4h-6h-8h per hour respectively and then we investigated transcriptional changes of BDNF, cFOS, apoptotic genes (caspase 3, Bax, Bcl2), heat shock genes (Hsp70 and Hsp 90) ER-Stress genes (grp78, atf6, and ire1) and oxidative stress genes (CAT, SOD, and GPx) and also immunoflourescence changes of BDNF and cFOSin rainbow trout brain. The results indicated that high temperature stress lead to physiological changes in the fish brain by causing a decrease in mRNA expression levels of CAT, SOD, GPx and Bcl2 and by causing an increase in mRNA expression of BDNF, cFOS, apoptotic genes (caspase 3, Bax), heat shock genes (Hsp70 and Hsp 90) ER-Stress genes (grp78, atf6, and ire1). This study will provide important information to elucidate the physiological mechanisms related to the effects of high water temperature on the fish brain., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

The aim of this study was to investigate neurophysiological responses in rainbow trout brain tissue exposed to natural/botanical pesticides. Fish were exposed to botanical and synthetic pesticides over a 21-day period. At the end of the treatment period, oxidative DNA damage (indicated by 8-OHdG (8-hydroxy-2'-deoxyguanosine), AChE activity (acetylcholinesterase) and transcriptional parameters (gpx (glutathione peroxidase), sod (superoxide dismutase), cat (catalase), HSP70 (heat shock protein 70) and CYP1A (cytochromes P450)) was investigated in control and application groups. Our results indicated that brain AChE activities decreased very significantly in fish treated with both insecticide types when compared with control (p < 0.05). 8-OHdG activity increased in a dose/time-dependent situation in the brain tissues of Oncorhynchus mykiss (p < 0.05). In addition, with regards to gene expression, gpx sod and, cat expressions were down-regulated, whereas CYP1A and HSP70 gene expression were up-regulated in fish treated with both insecticides when compared to the control group (p < 0.05). The data for this study suggests that bio-pesticides can cause neurophysiological changes in fish brain tissue.

In this study, we investigated the potential neuro-toxicological mechanism of the glufosinate in the brain of zebrafish larvae in terms of BDNF and c-Fos proteins by evaluating apoptosis, immunofluorescence BDNF, and c-FOS activation. We also measured survival rate, hatching rate, and body malformations during 96 h exposure time. For this purpose, zebrafish embryos were treated with graded concentrations of dosing solutions (0.5, 1, 3, and 5 ppm) of glufosinate. End of the treatment, acridine orange staining was used to detect apoptotic cells in the brain of zebrafish larvae at 96 hpf. Texas Red and FITC/GFP labeled protein-specific antibodies were used in immunofluorescence assay for BDNF and c-FOS, respectively. The results have indicated that exposure to glufosinate caused to embryonic death, hatching delay, induction of apoptosis, increasing of c-FOS activity and the level of BDNF in a dose-dependent manner. As a conclusion, we suggested that c-Fos might play a role in the regulation of BDNF which responses to prevent the cell from apoptosis even in case of unsuccessful in zebrafish larvae exposed to glufosinate., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Propyl gallate (PG) is a chemical compound obtained by esterification of propanol with gallic acid. Due to its antioxidative properties, it is widely used in cosmetics and pharmaceutical industries as well as to protect the oils in foods such as butter, milk-based desserts, chewing gum, mayonnaise, meat, soups, cereals, spices and seasonings from rancidity. This study has been designed to assessment 8-OHdG and 4-HNE activity, and histopathological changes in the brain tissues of zebrafish larvae, which is a lecithotrophic organism, after 96 h of PG exposure via microinjecting to yolk sac of embryo. To this end, approximately 5 nL of various concentrations of PG (1, 10, and 50 ppm) has been injected into yolk sac of fertilized embryo (final exposure concentrations are 5, 50, 250 pg/egg) with micro manipulator system. After 96 h exposure time, propyl gallate caused immunofluorescence positivity of 8-OHdG and 4-HNE in the brain tissues of zebrafish larvae. PG was not effect brain tissue histopathological in low concentrations (1 and 10 ppm) but highest concentration (50 ppm) caused degenerative changes in brain. These results suggests that PG treatment could lead oxidative DNA damage by causing an increase 8-OHdG and 4-HNE activities. This strategy will enable us to better understand the mechanisms of propyl gallate in brain tissues of zebrafish larvae., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The extensive use of imidacloprid, a neonicotinoid insecticide, causes undesirable toxicity in non-targeted organisms including fish in aquatic environments. We investigated neurotoxic responses by observing 8-hydroxy-2-deoxyguanosine (8-OHdG) activity, oxidative stress and acetylcholinesterase (AChE) activity in rainbow trout brain tissue after 21 days of imidacloprid exposure at levels of (5 mg/L, 10 mg/L, 20 mg/L). The obtained results indicated that 8-OHdG activity did not change in fish exposed to 5 mg/L of imidacloprid, but 10 mg/L and 20 mg/L of imidacloprid significantly increased 8-OHdG activity compared to the control (p < 0.05). An immunopositiv reaction to 8-OHdG was detected in brain tissues. The brain tissues indicated a significant increase in antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)) compared to the control and there was a significant increase in malondialdehyde (MDA) levels (p < 0.05). High concentrations of imidacloprid caused a significant decrease in AChE enzyme activity (p < 0.05). These results suggested that imidacloprid can be neurotoxic to fish by promoting AChE inhibition, an increase in 8-OHdG activity and changes in oxidative stress parameters. Therefore, these data may reflect one of the molecular pathways that play a role in imidacloprid toxicity., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Linuron is a widely used herbicide to control grasses and annual broad leaf weeds. It is known that linuron has toxic effects on different organisms. However, the toxic effects of linuron on aquatic organisms, especially fish, is completely unknown. Thus, we aimed to investigate changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) and nuclear factor kappa B (NFkB) activity, histopathological changes, antioxidant responses and acetylcholinesterase (AChE) activity in rainbow trout brain after exposure to linuron. Fish were exposed to 30μg/L, 120μg/L and 240μg/L concentrations of linuron for twenty-one days. Brain tissues were taken from fish for 8-OHdG and NFkB activity, histopathological examination and determination of superoxide dismutase (SOD), catalase (CAT) enzyme activity, lipid peroxidation (LPO), and reduced glutathione (GSH) levels. Our data indicated that high linuron concentrations caused a decrease in GSH levels, SOD and CAT activities in brain tissues (p<0.05). LPO levels were significantly increased by 240μg/L linuron. All concentrations caused a significant inhibition in brain AChE enzyme activity (p<0.05). Immunopositivity was detected for 8-OHdG and NFkB, and linuron exposure caused histopathological damage to the brain tissues. The results of this study can provide useful information for understanding of linuron-induced toxicity., (Copyright © 2016 Elsevier B.V. All rights reserved.)

The aim of this study was to determine the biochemical, immunohistochemical, and histopathological effects of nickel chloride (Ni) in the rainbow trout brain. Fish were exposed to Ni concentrations (1 mg/L and 2 mg/L) for 21 days. At the end of the experimental period, brain tissues were taken from all fish for c-Fos activity and histopathological examination and determination of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) enzyme activities, lipid peroxidation (LPO), and glutathione (GSH) levels. Our results showed that Ni treatment caused a significant increase in the brain SOD activity and in LPO and GSH levels (p < 0.05), but it significantly decreased AChE and CAT enzyme activities (p < 0.05). Strong induction in c-Fos was observed in some cerebral and cerebellar regions of fish exposed to Ni concentrations when compared with the control group. However, c-Fos activity was decreased in necrotic Purkinje cells. Brain tissues were characterized by demyelination and necrotic changes. These results suggested that Ni treatment causes oxidative stress, changes in c-Fos activity, and histopathological damage in the fish brain.

Chlorpyrifos is widely used to control agricultural pests associated with fruit, nut and vegetable crops, despite its toxic effects and potential brain alterations in aquatic organisms. This study was carried out to determine thein vivoandin vitroeffects of chlorpyrifos on rainbow trout brain acetylcholinesterase (AChE) enzyme activity. The fish were exposed to 2.25 µg/L (25% of 96 h LC50), 4.5 µg/L (50% of 96 h LC50) and 6.75 µg/L (75% of 96 h LC50) of chlorpyrifos for 24, 48, 72 and 96 h.In vitrostudies, inhibition constants (Ki) and half-maximal inhibitory concentration (IC50) values for chlorpyrifos were determined by Lineweaver–Burk graphs and by plotting activity percentage vs. [I], respectively. Enzyme activities were determined by a colorimetric method. In fish exposed to chlorpyrifos 2.25 and 4.5 µg/L, enzyme inhibition was not observed (p> 0.05); however, chlorpyrifos exposure to 6.75 µg/L for 72 and 96 h caused a significant decrease in enzyme activity (p< 0.05). The IC50value of chlorpyrifos was found to be 30 µg/L. These results show that chlorpyrifos may cause direct cellular injury in the brain, and suggest that AChE may be used as a bioindicator for toxicological studies. [ABSTRACT FROM PUBLISHER]

This study was designed to investigate the qualitative and quantitative changes in brain tissue following aluminum chloride (AlCl3) administration and to determine whether boric acid (BA) has a protective effect against brain damage induced by AlCl 3. For this aim, Sprague-Dawley rats were randomly separated into eight groups: (1) control, (2) AlCl3 (5 mg/kg/day), (3, 4 and 5) BA (3.25, 36 and 58.5 mg/kg/day), (6, 7 and 8) AlCl3 (5 mg/kg/day) plus BA (3.25, 36 and 58.5 mg/kg/day). After the animals were killed, the total numbers of neuron in the brain of all groups were determined using an unbiased stereological analysis. In addition to the stereological analysis, all brains were examined histopathologically by using light and electron microscopy. The stereological and histopathological results indicated a high damage of the rat brain tissues in the AlCl3 and AlCl3 + high dose BA (36 and 58.5) treatment groups. However, protective effects on neuron were observed in the AlCl3 + low dose BA (3.25) group when compared other AlCl3 groups. Our stereological and histopathological findings show that low-dose BA, as a proteasome inhibitor, can decrease the adverse effects of AlCl3 on the cerebral cortex. [ABSTRACT FROM AUTHOR]