Analyzing the impact of synthetic and natural steroids: a study of cytochrome P450 metabolism, morphological alterations through metabolomics, and histopathological Examination.

This study focuses on the comparative metabolic profiling and effects of two steroid types: natural and synthetic, specifically 17α-methyl testosterone (17α-MT) at varying concentrations (1.5, 2, and 3 mg/kg) in rainbow trout (Oncorhynchus mykiss). Over a 75-day feeding trial, growth metrics, such as feed efficiency, daily specific growth, live weight gain, total weight gain, and survival rate were systematically monitored every 15 days. At the end of the feeding trial, histopathology, immunohistochemistry, and metabolome analyses were performed in the high-concentration groups (3 mg/kg natural and 3 mg/kg synthetic), in which the lowest survival rate was determined. Key findings reveal that the type of hormone significantly influences growth parameters. While some natural steroids enhanced certain growth aspects, synthetic variants often yielded better results. The metabolomic analysis highlighted significant shifts in the metabolism of tryptophan, purine, folate, primary bile acids, phosphonates, phosphinates, and xenobiotics via cytochrome P450 pathways. Histopathologically, the natural hormone groups showed similar testicular, hepatic, muscular, gill, cerebral, renal, and intestinal tissue structures to the control, with minor DNA damage and apoptosis observed through immunohistochemistry. Conversely, the synthetic hormone groups exhibited moderate DNA damage and mild degenerative and necrotic changes in histopathology.

Testing the detoxification power of black cumin oil (Nigella sativa) over cypermethrin insecticide effects in rainbow trout (Oncorhynchus mykiss) at multiple scales.

This study investigated the curative effect of black cumin oil (Nigella sativa, NS), which is a phytotherapeutic agent against to cypermethrin (CYP), which is known to have adverse effects on rainbow trout (Oncorhynchus mykiss)'s behavioral changes, oxidative stress-mediated neurotoxicity, hematotoxicity and hepatotoxicity parameters.At the end of the trial period; (i) evaluation of critical swimming speed (Ucrit) (ii) hematology indices [white blood cell (WBC), red blood cell (RBC), hemoglobin (Hgb), hematocrit (Hct), mean cell volume (MCV), mean cell hemoglobin) (MCH), mean cell hemoglobin concentration (MCHC)] (iii) Elucidation of the mechanism of functional damage in brain tissue of O. mykiss by neurological parameter [acetylcholinesterase (AChE)] (iv) Evaluation of oxidative damage in oxidative stress-mediated neurotoxicity and hepatotoxicity in liver, gill and brain tissue of O. mykiss with antioxidant enzymes [(Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), Glutathione (GSH)] and [(detection by means of malondialdehyde (MDA)] (v) Obtaining applicable data in the toxicological field using a multi-biomarker approach to investigate the modulation of NS administration via target markers in the physiological pathway of O. mykiss were aimed.As a result of CYP application, it was determined that the Ucrit value of O. mykiss decreased significantly. It was determined that the changes in the values of RBC, Hgb and Hct, which are among the hematology parameters examined in the blood tissue, were statistically significant (p < 0.05). It was determined that WBC value was inhibited by CYP application and NS tried to make a positive contribution to WBC. It was determined that the AChE activity of O. mykiss in the brain tissue had a statistically significant inhibition in the CYP-treated group (p < 0.05). SOD, CAT, GPx, enzyme activities were found to be inhibited by CYP application and were statistically significant (p < 0.05). Acute toxicity of CYP was determined by antioxidant enzyme biomarkers in gill tissue. In the results obtained; While inhibitions were determined in SOD, CAT, GPx activities compared to the control group, an induction occurred in MDA value.NS administration was noted to be an important modulator of the SOD-CAT system against CYP exposure at both concentrations. Thus, it can be said that it indirectly functions as an effective antioxidant through the NS receptor protein and structurally stimulates the synthesis and activity of antioxidative enzymes under oxidative stress.

Effect of climate change on fillet quality and shelf-life of Oncorhynchus mykiss under controlled conditions.

BACKGROUND: Temperature, which affects numerous physiological processes, has been described as the 'main ecological factor' for fish. The aim of this modeling study is to explore the impact of climate-induced temperature changes on fish fillet quality and shelf life. RESULTS: Temperature stress in rainbow trout affected ash and moisture, and inhibited myofibril fragmentation in the fillets. However, with the increase in temperature, there was a decrease in the total amount of saturated fatty acids (∑SFA) and there were significant increases in the total amount of omega 3 (∑n3) and 22:6n-3 (DHA). It was determined that temperature increase had a negative effect on color, texture, water-holding capacity, water activity, pH, lactic acid, and glycogen levels in fillets, and it had a positive effect by delaying microbial spoilage, especially in cold storage. CONCLUSION: This study suggest that the effects of climate change on product quality and shelf life in fish requires further research. It highlights knowledge gaps to guide future research in this emerging field. © 2023 Society of Chemical Industry.

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.

Effect of climate change on hematotoxicity/hepatoxicity oxidative stress, Oncorhynchus mykiss, under controlled conditions.

Described as the 'main ecological factor', temperature, strongly affects the physiological stress responses of fish. In order to evaluate the effects of temperature variations on fish culture and food value chain, the present study was designed as a climate change model. Furthermore, the present study provides a theoretical basis for a better understanding of the mechanisms of the environmentally induced changes. In this direction, we examined the blood physiology and oxidative stress responses induced by temperature variation in the rainbow trout, a temperature-sensitive cold-water fish. The obtained results showed that climate changes promoted the inhibited activities' expressions and the development of potential tissue and hematological defense mechanisms against temperature-induced toxic damage. This study showed that climate change could be a subset of the studies on the stress physiology in aquaculture, which can be developed for new experimental designs and research collaborations. Furthermore, it highlights knowledge gaps to guide future research in this emerging field.

A laboratory investigation on the effect of biguanide- and pyridine-derived antiseptics on the adhesion of resin composites to dentin.

Optimal bonding of adhesive restorations to dentin is crucial to prevent microleakage and enhance the survival of root-filled teeth. The aim of this study was to investigate the effect of chlorhexidine (CHX), alexidine (ALX) and octenidine dihydrochloride (OCT) on the bond strength of resin composites to coronal dentin. Human coronal dentin specimens were treated with 2% CHX, 0.1% ALX, 0.1% OCT or saline then restored with traditional or bulk-fill resin composites. The adhesion strength between the resin and dentin was measured using the microtensile bond strength and failure mode was determined using a stereomicroscope. Treatment with ALX and OCT resulted in significantly greater µTBS compared with CHX and saline, irrespective of the resin composite used. Alexidine treatment predominantly resulted in mixed failure, while adhesive failures were frequently observed in CHX and saline-treated dentin. In conclusion, final irrigation with ALX or OCT improved the bonding of resin composites to dentin.

Mitigation potential of zingerone and rutin on toxicity mechanisms of nickel to zebrafish based on morphological, DNA damage and apoptosis outcome analysis.

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 (NiCl2) 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.

Recent insight into nanotechnology in fish processing: a knowledge gap analysis.

Fish and other seafood are fundamental nutritional ingredients for a healthy life that are consumed globally. However, the high degree of spoilage of these products has led to the progress of a prevalent variety of preservation, processing, and analytical techniques in this sector. Food safety, authenticity, nutritional quality, and freshness are important features of aquaculture quality. In seafood processing, developing nanotechnology (nanotech), by adapting to new and complex applications, has promising applications for all segments of the food supply chain, including quality assessment, packaging, and storage. In this review, the application of nanotech in food, and especially in seafood, and its positive contributions to processing, preservation, the packaging industry, and the toxicity potential of nanoparticles (NPs) in food and food safety are investigated, and an overview is given. In line with this perspective, by examining the current state of nanotech in seafood processing procedures, not only present practices and future expectations but also studies on this subject are reviewed, and future pathways/future lines of research are predicted is attempted to be formed. In light of this research, it is understood that, depending on their properties, NPs are effective in their fields of use, and their success is related to the application procedures for which they are used. It is seen that these substances, which are synthesized in different ways, especially in recent years, are preferred in applications for improving product quality, product development, storage, and packaging stages of green synthesis particles.

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.

Effect of coating with chitosan enriched with different borates on the shelf life of fish fillet.

BACKGROUND: In this study, the effects of biofilm coatings obtained by immobilization of different borates - namely borax (BX), colemanite (COL), and ulexite (UX) - with chitosan (Ch) on the shelf life of rainbow trout fillets were investigated. The immobilization and characterization of borates in Ch were confirmed by scanning electron microscopy, Fourier transform infrared spectroscopy, and zeta potential analysis. In determining the shelf life of fillets that were covered by immersion and stored for 15 days, microbiological (total aerobic mesophilic, psychrotrophic, lactic acid, Pseudomonas, and Enterobacteriaceae bacteria counts) and chemical analyses (total volatile basic nitrogen, thiobarbituric acid reactive substance, and pH levels) were performed at 3 day periodic intervals. In addition, the biodegradation of borates was determined using inductively coupled plasma mass spectrometry in biofilm-coated fillets on the 1st, 8th, and 15th storage days. RESULTS: The microbial results of the coatings enriched with borates (BX, COL, and UX) at different levels (0, 0.03, and 0.06 mg L-1 ) (due to the immobilization with Ch) show the shelf life was extended by 3-6 days in all of the treatment groups compared with the control. CONCLUSION: It was concluded that BX, COL, and UX coatings enriched by immobilization with Ch increase shelf life and improve fillet quality. In addition, the enrichment of BX, COL, and UX with Ch showed explicit natural protective effects. This study demonstrates that Ch-enriched coatings of BX, COL, and UX can be used as natural bioactive nanocarriers to provide bioactive food ingredients in the seafood processing industry. © 2023 Society of Chemical Industry.

Microplastic-induced oxidative stress response in turbot and potential intake by humans.

Microplastic (MP) pollution has become a health concern subject in recent years. Althoughann increasing number of studies about the ingestion of microplastics by fish, research on the oxidative stress response to MPs in natural environments is quite limited. In this study, the identification and characterization of MPs in gill (G), muscle tissues (M), and gastrointestinal tract (GI) of turbot (Scophthalmus maximus) were evaluated. Oxidative damage of MPs on the brain (B), liver (L), gill (G), and muscle (M) tissues as well as their effect on superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), paraoxonase (PON), arylesterase (AR) myeloperoxidase (MPO), and malondialdehyde (MDA) biomarkers were evaluated. The potential transmission of MPs from muscle tissues to humans was examined. Results showed that gills contain the highest amounts of MPs, ethylene propylene is the most dominant polymer type, black and blue are the most common MP color, fiber is the most common shape, and 50-200 µm is the most common MP size. Results showed that MPs cause oxidative stress of tissues with inhibiting effect on enzyme activities and promoting impact on lipid peroxidation. The oxidative damage mostly affected the liver (detoxification organ) followed by gill tissue. The intake of MPS in the European Union was estimated by EFSA as 119 items/year, while in Turkey it is 47.88 items/year. This study shows that more research is needed in terms of ecosystem health and food chain safety. The risk assessment of MPs in living organisms and environmental matrices including food safety and human health should be considered a public health issue.

Neutralization of iron oxide magnetic nanoparticle aquatoxicity on Oncorhynchus mykiss via supplementation with ulexite.

Nowadays, the unique features of nanoparticles (NPs) have encouraged new applications in different areas including biology, medicine, agriculture, and electronics. Their quick joining into daily life not only enhances the uses of NPs in a wide range of modern technologies but also their release into the aquatic environment causes inevitable environmental concerns. On the other hand boron exhibits key physiological effects on biological systems. This research was designed for evaluating the toxicity of magnetite nanoparticles (Fe3O4-MNPs) on aquatic organisms and obtaining data for the information gap in this area. In this study, Rainbow trout (Oncorhynchus mykiss) was considered as an aquatic indicator, and trials were designed as Ulexite (a boron mineral, UX) treatment against exposure to Fe3O4-MNPs. Synthesized and characterized Fe3O4-MNPs were exposed to rainbow trouts in wide spectrum concentrations (0.005-0.08 mL/L) to analyze its lethal dose (LC50) and cytoprotective properties by UX treatment were assessed against Fe3O4-MNPs applications for 96 h. For the initial toxicity analysis, hematological parameters (blood cell counts) were examined in experimental groups and micronucleus (MN) assay was performed to monitor nuclear abnormalities after exposure to NPs. Biochemical analyzes in both blood and liver samples were utilized to assess antioxidant/oxidative stress and inflammatory parameters. Also, 8-hydroxy-2'-deoxyguanosine (8-OHdG) assay was used to investigate oxidative DNA lesions and Caspase-3 analysis was performed on both blood and liver tissues to monitor apoptotic cell death occurrence. When antioxidant enzymes in blood and liver tissue were examined, time-dependent decreases in activity were determined in SOD, CAT, GPx, and GSH enzymes, while increased levels of MDA and MPO parameters were observed in respect to Fe3O4-MNPs exposure. It was found that TNF-α, Il-6 levels were enhanced against Fe3O4-MNPs treatment, but Nrf-2 levels were decreased at the 46th and 96th h. In the 96th application results, all parameters were statistically significant (p < 0.05) in blood and liver tissue, except for the IL-6 results. It was determined that the frequency of MN, the level of 8-OHdG and caspase-3 activity increased in respect to Fe3O4-MNPs exposure over time. Treatment with UX alleviated Fe3O4-MNPs-induced hematotoxic and hepatotoxic alterations as well as oxidative and genetic damages. Our findings offer strong evidence for the use of UX as promising, safe and natural protective agents against environmental toxicity of magnetite nanoparticles.

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.

Thermal processing implications on microplastics in rainbow trout fillet.

Heat treatment is an inevitable step in making meat and meat products ready for human consumption. Researches on ready-to-eat foods had shown that foods can also contain microplastics (MPs). The source of the presence of MPs in foods is: air, raw materials, food production stages, or plastics used in packaging. This study was carried out to evaluate the possible effects of the sous-vide (So-Vc) technique applied in rainbow trout (Oncorhynchus mykiss) fillets at different temperatures and time intervals on MPs degradation or migration mechanisms and the level of uptake by humans. For this purpose, 7 treatment temperature × 3 various cooking times and So-Vc technique were applied on rainbow trout fillets. Then, in these fillets, MP presence, size, and shape were researched, as well as polymer types and possible levels of MP uptake by humans were determined. In the analyses, 1.27 ± 0.54 MP/g was found in 1 g of fish tissue. Dimensionally, 67% of MPs was detected as <50 µm and 8% of 500-1000 µm. The dominant shape was determined as a fragment, and the color was black. Six polymer types were determined. The results showed that high temperature (> 65°C) applications promoted polymer degradation. MP migration from packaging material to fillets was not detected. By calculations made on these findings, the lowest intake level by a human was estimated as 6140 MPs units/year. The obtained data provided the initial data to explore and optimize the current understanding of thermally processed products in terms of MPs. This study proved that the sous vide method causes polymer degradation at high temperatures and longer time periods.

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.

Boron Compounds Exhibit Protective Effects against Aluminum-Induced Neurotoxicity and Genotoxicity: In Vitro and In Vivo Study.

Genetic, neuropathological and biochemical investigations have revealed meaningful relationships between aluminum (Al) exposure and neurotoxic and hematotoxic damage. Hence, intensive efforts are being made to minimize the harmful effects of Al. Moreover, boron compounds are used in a broad mix of industries, from cosmetics and pharmaceuticals to agriculture. They affect critical biological functions in cellular events and enzymatic reactions, as well as endocrinal and mineral metabolisms. There are limited dose-related data about boric acid (BA) and other boron compounds, including colemanite (Col), ulexite (UX) and borax (BX), which have commercial prominence. In this study, we evaluate boron compounds' genetic, cytological, biochemical and pathological effects against aluminum chloride (AlCl3)-induced hematotoxicity and neurotoxicity on different cell and animal model systems. First, we perform genotoxicity studies on in vivo rat bone marrow cells and peripheric human blood cultures. To analyze DNA and chromosome damage, we use single cell gel electrophoresis (SCGE or comet assay) and micronucleus (MN) and chromosome aberration (CA) assays. The nuclear division index (NDI) is used to monitor cytostasis. Second, we examine the biochemical parameters (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total antioxidant capacity (TAC) and total oxidative status (TOS)) to determine oxidative changes in blood and brain. Next, we assess the histopathological alterations by using light and electron microscopes. Our results show that Al increases oxidative stress and genetic damage in blood and brain in vivo and in vitro studies. Al also led to severe histopathological and ultrastructural alterations in the brain. However, the boron compounds alone did not cause adverse changes based on the above-studied parameters. Moreover, these compounds exhibit different levels of beneficial effects by removing the harmful impact of Al. The antioxidant, antigenotoxic and cytoprotective effects of boron compounds against Al-induced damage indicate that boron may have a high potential for use in medical purposes in humans. In conclusion, our analysis suggests that boron compounds (especially BA, BX and UX) can be administered to subjects to prevent neurodegenerative and hematological disorders at determined doses.

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.

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.

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.

Hematotoxic, oxidative and genotoxic damage in rainbow trout (Oncorhynchus mykiss) after exposure to 3-benzoylpyridine.

Pyridine is a basic heterocyclic organic compound. The pyridine ring is present in many important compounds, including agricultural chemicals, medicines and vitamins. Due to their widespread industrial use, bioaccumulation and non-target toxic effects are being considered as a great risk to human and environmental health. In this study, we aimed to evaluate the hematological, oxidative and genotoxic damage potentials by different concentrations (1, 1.5, and 2 g/L) of the ketone 3-Benzoylpyridine (3BP) on rainbow trout (Oncorhynchus mykiss). Alterations in the biomarker levels of oxidative DNA damage (8-hydroxy-2'-deoxyguanosine (8-OHdG)), apoptosis (Caspase-3), malondialdehyde (MDA) as well as antioxidant enzyme activities including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), myeloperoxidase (MPO), paraoxonase (PON), and arylesterase (AR) were assessed in brain, liver, gill and blood tissues. Acetylcholinesterase (AChE) activity was also determined in brain tissue. In addition, we analyzed micronucleus (MN) rates and hematological indices of total erythrocyte count (RBC), total leukocyte count (WBC), hemoglobin (Hb), hematocrit (Hct), total platelet count (PLT), mean cell hemoglobin concentration (MCHC), mean cell hemoglobin (MCH), and mean cell volume (MCV) in blood. LC50-96h value of 3BP was calculated as 5.2 g/L from the data obtained. A significant decrease in brain AChE activity was determined in clear time and dose dependent manners. While SOD, CAT, GPx, PON, and AR levels were decreased, MDA, MPO, 8-OHdG and Caspase-3 levels were increased in all tissues (p < 0.05). Again, the 3BP led to increases of MN formation at all applied concentrations in the rates of between 45.4 and 72.7%. Significant differences (p < 0.05) were found out in between all studied hematology parameters between 3BP-exposed and the control fish. In conclusion, ours study firstly indicated that the treatment doses of 3BP induced distinct hematological and oxidative alterations as well as genotoxic damage in rainbow trout.