Search

The toxic effects of microplastic (MP) pollution, which is a growing threat to the aquatic ecosystem, are constantly recorded by scientific reports at the organism and cellular levels. Despite this, the action mechanism of MP toxicity remains ambiguous. This research was designed to investigate the interactions with multiple biomarkers in the tissues of Oncorhynchus mykiss exposed to polyethylene microplastics (MPs-PE) under controlled conditions. In this context, fish were fed with MP-PE added feeding at different levels [MP-PE-I (10%) and MP-PE-II (20%)]. It was aimed to elucidate the MP abundance in gills, gastrointestinal system, on growth and hematological indexes in fish, as well as possible oxidative, DNA damage in target tissues (brain, gill, liver and muscle) and a number of biochemical events underlying apoptosis. MPs-PE tested at different concentrations led to changes in growth parameters and hematologic indices in fish. In all tissues targeted for the follow-up of oxidative stress, inhibitions in GSH levels and antioxidant enzyme activities were determined, while MDA, ROS, DNA damage and apoptosis significantly changed the expression profile upwards. MPs-PE significantly inhibited neurotransmission in rainbow trout. In conclusion, the outcomes of this study revealed that MPs-PE induced dose-dependent ROS-mediated apoptotic responses/ DNA damage in rainbow trout. The data are also a first record for rainbow trout and will help unravel different mechanisms with the potential to model for other MPs-PE-based toxicity studies. [Display omitted] [ABSTRACT FROM AUTHOR]

Although nickel (Ni) is an important cofactor for various enzymes in biological systems, it can cause serious problems when insufficient or excessive in an organism. Therefore, it is very important to investigate Ni in biological systems, especially in cells with its related pathogenic mechanism. This study was carried out to demonstrate the effects of zingerone (ZO) and rutin (RN) administration against nickel chloride (NiCl 2) toxicity on neurobehavioral performance and brain oxidative status in zebrafish (Danio rerio) embryos/larvae on histological perspective. The experimental design of the study, which included twenty groups of fish, each containing 10 embryos, was prepared as semi-static and the trial continued for 96 hpf. In the obtained findings, it was determined that ZO and RN had a mitigating effect in this toxicity table where Ni caused oxidative stress in zebrafish larvae, induced DNA damage and apoptosis. A similar picture is valid for malformation processes as well as survival and hatching rates. These results showed that nickel is toxic to developing embryos via acting different mechanisms. In conclusion, we observed that ZO and RN have a greater effect on physiology, DNA damage and apoptosis than gross morphology, with a significant ameliorative effect. [ABSTRACT FROM AUTHOR]

We investigated changes in nuclear factor kappa B (NFkB) activity, antioxidant responses and histopathological effects in the liver, gill and kidney tissues of rainbow trout exposed to nickel chloride (Ni). Two different concentrations (1 mg/L and 2 mg/L) were administrated to fish for 21 days. Tissues were taken from all fish for NFkB activity, histopathological examination and determination of superoxide dismutase (SOD), catalase (CAT) enzyme activity and of lipid peroxidation (LPO), and glutathione (GSH) levels. The findings of this study indicated that Ni exposure led to a significant increase in LPO indicating peroxidative damage and antioxidant enzymes SOD and CAT activity in tissues (p < 0.05), but 2 mg/Ni concentration caused a significant decrease in CAT activity in kidney tissues (p < 0.05). One of mechanism in the antioxidant defense system seems to be GSH, which increased in gill and kidney tissues of fish exposed to Ni (p < 0.05). NFkB immunopositivity was detected in all tissues. Ni exposure caused lamellar thickening, cellular infiltration in gill tissues, hydropic degeneration of hepatocytes in liver tissues, hyalinous accumulation within the glomeruli and tubular degeneration in kidney tissues. Our results suggested that Ni toxicity may disturb the biochemical and physiological functions of fish by causing changes in NFkB activity and oxidative and histopathological damage in the tissues of rainbow trout. This study can provide useful information for understanding of Ni-induced toxicity. [ABSTRACT FROM AUTHOR]

Graphene oxide (GO) and their natural/synthetic composites are encouraging tools for humanity. There is a need to address critical challenges and potential risk possibilities in GO-based architectures, which have a wide range of uses. In this study, ecotoxicological levels as well as GO-based nanoparticle synthesis, characterization, interaction mechanism and toxicity detection levels for potential biomedical applications were determined on zebrafish (Danio rerio). The effects of GO-ED-BA NP (graphene oxide-boramidic acid nano particles) which was characterized by FT-IR, SEM, TEM, and BET on survival rate, morphological abnormalities (yolk sac edema, lordosis/kyphosis, pericardial edema, and tail malformation), hatching rate as well as neuronal degeneration /necrosis, 8 OHdG and TNF-α expression were observed in D. rerio embryos and larvae. In the obtained findings, it was determined that the toxicity profile of GO-ED-BA NP appeared similar, in high-dose application with single GO use, causing a cytotoxic, pro-inflammatory response and triggering oxidative stress. However, increased malformation rates and mortality at the highest concentration were due to nanoparticle sizes and GO. The presence of boramidic acid unit on graphene nanostructure changed the GO's toxicity profile and positively directed the proinflammatory and oxidative stress response. Synthesizing of graphene oxide-boramidic acid and its toxicity panels compared to graphene oxide are reported for the first time in this study. [Display omitted] • GO exerted higher oxidative and genotoxic stress on cells than GO-ED-BA. • GO-induced stress increases TNF-α levels. • GO-ED-BA changed the GO's toxicity profile and positively directed the proinflammatory and oxidative stress response. [ABSTRACT FROM AUTHOR]

Acrylamide(AA) is a compound with wide usage areas including paper, dyes, and plastics industries. Due to its broad spectrum and water solubility suggest that this vinyl compound may cause serious environmental problems. AA was shown to exhibit neurotoxic, immunotoxic, reproductive toxicant as well as carcinogenic potency on animals. Especially in recent years, the therapeutic effects of boron and boron containing compounds like borax(BX), ulexite(ULX) and colemanite(COL) had been reported. However, the ameliorative potential by boron compounds against AA-induced toxicities had not been investigated yet. Therefore, in this investigation rainbow trout were exposed acutely to AA in the presence and absence of BX. The hematological indices and genotoxic end-points were examined in the fish blood tissue. In addition to oxidative stress response, the levels of DNA damage, CASP3, TNF-α, Nrf-2 as well as IL-6 amounts were determined in both blood and liver tissues of fish. The obtained results executed that AA induced toxic conditions in both tissues. In fact, an increase in the amount of oxidative stress and ROS, and a decrease in GSH levels were observed. AA exposure led to an increase in CASP3levels and 8-OHdG formation. It was also found that Nrf-2 pathway contributed to the initiation of oxidative stress that associated with AA-induced toxicity. On the contrary, our findings indicated that co-exposure of BX with AA elicited oxidative stress and cell death. In a conclusion BX was suggested as a useful and effective natural agent for the prevention and early treatment of AA toxicity in fish. [Display omitted] • BX significantly attenuated the hematological, genetic and oxidative damage induced by AA. • BX has the potential to be developed as an antioxidant. • BX clearly activating the Nrf-2/ROS signaling pathway. • BX has protective effect against AA. [ABSTRACT FROM AUTHOR]

We investigated apoptotic effects and changes in glucose-6-phosphate dehydrogenase (G6PD) enzyme activity in liver and gill tissues of fish exposed to chlorpyrifos. Three different chlorpyrifos doses (2.25, 4.5 and 6.75 μg/L) were administrated to rainbow trout at different time intervals (24, 48, 72 and 96 h). Acute exposure to chlorpyrifos showed time dependent decrease in G6PD enzyme activity at all concentrations ( p < 0.05). Immunohistochemical results showed that chlorpyrifos caused mucous cell loss in gill tissue and apoptosis via caspase-3 activation in fish. The present study suggested that chlorpyrifos inhibits G6PD enzyme and causes mucous cell loss in gill and apoptosis in gill and liver tissues. [ABSTRACT FROM AUTHOR]

In recent years, therapeutic targets and the development of new drugs have shifted research towards inflammatory and oxidative stress pathways. Ferrocene (FcH) is a stable, small molecule that exhibits immunostimulatory and anti-tumor properties by a different mechanism and is effective at low doses in oral administration. However, it was surprising that there has been no performed investigation using FcH on aquaculture. On the other hand, recent papers reveal the key biological functions and health benefits due to daily boron intake in animals and humans. Therefore, we investigated the neurotoxic damage potential of FcH and its related neurotoxicity action mechanism in aquatic environments. In addition, the protective potential of borax (BX, or sodium borate) were evaluated againt in vivo neurotoxicity by FcH. Neurotoxicity assessment was performed in rainbow trout brain tissue, acutely under semi-static conditions via determining a vide range of parameters including catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) activities as well as glutathione (GSH), myeloperoxidase (MPO), glutathione (GSH), malondialdehyde (MDA levels), DNA damage (8-OHdG), apoptosis (caspase 3), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), nuclear factor erythroid-2 (Nrf-2), acetylcholinesterase (AChE) and brain-derived neurotrophic factor (BDNF) levels. In addition, the LC 50 96 h level of FcH was determined for the first time in rainbow trout in this study. In the obtained results, while FcH caused inhibition in enzyme activities, it showed an inducing effect on MDA, MPO, BDNF, Nrf2, TNF-α and IL-6 levels. It was determined that this oxidative damage related alterations were significantly different (p < 0.05) in comparison between FcH treated and controls. Again, the LC 50 96 h value in rainbow trout was determined as 11.73 mg/L, which is approximately 5% less than the value given for freshwater fish (12.3 mg/L). On the contrary, it was observed that BX has a mitigating effect on FcH-induced neurotoxicity. The present study suggests that borax may be useful for preventing or alleviating neurotoxicity induced by environmental contaminants or toxic chemicals. [Display omitted] • BX has a significant neuroprotective effect on the FcH in fish brain tissue. • BX activating the BDNF/Nrf2 pathway, inhibiting apoptosis and decreasing DNA damage levels. • BX may be useful for preventing or treating brain disorders associated with neuronal damage. [ABSTRACT FROM AUTHOR]

Fish and other fishery products are among the foods recommended for the prevention and treatment of diseases with their high nutritional properties. The demand for fish caviar has increased in recent years due to the increase in fish consumption and their high nutritional and commercial value. In order to meet this increasing demand, caviar substitutes obtained from different fish species have been investigated, however in these limited studies, generally, information about products and markets are provided. In this study, caviar obtained from 30 female rainbow trout (Oncorhynchus mykiss , raised under farm conditions) were processed with different salt concentrations (2, 4 and 8%). Physicochemical [lipid peroxidation (with Thiobarbituric Acid Reactive Substance (TBARS), protein degradation (with Sodium Dodecyl Sulfate - PolyAcrylamide Gel Electrophoresis (SDS-PAGE), color (L*, a*, b*) and salt content of caviar formed by salting process)] and microbiological [total aerobic bacteria (TAB)] quality parameters on certain days of 21-day storage (4 °C) (0., 3., 6., 9., 12., 15., 18., and 21.) was investigated. As a result of the study, the changes in TAB, TBARS, L *, a *, b * values and salinity levels during storage were determined as important (p < 0.05). At the end of storage, it was detected in different profiles as well as phosphoprotein and glycoproteins as major protein groups in the SDS-PAGE analysis. In terms of microbiology, 8% salt concentration was found to be very low compared to control and other salt applications. Considering all the research findings, high salt concentrations were determined to have a positive effect on the preservation of quality. [ABSTRACT FROM AUTHOR]

Imidacloprid (IMI) pesticide has significant environmental and ecotoxicological pollution effects. Also, its high potential to enter the aquatic environment reveals the importance of early evaluation of the toxic effects of this compound. This study aimed to evaluate organ responses that can be associated with outcomes at higher levels of biological organization in fish. In this respect, the toxicity mechanism and recovery response process of IMI in rainbow trout (Oncorhyncus mykiss)' s different tissues (blood, brain, gill and liver) were analyzed with important biomarkers [(hematological indices (RBC, WBC, Hg, Hct, MCV, MCH, MCHC), antioxidant enzyme activities (SOD, CAT, GPx, GSH), MDA, DNA damage (8-OHdG), apoptosis (caspase 3), AChE, TNF α, interleukin 6, Nrf-2, NF-kB activities, histopathological and immunofluorescence analyses (NeuN, BDNF, JNK and Nop10]. Exposure to different concentrations of IMI caused a decrease in RBC, WBC, Hg and Hct levels in O. mykiss. The effect of the same application on brain, gill and liver tissues was determined as inhibitions in antioxidant enzyme activities (SOD, CAT and GPx) and GSH level, inductions on MDA level, DNA damage, caspase-3, TNF α, IL- 6, Nrf-2 and NF-kB activities. As a result of three tissues' histopathological examination; the degeneration, necrosis and hyperemia in the brain and liver, adhesion, desquamation and inflammation in the lamellar epitheliums has been determined in company with stress-induced responses inducing DNA damage. In the reflection of this situation on histomap results, increases were recorded in BDNF and NeuN levels. In the recovery response, tissue damage profile and detoxification process were differentiated according to dose and marker, and it manifested itself with moderate and mild symptoms. These findings revealed that IMI-mediated oxidative stress was effective in the Nrf-2/GSH/NF-kB pathways, showing strong hemato/hepato, and neurotoxic effects. It has become clear that the severity of the effects caused by IMI exposure is felt more in the brain and liver tissues, and that such contaminants should be taken into account in the risk assessment. During the post-exposure recovery period (after 15 days), AChE activity increased by 21% at high-dose administration. The recovery period was effective in regulating the oxidant/antioxidant balance of the organism by exhibiting serious induction/inhibition in each tissue and biomarker performance. [Display omitted] [ABSTRACT FROM AUTHOR]

Fe2+ in ferrocene facilities the oxidation. Based on this phenomenon, increased iron (Fe) level in freshwater ecosystems is thought as an important environmental problem in many geographic regions. In addition to increased mobilization of Fe from sediment due to changes in land use, mining, industrial activity, and elevated acid deposition are also proposed to be possible factors contributing to the increased Fe loading in freshwater environments. Ferrocene is useful in the modern organometallic chemistry industry due to its versatile applications. In this study, the toxicity potential and related toxicity mechanisms of acute ferrocene exposure as well as the protective potential of borax supplementation against ferrocene were investigated in rainbow trout during 96 h under semi-static conditions. In target tissues multiplexed endpoints of hematological indices, genotoxicity, oxidative stress response, DNA damage and apoptosis levels, as well as tumor necrosis factor alpha, and interleukin-6 activities were assessed in blood tissue. In liver tissue, in addition to the parameters studied in blood tissue (except cortisol), the nuclear factor erythroid-2, which regulates the expression of detoxification enzymes, was investigated. When the results obtained from blood analyzes were examined, ferrocen treatment caused different reactions (increase/decrease) in blood indexes, and these findings were confirmed by MN tests. In ferrocene-induced hematoxicite, the healing effect of borax application has been observed to increase inhibited values and decrease in indexes with increasing tendencies. Besides, this hematoxicity was also supported by cortisol increases. Our findings showed that ferrocene inhibited antioxidant enzyme activities and increased lipid peroxidation, 8-OH-dG, caspase 3, TNF-α, and IL-6 levels in both blood and liver tissues. Similarly, cortisol level (in blood tissue) and Nrf-2 level (in liver tissue) increased with ferrocene application. In the ferrocen+borax group, the MDA level decreased 11 % at the end of the 96th hour compared to the 48th hour, and the Nrf2 level increased 9 %. In general, enzyme inhibitions in blood and liver tissues have shown that ferrocen-mediated toxicity occurs in induced ROS, DNA damage, apoptos activity, and BX applications have a positive effect on the correction of toxicity in the direction of hormesis. In a conclusion, the present study suggested that borax migt exhibite ameliorative potential against ferrocene-induced toxicity in O. mykiss blood and liver via regulating the ROS/TNF-α/Nrf-2 pathway. [Display omitted] [ABSTRACT FROM AUTHOR]

In recent years, n-butanol has growing use in many areas, including the food industry. In this study, acute toxic effects of n-butanol to zebrafish (Danio rerio) larvae by applying different concentrations (10, 50, 250, 500, 750, 1000 and 1250 mg/L) to embryos were evaluated. For this purpose the data of oxidative stress, antioxidant - acetyl cholinesterase enzyme activities, malondialdehyde level and apoptosis were taken into consideration. At the end of the 96 h, antioxidant (Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)) and acetylcholinesterase (AChE) enzyme activities were decreased, however lipid peroxidation level, apoptotic cells, and reactive oxygen species increased (p <.05). As a result, it has been observed that high concentrations of n-butanol with its amphiphilic structure causes quite intense toxic effects in zebrafish embryos. Unlabelled Image • n-Butanol induced oxidative stress by promoting ROS production in zebrafish. • It has been found that different doses of n-Butanol induce apoptosis. • n-Butanol caused enzyme inhibition in zebrafish. [ABSTRACT FROM AUTHOR]

Fish, which are in constant contact with water, serve as an important ecological indicator of aquatic environment health. Therefore, in this study, in the name of neural degeneration, thiamethoxam (TMX) insecticide in the cerebral tissue of Oncorhynchus mykiss ; neurotoxic endpoints such as biomarkers of oxidative stress, DNA damage and the status of antioxidant enzymes have been identified. Antioxidant enzyme (CAT, SOD, GPx, GSH) activities were significantly inhibited by TMX administration, and MDA and MPO values increased as a result of the stimulation of ROS (p < 0.05). It was interpreted that ulexite (UX) added to the medium was effective in favor of antioxidants and tried to prevent MDA and MPO levels. It was determined that Nrf-2, one of the inflammation parameters, was inhibited as a result of TMX application, and the supplementation of UX to the medium created merits similar to the no treatment group. In the 48th and 96th hour analyses of cerebral tissue, it was determined that IL-6 and TNF-α values were induced in TMX applied groups and UX tried to inhibit this situation. It was commented that TMX induced DNA damage and apoptosis at 48th–96th h, whereas UX suppressed this situation. The results provide possible in vivo evidence that UX supplements can reduce TMX-mediated oxidative stress and brain damage in O. mykiss brain tissue. [Display omitted] • TMX-mediated stress induced oxidative stress, inflammation and DNA damage in cerebral tissue • Administration with UX suppressed the accumulation of 8-OHdG adducts and caspase-3 levels as compared to only TMX treatment • The results provide possible in vivo evidence that UX supplements can reduce TMX-mediated oxidative stress and brain damage in O. mykiss brain tissue. [ABSTRACT FROM AUTHOR]

Contamination of the aquatic environment with different insecticides is a major concern in the aquatic ecosystem today. For this reason, in the designed study, Thiamethoxam (TMX) for which there is limited information on its negative effects on Oncorhynchus mykiss was investigated, its effects on hematotoxicity, oxidative status, cytotoxicity, DNA damage and apoptotic status indicators in blood/liver tissue. However, the antitoxic potential of ulexite (UX) supplementation in the elimination of TMX-mediated toxicity has been determined. LC 50- 96h value determined for TMX 0.73 mg/L has been determined. As a result of hematology profile, TMX application, RBC, Hgb and Hct values showed a temporal decrease compared to the control group, while increases were determined in MCV, MCH and MCHC values. It was determined that the inhibition/induction of hematological parameters was slowed down by adding UX to the medium. During the trial (48th and 96th hours), it was noted that TMX induced cortisol level, while UX supplementation slowed this induction at 48th hour. Antioxidant enzyme activities were significantly inhibited by TMX application, and MDA and MPO values increased as a result of the stimulation of ROS. It was determined that UX added to the medium showed activity in favor of antioxidants and tried to inhibit MDA and MPO levels. When Nrf-2, one of the inflammation parameters, was compared with the administration and control groups, it was determined that it inhibited depending on time, TNF-α, IL-6, DNA damage and apoptosis were induced, and UX suppressed this situation. The results obtained were evaluated as statistically meaningful. Briefly, it was determined that TMX induced oxidative damage in all tissues at 48th - 96th hours, whereas UX mitigated this situation. The results provide possible in vivo evidence that UX supplements can reduce TMX-mediated oxidative stress and tissues damage in O. mykiss blood and liver tissues. • UX conferred a protection against TMX induced toxic insults in fish. • UX suppressed the accumulation of 8-OHdG adducts and caspase-3 levels as compared to TMX treatment. • UX exerted significant protection potency against TMX induced hematotoxic, oxidative, and cytotoxic damages. • UX could be a new source of natural protective agents in environment. [ABSTRACT FROM AUTHOR]

Abstract: The aim of this study was to investigate the therapeutic effect of N-acetylcystein (NAC) against oxidative stress induced by Cypermethrin pesticide in rainbow trout (Oncorhynchus mykiss). The experiment was designed as 5 groups (A, B, C, D, and E). Group A was organized as control group and had no treatment. The other groups were treated with Cypermethrin for 14 days. At the end of this period, Groups B (1.0 mM NAC) and D (0.5 mM NAC) was performed with NAC for 96 h. Group C was not administered NAC, the recovery process was evaluated with this group. Group E was exposed to cypermethrin during 14 days and sampled. Acetylcholinesterase (AChE), malondialdehyde (MDA), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), paraoxonase (PON), arylesterase (AR), myeloperoxidase (MPO) activities, oxidative DNA damage (8-hydroxy-2′-deoxyguanosine (8-OHdG)), caspase-3 levels, and trace elements contents analyses were performed in all fish brains. According to the results, MDA, MPO, 8-OHdG and caspase-3 levels were significantly decreased compared to the other groups (pesticide and recovery) (p < 0.05), AChE, SOD, CAT, GPx, PON, and AR activities increased (p < 0.05). In brain tissue, no statistically significant difference was observed in trace element analysis of all application groups. According to the obtained data, the positive effect of N-acetylcysteine on protein synthesis, detoxification, and diverse metabolic functions against cypermethrin toxicity has been more effective in 1.0 mM NAC. NAC has important therapeutic effect on pesticide-induced neurotoxicity for fish in terms of all data. It was concluded that NAC has an antioxidant effect against pesticide-induced oxidative stress and the selected biochemical markers are useful for such studies. Graphical abstract Image 1071 Highlights • A: Control; B: 1.0 mM NAC; C: Recovery; D: 0.5 mM NAC; E: Pesticide treatment. • There is no statistical differences among shown same capital (a, b, c). • The study findings showed that cypermethrin produced neurotoxicity in brain cells by apoptotic ways. • It was concluded that NAC may be a potential antidote in pesticide toxicities according to all parameters researched. [ABSTRACT FROM AUTHOR]

Abstract The aim of this study was to evaluate the effectiveness of borax (BX) against heavy metal exposure on the transcriptional and biochemical reaction in vivo and alleviating effect on gill and liver tissues of rainbow trout. Due to this aim, fish were fed with different level of BX and/or copper (Cu) (1.25, 2.5 and 5 mg/kg of BX; 500 and 1000 mg/kg of Cu) for 21·days in pre- and co-treatment options. The transcriptional parameters [(heat-shock protein 70 (hsp70), and cytochromes P450 (cyp1a), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT))], antioxidant enzyme activities (SOD, CAT and GPx), malondialdehyde (MDA), oxidative DNA damage (8-hydroxy-2′-deoxyguanosine (8-OHdG) and caspase-3 levels were investigated in different tissues samples of treated and control fish. Our results revealed that antioxidant enzyme activity was increased and levels of 8-OHdG, Caspase-3 and MDA were decreased in the BX and BX combined groups as compared to the copper combination group and to copper-only application during pre- and co-treatment (p < 0.05). Similarly, hsp70 and cyp1a gene expressions were decreased after treatment with BX. As conclusion, we suggest that borax itself is not an antioxidant it supportes antioxidant defense mechanism of fish disrupted by heavy metals. Graphical abstract Unlabelled Image [ABSTRACT FROM AUTHOR]

The goal of this study was to determinate toxicity mechanism of biopesticide with antioxidant enzymes parameters such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA) levels, oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)), transcriptional changes of heat shock protein 70 (HSP70), and cytochromes P4501A (CYP1A), sod , cat , and gpx in liver and gill tissues of Oncorhynchus mykiss . For this aim, plant-based (natural pesticides, azadirachtin (AZA)) and synthetic pesticides (deltamethrin (DLM)) were exposed on the fish at different concentrations (0.0005 and 0.00025 ppm of DLM; 0.24 and 0.12 ppm of AZA) for 21 days. According to the results of the study, the activity of SOD, CAT and GPx decreased, but malondialdehyde (MDA) level and activity of 8-OHdG increased in the gill and liver of rainbow trout (p < 0.05). Additionally sod , cat and gpx were down regulated; HSP70 and CYP1A were up regulated for transcriptional observation. The downwards regulation of antioxidant ( sod , cat and gpx ) and the upregulation of HSP70 and CYP1A was obvious with doses of AZA or DLM (p < 0.05). The findings of this study suggest that biopesticide can cause biochemical and physiological effects in the fish gill and liver by causing enzyme inhibition, an increase in 8-OHdG levels and changes in both transcriptional parameters ( sod , cat , gpx , HSP70 and CYP1A). We found that excessive doses of plant-based pesticide are nearly as toxic as chemical ones for aquatic organisms. Moreover, 8-OHdG, HSP70 and CYP1A used as a biomarker to determinate toxicity mechanism of biopesticide in aquatic environment. [ABSTRACT FROM AUTHOR]

Industrial products containing PdCu@GO can gain access to the aquaculture environment, causing dangerous effects on living biota. In this study, the developmental toxicity of zebrafish treated with different concentrations (50, 100, 250, 500 and 1000 μg/L) of PdCu@GO was investigated. The findings showed that PdCu@GO administration decreased the hatchability and survival rate, caused dose-dependent cardiac malformation. Reactive oxygen species (ROS) and apoptosis were also inhibited in a dose-dependent manner, with acetylcholinesterase (AChE) activity affected by nano-Pd exposure. As evidence for oxidative stress, malondialdehyde (MDA) level increased and superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) activities and glutathione (GSH) level decreased due to the increase in PdCu@GO concentration. Our research, it was determined that the oxidative stress stimulated by the increase in the concentration of PdCu@GO in zebrafish caused apoptosis (Caspase-3) and DNA damage (8-OHdG). Stimulation of ROS, inflammatory cytokines, tumor Necrosis Factor Alfa (TNF-α) and interleukin – 6 (IL-6), which act as signaling molecules to trigger proinflammatory cytokine production, induced zebrafish immunotoxicity. However, it was determined that the increase of ROS induced teratogenicity through the induction of nuclear factor erythroid 2 level (Nrf-2), NF-κB and apoptotic signaling pathways triggered by oxidative stress. Taken together with the research findings, the study contributed to a comprehensive assessment of the toxicological profile of PdCu@GO by investigating the effects on zebrafish embryonic development and potential molecular mechanisms. • PdCu@GO decreased the hatchability and survival rate. • PdCu@GO caused dose-dependent cardiac malformation. • ROS, AChE and apoptosis were also inhibited in a dose-dependent manner. • DNA damage, TNF-α and IL-6 were induced by PdCu@GO in zebrafish. • PdCu@GO has effects on zebrafish embryonic development. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

In this study, it has been investigated that the effects of glyphosate, which is a herbicide within organophosphate and unselective widely used in agriculture on enzyme activity of carbonic anhydrase, production of reactive oxygen species, cell apoptosis and body morphology during the embryonic development of zebrafish. To this end, it has been treated embryo with 1, 5, 10 and 100 mg/L gyphosate at 96 h. The embryos treated with glyphosate from 4 hpf were evaluated by considering the survival rates, hatching rates, body malformations under the stereo microscope in 24, 48, 72 and 96th hours. In order to clarify the mechanism of the abnormalities ROS, enzyme activity of carbonic anhydrase and cellular death were detected end of the 96th hour. The data obtained in the present study have shown that glyphosate treatment inhibited CA activity, caused production of ROS especially branchial regions, triggered cellular apoptosis and caused several types of malformations including pericardial edema, yolk sac edema, spinal curvature and body malformation in a dose-dependent manner. As a conclusion, in light of present and previous studies, we can deduce that (1) the probable reason of ROS production was CA inhibition via decreasing of CO 2 extraction and developing respiratory acidosis (however, one needs to clarify), (2) abundance of ROS triggered cellular apoptosis and (3) as a result of cellular apoptosis malformations increased. These data will enable us to further understand potential toxic mechanism of glyphosate on embryonic development stage of zebrafish and may be useful for assessment in the toxicology studies. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 30 μg/L, 120 μg/L and 240 μg/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 240 μg/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. [ABSTRACT FROM AUTHOR]

[Display omitted] • BX can be use for preventing neurological and neurodegenerative as a natural supplement. • AH induced oxidative stress, disrupted the Nrf-2 pathway, and gave rise to neurotoxicity. • BX clearly activating the Nrf-2/ROS signaling pathway. The current study was designed to assess the possible neuroprotective effect of borax (BX) against the toxicity of aluminum hydroxide [AH, Al (OH) 3 ] on brain of rainbow trout (Oncorhynchus mykiss) with multibiomarker approaches. For this purpose, the presence of the neuroprotective action by BX against the AH exposure was assessed by the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), myeloperoxidase (MPO), acetylcholinesterase (AChE). In addition, we evaluated glutathione (GSH), malondialdehyde (MDA), DNA damage (8-OHdG), apoptosis (caspase 3), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), nuclear factor erythroid-2 (Nrf-2), and brain-derived neurotrophic factor (BDNF) levels in 96 h semi-static treatment. In the 48th and 96th hour samplings, apoptosis induced by AH in the Nrf-2/BDNF/AChE pathways in rainbow trout brain tissue was revealed by DNA damage, enzyme inhibitions and lipid peroxidations. On the contrary applications of BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage. BX also increased the BDNF levels and AChE activity. Moreover, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels. It can be concluded that the combination of borax with AH modulated the toxic effects of AH. [ABSTRACT FROM AUTHOR]

The effects of salinity on the fatty acid profiles of liver, gonad, muscle and adipose tissues of rainbow trout (Oncorhynchus mykiss) kept in cages suspended in a seawater (SW) and freshwater (FW), respectively, and fed with the same commercially available diets before marketing, were investigated.In muscle tissue, the effect of salinity (0.17%) was found to be insignificant in terms of the total monounsaturated fatty acid (MUFA), total polyunsaturated fatty acid (n-3, n-6 PUFA) and total saturated fatty acid (SFA), but significant in terms of the eicosapentaenoic acid (EPA)/docosahexaenoic acid (DHA) ratio. In gonad and liver tissues, MUFA and n-3 PUFA were found to be significantly affected by salinity, but not SFA or n-6 PUFA. In adipose tissues, all the parameters were significantly affected by salinity. Also n-3/n-6 PUFA and EPA/DHA ratios were characteristic for FW and SW fish.While the salinity significantly affected the n-3/n-6 ratio in the adipose and liver tissues, it did not have any significant effect in the muscle and gonads. Additionally, the EPA/DHA ratio was found to be significantly affected by the salinity in all the tissues examined. [Copyright &y& Elsevier]

• Low doses of UX did not cause any oxidative stress. • Low doses of UX promoted all enzyme activities in liver of zebrafish. • UX exhibits beneficial roles on blood and liver tissues of zebrafish at lower doses. • This applications did not alter the MN rates in zebrafish erythrocytes. The ulexite (UX), a borate mineral, is used as boron source and commonly used in various industrial processes. The hematological and hepatic effects of UX were investigated by exposing adult zebrafish to UX (5, 10, 20 and 40 mg/L) over 96 hours. The blood and liver tissues were taken at the end of the trial period then micronucleus (MN) rates, oxidative DNA damage (8-OHdG), apoptosis (Caspase-3), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), myeloperoxidase (MPO), paraoxonase (PON), arylesterase (AR) and lipid peroxidation (MDA) levels were determined. Genotoxic damage by UX occurred only at 40 mg/L in the blood MN assay. Oxidative stress, oxidative DNA damage and apoptosis in liver also occurred at this dose. Moreover, 5-20 mg/L doses led to decreases of DNA damage and apoptosis levels via promoting antioxidant system in liver tissues. UX exhibits beneficial roles on blood and liver tissues of zebrafish at relatively lower doses, which may be relevant to nutritional and medicinal industries. [ABSTRACT FROM AUTHOR]