Search

We investigated changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) activity which is a product of oxidative DNA damage, histopathological changes and antioxidant responses in liver and gill tissues of rainbow trout, following a 21-day exposure to three different concentrations of linuron (30 µg/L, 120 µg/L and 240 µg/L). Our results indicated that linuron concentrations caused an increase in LPO levels of liver and gill tissues ( p < 0.05). While linuron induced both increases and decreases in GSH levels and SOD activity, CAT activity was decreased by all concentrations of linuron ( p < 0.05). The immunopositivity of 8-OHdG was detected in the hepatocytes of liver and in the epithelial and chloride cells of the secondary lamellae of the gill tissues. Our results suggested that linuron could cause oxidative DNA damage by causing an increase in 8-OHdG activity in tissues, and it induces histopathological damage and alterations in the antioxidant parameters of the tissues.

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., (Copyright © 2016 Elsevier Ltd. 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.

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. [Display omitted] • We evaluated transcriptional changes in fish brain after high water temperature. • High temperature stress lead physiological changes in the fish brain. • High water temperature stress leads physiological changes by causing transcriptional fluctuations in the fish brain. [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]

The toxicity of sodium carboxymethyl cellulose (CMC), which has GRAS status and has been determined as "ADI non specified", was re-evaluated with a new modelling and molecular-based data. For this purpose, CMC, a food additive, was injected to the yolk sac (food) of the zebrafish embryo by the microinjection method at the 4th hour of fertilization at different concentrations. As a result, it was found that CMC showed no toxic effects within the framework of the parameters studied. But, we determined increasing lipid accumulation in zebrafish embryos exposed to CMC in a dose-dependent manner. To elucidate the mechanism underlying this lipid accumulation, the expression levels of genes related to obesity-linked lipid metabolism were examined. Our findings show that while CMC does not cause a toxic effect in zebrafish embryos, it can lead important effects on lipid metabolism by causing changes in the expression of some genes associated with obesity. Unlabelled Image • The toxicity of CMC was evaluated using a new modelling. • No teratogenic and neurotoxic effects of CMC were detected in zebrafish embryos. • But, this study contains strong evidence that CMC can trigger obesity. [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]

Eprinomectin (EPM), a member of avermectin family, is a semi-synthetic antibiotic. It has been known that avermectin family enters the aquatic environments and adversely affects the aquatic organisms. Effects of EPM is fully unknown in aquatic organisms especially fish, thus the aim of the present study was to investigate transcriptional changes ( sod, cat, gpx) and activities of some antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA) levels, oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)) and transcriptional changes of heat shock protein 70 (HSP70), and cytochromes P4501A (CYP1A) in liver tissues of rainbow trout exposed to sublethal EPM concentration (0.001 μg/L, 0.002 μg/L, 0.01 μg/L, 0.05 μg/L) for 24 h, 48 h, 72 h and 96 h. The decrease in antioxidant enzyme (SOD, CAT and GPx) activity, transcriptional changes ( sod, cat, gpx , HSP70 and CYP1A genes) and increase in MDA level and activity of 8-OHdG in a dose–time-dependent manner in the liver of rainbow trout were observed. The down-regulated of antioxidant ( sod, cat and gpx ), HSP70 and CYP1A obviously, the severity of which increased with the concentration of EPM and exposure time. The results imply that EPM could induce oxidative damage to the liver tissue of rainbow trout. The information presented in this study is helpful to understand the mechanism of veterinary pharmaceuticals–induced oxidative stress in fishes. [ABSTRACT FROM AUTHOR]