Modulatory role ulexit against thiamethoxam-induced hematotoxicity/hepatotoxicity oxidative stress and immunotoxicity in Oncorhynchusmykiss.

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. LC50-96h 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.

Evaluation of cholinergic enzymes and selected biochemical parameters in the serum of patients with a diagnosis of acute subarachnoid hemorrhage.

Background: Spontaneous subarachnoid hemorrhage (SAH) is the most severe form of hemorrhagic stroke and accounts for 5-7% of all strokes. Several chemical enzymes and cytokines are thought to cause reactions that may affect the mortality and morbidity of SAH patients. This study aimed to examine the possible relationships between these parameters and the occurrence of SAH and the clinical-radiological parameters in patients with acute SAH. Methods: This study evaluated 44 patients, including 20 with SAH and 24 controls. We obtained blood from the patients and control groups, which was stored in heparinized tubes and used in determining tumor necrosis factor alpha (TNF-α), brain-derived neurotrophic factor (BDNF), acetylcholinesterase (AChE), caspase-3, and butyrylcholinesterase (BChE) enzymes. Results: TNF-α, BDNF, AChE, and BChE enzyme levels were not related to the Glasgow Coma scale (GCS) score in the patient group (p > 0.05), whereas higher enzyme levels of caspase-3 were associated with lower GCS scores (p < 0.05). The difference between the control and patient groups in terms of mean TNF-α levels was statistically significant (p < 0.01). The BDNF levels were statistically insignificant in the patient groups (p > 0.05). Caspase-3, AChE, and BChE levels were significantly different between the control and patient groups (p < 0.01). Conclusions: Our results may be valuable for predicting the prognosis, diagnosis, and follow-up of patients with SAH. However, further studies are required to elucidate the relationship between the clinical and radiological results in patients with SAH and certain enzymes, cytokines, and growth factors.

Has PdCu@GO effect on oxidant/antioxidant balance? Using zebrafish embryos and larvae as a model.

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.

Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain.

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.

Ulexite modulates the neurotoxicological outcomes of acetylferrocene-exposed rainbow trout.

In this study, the neuroprotective action potential by ulexite (UX) (18.75 mg/L) against acetylferrocene (AFC) (3.82 mg/L) induced neurotoxicity was aimed to investigate in brain tissues of Oncorhynchus mykiss. For this purpose, the effects on neurotoxicity markers, proinflammatory cytokines, antioxidant immune system, DNA, and apoptosis mechanisms were assessed on brain tissues in the 48-96  h of the 96- trial period. In this research, it was determined that brain-derived nerve cell growth factor (BDNF) level and acetylcholinesterase (AChE) activity were inhibited in the brain tissue compared to the control group by AFC. In addition, inhibition in glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH) values (which are antioxidant system biomarkers), and inductions in malondialdehyde (MDA) and myeloperoxidase (MPO) amounts (which are indicators of lipid peroxidation) were determined (p < 0.05) after exposure to AFC. And, while tumor necrosis factor-α (TNF-α) and IL-6 levels were increased in the AFC-exposed group, Nrf-2 levels were found to be remarkably decreased. Upregulation was also detected in 8-hydroxydeoxyguanosine (8-OHdG) and caspase-3 levels, which are related to DNA damage and apoptosis mechanism. On the contrary, UX (single/with AFC) suppressed the AChE and BDNF inhibition by AFC. Moreover, UX mitigated AFC-induced oxidative, inflammatory, and DNA damage and attenuated AFC-mediated neurotoxicity via activating Nrf2 signaling in fish. Collectively, our findings revealed that UX supplementation might exert beneficial effects and may be considered as a natural and promising neuroprotective agent against AFC-induced toxicity.

Borax relieved the acrylamide-induced hematotoxic, hepatotoxic, immunotoxic and genotoxic damages in rainbow trout by regulating apoptosis and Nrf2 signaling pathway.

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.

Borax exerts protective effect against ferrocene-induced neurotoxicity in Oncorhynchus mykiss.

BACKGROUND: 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. METHODS: 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 LC50 96 h level of FcH was determined for the first time in rainbow trout in this study. RESULTS: 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 LC50 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. CONCLUSION: The present study suggests that borax may be useful for preventing or alleviating neurotoxicity induced by environmental contaminants or toxic chemicals.

Magnetic nanoparticles-induced neurotoxicity and oxidative stress in brain of rainbow trout: Mitigation by ulexite through modulation of antioxidant, anti-inflammatory, and antiapoptotic activities.

The prevalent exposition of metallic nanoparticles (MNPs) to the aquatic medium and their negative influence on human life is one of the major concerns global. Stress mechanization, as a non-specific and pervasive response, involves all physiological systems, particularly the closely interconnected neuroendocrine and immune systems. In this study, which was designed to obtain more data on the biological effects of ulexit, which prevents oxidative DNA damage by protecting against toxicity damage and offers new antioxidant roles. The concomitant use of ulexite (UX, as 18.75 mg/l) as a natural therapeutic agent against exposure to magnetic nanoparticles (Fe3O4-MNPs/0.013 ml/l) on Oncorhynchus mykiss was investigated for 96 h. The brain tissues were taken at the 48th and 96th hours of the trial period, the effects on neurotoxic, pro-inflammatory cytokine genes, antioxidant immune system, DNA and apoptosis mechanisms were analyzed. In the present study, it was determined that AChE activity and BDNF level in the brain tissue decreased over time in the Fe3O4-MNPs group compared to the control, and UX tried to depress this inhibition. While inhibition was determined in antioxidant system biomarkers (SOD, CAT, GPx, and GSH values), an induction was observed in lipid peroxidation indicators (MDA and MPO values) in Fe3O4-MNPs applied group. The same group data showed that TNF-α, IL-6, 8-OHdG and caspase-3 levels were increased, but Nrf-2 levels were decreased. The alterations in all biomarkers were found to be significant at the p < 0.05 level. In general, it was determined that Fe3O4-MNPs caused stress in O. mykiss and UX exhibited a positive effect on this stress management.

Neurotoxic responses of rainbow trout (Oncorhynchus mykiss) exposed to fipronil: multi-biomarker approach to illuminate the mechanism in brain.

Insecticides have potential to non-target organisms, disrupting the healthy functioning of the aquatic environment as they are the ultimate receptor of the aquatic ecosystem. Insecticides, which are widely used in agriculture, have high neurotoxicity on aquatic organisms. In this study, the acute alterations [catalase (CAT), arylesterase (ARE), malondialdehyde (MDA), myeleperoxidase (MPO), paraoxonase (PON), glutathione peroxidase (GPX), superoxide dismutase (SOD), 8-hydroxy-2-deoxyguanosine (8-OHdG) level, caspase-3 activity, and Acetylcholinesterase (AChE) enzyme activity] caused by the different concentrations of Fipronil (FP) insecticide (0.05, 0.1, and 0.2 mg/L) on rainbow trout (Oncorhynchus mykiss) brain tissue were investigated. It has been determined that superoxide dismutase -catalase - glutathione peroxidase - paraoxonase and arylesterase enzyme activities were inhibited but MDA and MPO induced depending on the concentration in brain tissue. When compared with the control group, the changes between the pesticide exposed groups were found statistically significant (p < 0.05). In brain tissue, while AChE enzyme activity was decreased depending on concentration, caspase-3 activity increased with 8-OHdG level. As a result, it has been determined that FP is a dangerous environmental pollutant for aquatic organisms, even at low concentrations, inducing oxidative stress, damaging the brain tissue of fish and stimulating apoptosis.

Antioxidant Potential of Ulexite in Zebrafish Brain: Assessment of Oxidative DNA Damage, Apoptosis, and Response of Antioxidant Defense System.

In recent years, because of its significant biological roles, the usage of boron has been started in animal feeding. In this research, it was aimed to investigate the ulexite's action mechanism on the zebrafish brain with an evaluation of the oxidative parameters. The adult zebrafish were exposed to four ulexite doses (5, 10, 20, and 40 mg/l) in a static test apparatus for 96 h. For assessing the oxidative responses, multiple biochemical analyses were performed in brain tissues. The results indicated the supporting potential of low ulexite doses on the antioxidant system (< 40 mg/l) and that low-dose ulexite does not lead to oxidative stress in the zebrafish brain. Again, our results showed that low ulexite concentrations did not cause DNA damage or apoptosis. As a final result, in aquatic environments, ulexite (a boron compound) can be used in a safe manner, but it would be useful at higher concentrations to consider the damages of the cells that are probable to develop because of the oxidative stress.

Hematological and Hepatic Effects of Ulexite in Zebrafish.

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.

Determination of Fipronil toxicity by different biomarkers in gill and liver tissue of rainbow trout (Oncorhynchus mykiss).

Insecticides that disrupt the healthy functioning of the ecosystem have toxic potential on non-target organisms. Fish, an important component of the aquatic ecosystem, are exposed to these pesticides in different ways. The stress response is regarded as an adaptive mechanism that allows the fish to cope with the perceived stressor to maintain its normal or homeostatic state. This mechanism is determined by antioxidant parameters and oxidative stress indicators measured in gill and liver tissue of rainbow trout. Accordingly, the effects of fipronil (FP) insecticide on the physiology of rainbow trout (Oncorhynchus mykiss) were determined with using the different biomarkers (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), malondialdehyde (MDA), paraoxonase (PON), arylesterase (ARE), myeloperoxidase (MPO), 8-hydroxy-2-deoxyguanosine (8-OHdG)), and caspase 3 activity) in this study. Different doses of FP inhibited antioxidant enzyme activities in rainbow trout liver and gill tissues while inducing oxidative stress parameter (MDA, MPO, and 8-OHdG) levels. Also, caspase-3 activity was increased in liver and gill tissue, but this increase was statistically significant only in gill tissue (p < 0.05). When the results of the study were taken into consideration, it was concluded that different doses of FP insecticide caused physiological changes in rainbow trout and the studied parameters were usable biomarkers in explaining the adaptive response of stress factor.

The effect of N-acetylcysteine supplementation on the oxidative stress levels, apoptosis, DNA damage, and hematopoietic effect in pesticide-exposed fish blood.

Cysteine is important for protein synthesis, detoxification, and diverse metabolic functions. However, cysteine metabolism has been poorly described in fish, and the role of the therapeutic effect in pesticide toxicology on aquatic organisms is unknown. The aim of this study was to determine the effects of regular cysteine treatment on the hematology, biochemistry, apoptosis, oxidative DNA damage, and antioxidant parameters in fish blood after chemical application. Therefore, fish were exposed to cypermethrin for 2 weeks. Then two different concentrations of N-acetylcysteine (NAC) were applied for a 4-day treatment period and compared with the group of the self-healing process. At the end of the treatment, the hematological index, blood biochemical parameters, paraoxonase (PON), arylesterase (ARE), and myeloperoxidase (MPO) activities in the fish blood samples were investigated. With regard to the hematological parameters, statistical differences were obtained except for mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) (P < 0.05). Enzyme activities (ARE, PON, and MPO), as well as some biochemical parameters (creatinin [Cre], alanine amino transferase, total glyceride, alkaline phosphatase, iron, calcium, low density lipoprotein-cholesterol [LDL-C], sodium, and potassium), were found to be importantly different among all groups at the P < 0.05 level, while 8-hydroxydeoxyguanosine and caspase-3 levels were determined to be high in the pesticide group but decreased significantly in NAC-treated groups ( P < 0.05). According to the results of the study, acute cysteine treatment showed an ameliorative effect on the hematological index, biochemical parameters, PON, MPO, and ARE in the blood in the all the treatment group fish. The positive effect of NAC on protein synthesis, detoxification, and diverse metabolic functions against cypermethrin toxicity was more effective in 1.0 mM NAC. NAC has an important therapeutic effect on pesticide-induced hematoxicity for fish in terms of all the data.

Borax Alleviates Copper-Induced Renal Injury via Inhibiting the DNA Damage and Apoptosis in Rainbow Trout.

The aim of this study was to determine the therapeutic potential of borax against copper in the kidney tissue of the rainbow trout fed with added borax (BX) (1.25, 2.5, and 5 mg/kg) and/or copper (Cu) (500,1000 mg/kg) contents. For this purpose, two treatment groups had designed, and glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) enzyme activities were determined. Besides, oxidative DNA damage (8-hydroxy-2'-deoxyguanosine, 8-OHdG), caspase-3, and malondialdehyde (MDA) levels were assessed in kidneys of all treatment groups. In molecular pathway, hsp70, CYP1A, and antioxidant gene expression levels were determined. In the results of the analysis, antioxidant enzyme activity and gene expression were increased; 8-OHdG, caspase-3, and MDA levels were decreased in groups fed with borax supplemented feeds compared to the copper-treated group. The alterations among the groups were found as significant (p < 0.05). CYP1A and hsp70 gene expressions were upregulated in copper and copper combined groups (p < 0.05). The findings of present research showed that borax had alleviative effect on copper-induced toxicity and could be used as an antidote in fish nutrition.

Therapeutic effect of N- acetyl cysteine as an antioxidant on rainbow trout's brain in cypermethrin toxicity.

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.

The protective effect exerted by dietary borax on toxicity metabolism in rainbow trout (Oncorhynchus mykiss) tissues.

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.

Neuroprotective effects of dietary borax in the brain tissue of rainbow trout (Oncorhynchus mykiss) exposed to copper-induced toxicity.

We aimed to investigate the modulating effects of dietary borax on the pathways in rainbow trout brain exposed to copper. For this aim, a comprehensive assessment was performed including biochemical (acetylcholinesterase (AChE), malondialdehyde (MDA), oxidative DNA damage (8-hydroxy-2'-deoxyguanosine (8-OHdG), and caspase-3 levels) and transcriptional parameters (heat shock protein 70 (HSP70) and cytochromes P450 (CYP1A), glutathione peroxidase (gpx), superoxide dismutase (sod), and catalase (cat)) parameters and immunohistochemically staining of 8-OHdG. Special fish feed diets were prepared for the trial. These diets contained different concentrations of borax (1.25, 2.5, and 5 mg/kg) and/or copper (500 and 1000 mg/kg) at the period of pre- and co-treatment strategies for 21 days. At the end of the treatment periods, brain tissue was sampled for each experimental group. As a result, the biochemical parameters were increased and AChE activity decreased in the copper and copper-combined groups in comparison with the control group and also with only borax applications (p < 0.05). We observed an increase or decrease in particular biochemical parameters for the borax group in every application and we established that borax had protective effect against copper toxicity by decreasing and/or increasing the relevant biochemical parameters in brain tissue of fish. The biochemical results of borax and its combinations corresponded to the observations of gene expression data, which similarly concluded that HSP70 and CYP1A genes were strongly induced by copper (p < 0.05). In addition, the expression levels of the sod, cat, and gpx genes in the fish brains exposed to borax and the borax combination groups were significantly higher than the only copper-treated groups. In conclusion, borax supplementation provided significant protection against copper-induced neurotoxicity in trout.

Serum levels of trace minerals and heavy metals in severe COPD patients with and without pulmonary hypertension.

Aim: The aim of the current study was to assess the serum levels of trace minerals/heavy metals in COPD patients with and without pulmonary hypertension (PH) and to investigate their correlations to demographic, clinical, and biochemical variables. Materials and methods: This cross-sectional study was performed in Van Yuzuncu Yil University Medical Faculty between April 2013 and July 2013. Cases were allocated into three groups: Group 1 consisted of severe COPD patients; Group 2 was made up of COPD patients with PH; and healthy controls constituted Group 3. Demographic, radiological, and biochemical variables, as well as the serum levels of trace minerals and heavy metals, were noted and compared in these three groups. Results: COPD patients were older and had higher rates of smoking habit, diabetes mellitus, and hypertension compared to the control group. Carotid intima-media thickness was increased bilaterally, and serum levels of Co, Cu, and Fe were higher in COPD patients. Left carotid intima-media thickness was increased, and serum levels of Cd, Co, and Fe were found to be higher in COPD cases with PH compared to COPD patients without PH. Conclusion: Our results show that serum levels of trace minerals and heavy metals may be altered in COPD and PH.

Assessment of 8-hydroxy-2-deoxyguanosine activity, gene expression and antioxidant enzyme activity on rainbow trout (Oncorhynchus mykiss) tissues exposed to biopesticide.

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 0.00025ppm of DLM; 0.24 and 0.12ppm 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.