Increased Levels Of Lipid Peroxidation Research Articles

Responses of salicylic acid encapsulation on growth, photosynthetic attributes and ROS scavenging system in Lactuca sativa exposed to polycyclic aromatic hydrocarbon pollution

Salicylic acid (SA) is a phytohormone that plays a key role in the regulation of the defense response against environmental variables in plants, and it provides increased yield and stress tolerance when exogenously applied to plants as a growth regulator. The role of SA-mediated signals in abiotic stress tolerance varies according to the species, stressor, application method, and dose. This study investigated the effects of salicylic acid (SA, 0.1 mg ml−1) or β-cyclodextrin encapsulated salicylic acid (e-SA, 0.1 mg ml−1) treatments on growth parameters, gas exchange, photosynthesis efficiency, and antioxidant capacity in lettuce seedlings exposed to polycyclic aromatic hydrocarbon pollution. Fluorene (FLN, 100 mg L−1) contamination resulted in a 27% growth rate and a 14% water content reduction in lettuce leaves. Significant suppressions of stomatal conductance, carbon assimilation, and PSII photochemistry were detected in plants under stress. FLN + SA and FLN + e-SA treatments regulated plant-water relations by stimulating proline accumulation and relieving stomatal limitations. As indicated by the high Fv/Fm ratio, photosynthesis efficiency was recovered in FLN + SA and FLN + e-SA group plants. FLN stress caused high oxidative stress in lettuce leaves and increased lipid peroxidation level by 40%. However, especially e-SA application to plants under stress, increased SOD activity by 3-fold and CAT activity by 80% and was successful in preventing H2O2 accumulation and lipid peroxidation. Both SA and e-SA treatments partially activated the AsA-GSH cycle. As a result, direct SA application was effective in mitigating stress-induced physiological limitations with high SA accumulation in the tissues, while encapsulated SA treatment was more effective in regulating photosynthetic and biochemical reactions, alleviating oxidative damage by activating the antioxidant defense, and promoting growth under stress with moderate SA accumulation.

Olea europaea L. leaf extract mitigates oxidative and histological damage in rat heart tissue exposed to combined noise and toluene: An experimental study

In many occupational settings, workers are frequently exposed to toluene and noise. However, the individual and combined effects of these exposures on the cardiovascular system have not been fully elucidated. Therefore, this study aimed to investigate the impact of simultaneous exposure to toluene and noise on the rat heart, while also evaluating the potential preventive effect of olive leaf extract (OLE). Forty-eight male Wistar rats were randomly assigned to eight groups (n = 6/group): control group (C), control group that received OLE (C + OLE), group exposed to noise (N), group exposed to noise and receiving OLE (N + OLE), group exposed to toluene (T), group exposed to toluene and receiving OLE (T + OLE), group co-exposed to noise and toluene (NT), and group co-exposed to noise and toluene and receiving OLE (NT + OLE). The rats in this study were subjected to simultaneous exposure to toluene and noise for a duration of six weeks, within a custom-built plexiglass chamber. Toluene was administered at a concentration of 300 ppm, while the noise level was set to 85 dB(A). The exposure chamber was equipped with a generation system, an exposure system, and a monitoring system, ensuring precise and accurate exposure conditions. After the six-week period, heart and blood samples were collected from the rats for subsequent analysis. Plasma levels of cholesterol (CHOL), triglycerides (TG), lactate dehydrogenase (LDH), and creatine kinase (CK) were measured, and histopathological investigation was conducted using HE staining. Additionally, superoxide dismutase (SOD) and catalase (CAT) activities, as well as malondialdehyde (MDA) levels in heart tissue were measured. Our results showed that simultaneous exposure to noise and toluene altered CHOL, TG, LDH, and CK levels, and also caused an increase in lipid peroxidation levels and superoxide dismutase activity, along with a decrease in catalase activity in the heart. A significant alteration in the myocardium was also observed. However, treatment with OLE was found to modulate these oxidative and histological changes, ultimately correcting the deleterious effects induced by the combined exposure to noise and toluene. Therefore, our study suggests that OLE could be a potential preventive measure for individuals exposed to toluene and noise in industrial settings.

Testosterone ameliorated the behavioural deficits of gonadectomised rats and counteracted free radicals in a dosage-dependent manner

Testosterone deficiency may induce behavioural changes in individuals. Oxidative stress resulting from a redox imbalance may be implicated in the initiation and progression of neurobehavioural disorders. However, whether exogenous testosterone intervention in male gonadectomised (GDX) rats ameliorates oxidative stress and plays a neuroprotective role remains unknown. Therefore, we examined this hypothesis by performing sham or gonadectomy surgeries on Sprague–Dawley rats with or without supplementation with different doses of testosterone propionate (TP). Open field and Morris water maze tests were performed, the serum and brain testosterone levels, and oxidative stress markers were analysed. GDX and lower TP doses (0.5 mg/kg) induced reduced exploratory and motor behaviours, but impaired spatial learning and memory compared to Sham rats. Administration of physiological TP levels (0.75–1.25 mg/kg) to the GDX rats restored the behaviour observed in the intact rats. However, higher TP doses (1.5–3.0 mg/kg) induced increased exploratory and motor behaviours but impaired spatial learning and memory. These behavioural impairments were accompanied by a marked decrease in levels of antioxidant enzymes (superoxide dismutase and catalase) and an increase in lipid peroxidation levels in the substantia nigra and hippocampus. These findings indicate that TP administration can alter behavioural performance and induce memory and learning impairment, which may result from changes in redox homeostasis in male GDX animals.

Assessment of arsenic induced physiological and lipid peroxidation response in two indica rice cultivars

Aim: To investigate the potential of sodium arsenite to induce physiological as well as oxidative stress at its low level exposure in tolerant and sensitive indica rice cultivars. Methodology: Rice seeds were surface sterilized using 0.1% HgCl2 for 15 min, followed by washing with distilled water. Twelve days after germination, the seedlings in one tray was kept aside as control and other trays were exposed to 50, 100, 150 and 200 μM of sodium arsenite. After treatment for 24 and 48hr, leaves were harvested and washed with distilled water to estimate the level of lipid peroxidation as well as physiological stress parameters. Results: The oxidative damage increased with corresponding increase in the sodium arsenite concentration in both the succeptible IR-64 and tolerant Nonabokra cultivars, the effect being more prononced in IR-64 than Nonabokra. The status of lipid peroxidation was assessed through quantification of its secondary product malondialdehyde by TBARS assay (P≤0.05). Significant increase in lipid peroxidation levels were observed in all the arsenic exposed groups of rice plants. Interpretation: The detrimental effect of arsenic was reflected as more chlorophyll loss, decrease in water content and significant reduction in the length of root as well as shoot of rice plants. Besides, significant elevated levels of LPO indicated drastic cellular damage in all the arsenic exposed groups of rice plants. Key words: Chlorophyll loss, Indica rice, Lipid peroxidation, Sodium arsenite, Water content

Increased levels of lipid and protein oxidation in rat prefrontal cortex after treatment by lithium, valproic acid, and olanzapine.

Oxidative stress is widely accepted to contribute to the pathogenesis of several psychiatric diseases. Many antipsychotic drugs and mood stabilizers act through restoration of the dysregulated oxidative homeostasis in the brain. However, the long-term effect of these drugs per se in terms of their potential to interfere with the oxidative status in the brain remains largely controversial. The present study aimed to investigate the sole effect of three commonly used psychoactive drugs, lithium, valproic acid, and olanzapine, on lipid and protein oxidation status in the prefrontal cortex of healthy rats. A total of 80 adult male albino Wistar rats were used, and groups were treated with saline (control), lithium, valproic acid, or olanzapine daily for 30days. Following sacrification, right prefrontal cortexes were dissected and homogenized. Lipid peroxidation (LPO) and protein oxidation (AOPP) assays were performed by ELISA. LPO levels were significantly higher in lithium and valproic acid-treated rats by 45% and 40%, respectively. Olanzapine treatment caused a mild 26% increase in LPO levels, but the effect was non-significant. Lithium, valproic acid, and olanzapine treatments significantly increased AOPP levels by 58%, 54%, and 36.5%, respectively. There was a strong positive correlation between the lipid peroxidation and protein oxidation levels. Our results call attention to the need to consider the pro-oxidative capacity of antipsychotic drugs per se and their potential to disturb the oxidative homeostasis in the brain during long-term medication for psychiatric diseases.

Pravastatin Prevents Increases in Activity of Metalloproteinase-2 and Oxidative Stress, and Enhances Endothelium-Derived Nitric Oxide-Dependent Vasodilation in Gestational Hypertension.

Pre-eclampsia (PE) is a hypertensive disorder of pregnancy and has been associated with placental growth restriction. The pre-eclamptic placenta releases free radicals to maternal circulation, thus increasing oxidative stress. An impaired redox state leads to reduction in circulating nitric oxide (NO) levels and activation of extracellular matrix metalloproteinases (MMPs). However, activation of MMPs induced by oxidative stress is still unclear in PE. Antioxidant effects have been demonstrated with the use of pravastatin. Therefore, we hypothesized that pravastatin protects against oxidative stress-induced activation of MMPs in a rat model of PE. The animals were divided into four groups: normotensive pregnant rats (Norm-Preg); pregnant rats treated with pravastatin (Norm-Preg + Prava); hypertensive pregnant rats (HTN-Preg); and hypertensive pregnant rats treated with pravastatin (HTN-Preg + Prava). The deoxycorticosterone acetate (DOCA) and sodium chloride (DOCA-salt) model was used to induce hypertension in pregnancy. Blood pressure, and fetal and placental parameters were recorded. The gelatinolytic activity of MMPs, NO metabolites and lipid peroxide levels were also determined. Endothelium function was also examined. Pravastatin attenuated maternal hypertension, prevented placental weight loss, increased NO metabolites, inhibited increases in lipid peroxide levels, and reduced the activity of MMP-2, and these effects were observed along with enhanced endothelium-derived NO-dependent vasodilation. The present results provide evidence that pravastatin protects against activation of MMP-2 induced by oxidative stress in pre-eclamptic rats. These findings may also involve improvement in endothelial function related to NO and antihypertensive effects of pravastatin, thus suggesting pravastatin as a therapeutic intervention for PE.

The Role of Selected Trace Elements in Oxidoreductive Homeostasis in Patients with Thyroid Diseases.

Impaired levels of selenium (Se), zinc (Zn), copper (Cu), iron (Fe), manganese (Mn) and iodine (I) in the organism may adversely affect the thyroid endocrine system. These trace elements play a role in the fight against oxidative stress as components of enzymes. Oxidative-antioxidant imbalance is considered a possible factor in many pathological conditions, including various thyroid diseases. In the available literature, there are few scientific studies showing a direct correlation of the effect of supplementation of trace elements on slowing down or preventing the occurrence of thyroid diseases in combination with the improvement of the antioxidant profile, or through the action of these elements as antioxidants. Among the available studies, it has been shown that an increase in lipid peroxidation levels and a decrease in the overall antioxidant defense status occur during such thyroid diseases as thyroid cancer, Hashimoto's thyroiditis and dysthyroidism. In studies in which trace elements were supplemented, the following were observed: a decrease in the level of malondialdehyde after supplementation with Zn during hypothyroidism and reduction in the malondialdehyde level after Se supplementation with a simultaneous increase in the total activity status and activity of antioxidant defense enzymes in the course of autoimmune thyroiditis. This systematic review aimed to present the current state of knowledge about the relationship between trace elements and thyroid diseases in terms of oxidoreductive homeostasis.

Contribution of Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress and Autophagy Pathways to the Ameliorative Effects of Hesperidin in NaF-Induced Testicular Toxicity.

The ameliorative effects of hesperidin (HES) on the toxicities created by sodium fluoride (NaF) in the testes tissue of rats were studied via oxidative stress, apoptosis and endoplasmic reticulum (ER) stress pathways. The animals were divided into five distinct groups (7 rats in each group). Group 1 was control group, group 2 received NaF-only (600 ppm), group 3 received HES-only (200 mg/kg bw); group 4 received NaF (600 ppm)+HES (100 mg/kg bw) and group 5 received NaF (600 ppm)+HES (200 mg/kg bw) for 14 days. NaF-induced testes tissue damage by reducing activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) and levels of glutathione (GSH), and increasing lipid peroxidation levels. NaF treatment significantly downregulated the mRNA levels of SOD1, CAT and GPx. NaF supplementation caused apoptosis in the testes by upregulating p53, NFkB, caspase-3, caspase-6, caspase-9, and Bax and downregulating Bcl-2. Furthermore, NaF caused ER stress via increasing mRNA transcript levels of PERK, IRE1, ATF-6 and GRP78. NaF treatment led to autophagy via upregulation of Beclin1, LC3A, LC3B and AKT2. In testes tissue, however, co-treatment with HES at doses of 100 and 200 mg/kg significantly reduced oxidative stress, apoptosis, autophagy and ER stress. Overall, the findings of this study suggest that HES may help to reduce testes damage caused by NaF toxicity.

Oxidation of biological molecules with age and induced oxidative stress in different growth phases of Saccharomyces cerevisiae.

One of the mechanistic approaches for explaining ageing is the oxidative stress theory of ageing. Saccharomyces cerevisiae has been used as a model to study ageing due to many factors. We have attempted to investigate if the differential ability to withstand oxidative stress can be correlated with their lifespans. In all the four strains studied (AP22, 699, 8C, and SP4), there was no age-associated increases in lipid peroxidation levels measured as thiobarbituric acid reactive substances (TBARS). Under induced oxidative stress conditions, there was an increased TBARS level in both the ages assessed with a quantum-fold increase in the stationary phase cells of AP22.In contrast, the late stationary phase cells of 8C exhibited the least susceptibility to induced oxidative stress. The level of TBARS in both exponential and late stationary phase cells of 699 was overall more than that in the other three strains. Protein carbonylation increased with age in 8C and 699. Induced stress increased carbonylation in the exponential cells of SP4 and 699 and the stationary phase cells of all four strains. Protein carbonylation data indicate that the AP22 cells exhibit decreased protein carbonylation vis-à-vis the other strains. Induced stress data showed that while the exponential cells of 699 are susceptible, the late stationary phase cells of 699 are most resistant. Western blotting analysis using anti-HNE antibodies showed two proteins of molecular mass ~ 56 and ~ 84kDa that were selectively modified with age in all the strains. Under induced stress conditions, an additional protein of ~ 69kDa was oxidized. Our investigation shows that the difference in lifespan between the four strains of S. cerevisiae may be regulated by oxidative stress. Knowledge of the identity of the oxidized proteins will significantly facilitate a better understanding of the effect of oxidative stress conditions on the cells of S. cerevisiae.

Zoledronic acid induces ferroptosis by reducing ubiquinone and promoting HMOX1 expression in osteosarcoma cells.

Aims: Ferroptosis plays important roles in tumorigenesis and cancer therapy. Zoledronic acid is known to inhibit the activity of farnesyl pyrophosphate synthase, a key enzyme in the mevalonate pathway. We examined whether zoledronic acid can inhibit the growth of osteosarcoma cells by inducing ferroptosis. Methods: Cell viability was analyzed by using CCK8 reagent and counting cells with trypan blue exclusion. Ferroptosis markers including lipid peroxide and PTGS2 expression were examined by flow cytometry, western blot, and quantitative PCR analyses. Cellular ubiquinone content was determined using high performance liquid chromatography. Ferrostatin-1 and RSL3 were used as the ferroptosis inhibitor and inducer respectively. Results: Zoledronic acid treatment decreased cell viability and promoted the increase in lipid peroxide content and PTGS2 expression. Addition of ferrostatin-1 reverted these effects of zoledronic acid on osteosarcoma cells, supporting a role of zoledronic acid in inducing ferroptosis. Mechanistically, zoledronic acid significantly decreased ubiquinone, a metabolite of the mevalonate pathway. Treating cells with exogenous ubiquinone prevented zoledronic acid-induced ferroptosis and decrease in the growth of osteosarcoma cells. In addition, zoledronic acid enhanced the expression of HMOX1, whereas knockdown of HMOX1 inhibited the zoledronic acid-induced increase in lipid peroxide level and decrease in cell growth. Finally, zoledronic acid together with RSL3 significantly enhanced the inhibitory effect on the growth of osteosarcoma cells. Conclusion: Our results indicate that zoledronic acid induces ferroptosis by decreasing ubiquinone content and promoting HMOX1 expression in osteosarcoma cells. Zoledronic acid together with ferroptosis inducer may be a promising new strategy for the treatment of osteosarcoma.

Chemical characterization of Hymenocardia acida stem bark extract and modulation of selected enzymes in Kidney and Heart of Wistar rats

Hymenocardia acida tul leaf and stem bark are used in treatment of several diseases in Africa. We examined the chemical constituents of the stem bark extract and its effects on some antioxidant indices and esterases in Wistar rats. Hymenocardia acida stem bark extract (HASBE) was obtained by Soxhlet extraction using methanol, followed by Atomic Absorption Spectroscopy (AAS), Fourier-Transform Infrared (FT-IR) spectroscopy, ultraviolet (UV) spectroscopy, High-performance liquid chromatography (HPLC) and Gas Chromatography-Flame ionization detection (GC-FID). Forty-eight male Wistar rats were assigned into eight groups (6 rats each), and administered orally with normal saline (Control), 50, 100, 150, 200, 250, 300, 350 mg/kg of HASBE twice per week for eight weeks. The rats were sacrificed under chloroform anesthesia, and kidneys and heart were excised, and processed into homogenates. Superoxide dismutase (SOD), catalase, lipid peroxidation (LPO), glutathione peroxidase (GPx), acetylcholinesterase (AChE) and carboxylesterases (CES) were determined spectrophotometrically. The AAS of HASBE detected Cobalt, Copper, Zinc, Iron, Nickel, Chromium, Manganese and Magnesium. The FT-IR shows four peaks as 2961.4, 2926.0, 1056.7 and 1034.3 cm-1, while UV shows absorbance between 250 nm and 650 nm. The HPLC identified orientin, β-sitosterol, rutin and betulinic acid, while GC-FID identified rutin, orientin, stigmasterol, hymenocardine and homopterocarpin as prominent compounds. The SOD significantly (p < 0.05) reduced in kidneys, while catalase was elevated in kidney and heart, with an increase in LPO level only in heart, relative to controls. The GPx, AChE and CE activities in kidneys were increased by HASBE, whereas, CE activity was lowered in heart. This study has demonstrated that Hymenocardia acida stem bark extract majorly contains iron, nickel, orientin, rutin, stigmasterol, hymenocardine, β-sitosterol, homopterocarpin and betulinic acid, and could possibly modulate the activities of antioxidant and esterase enzymes in kidney and heart of Wistar rats.

First approach to assess the effects of nanoplastics on the soil species Folsomia candida: A mixture design with bisphenol A and diphenhydramine

The terrestrial environment is one of the main recipients of plastic waste. However, limited research has been performed on soil contamination by plastics and even less assessing the effects of nanoplastics (NPls). Behind the potential toxicity caused per se, NPls are recognized vectors of other environmental harmful contaminants. Therefore, the main aim of the present study is to understand whether the toxicity of an industrial chemical (bisphenol A – BPA) and a pharmaceutical (diphenhydramine – DPH) changes in the presence of polystyrene NPls to the terrestrial invertebrate Folsomia candida. Assessed endpoints encompassed organismal (reproduction, survival and behavior) and biochemical (neurotransmission and oxidative stress) levels. BPA or DPH, 28 d single exposures (1 to 2000 mg/kg), induce no effect on organisms' survival. In terms of reproduction, the calculated EC50 (concentration that causes 50% of the effect) and determined LOEC (lowest observed effect concentration) were higher than the environmental concentrations, showing that BPA or DPH single exposure may pose no threat to the terrestrial invertebrates. Survival and reproduction effects of BPA or DPH were independent on the presence of NPls. However, for avoidance behavior (48 h exposure), the effects of the tested mixtures (BPA + NPls and DPH + NPls) were dependent on the NPls concentration (at 0.015 mg/kg – interaction: no avoidance; at 600 mg/kg – no interaction: avoidance). Glutathione S-transferase activity increased after 28 d exposure to 100 mg/kg DPH + 0.015 mg/kg NPls (synergism). The increase of lipid peroxidation levels found after the exposure to 0.015 mg/kg NPls (a predicted environmental concentration) was not detected in the mixtures (antagonism). The results showed that the effects of the binary mixtures were dependent on the assessed endpoint and the tested concentrations. The findings of the present study show the ability of NPls to alter the effects of compounds with different natures and mechanisms of toxicity towards soil organisms, showing the importance of environmental risk assessment considering mixtures of contaminants.

An iron-containing ferritin-based nanosensitizer for synergistic ferroptosis/sono-photodynamic cancer therapy.

Ferroptosis is a newly detected iron-dependent form of regulated cell death. Sono-photodynamic therapy (SPDT) can generate reactive oxygen species (ROS) and induce cell death under light and ultrasound. Due to the complexity of tumor physiology and pathology, single-modality often fails to achieve a satisfactory therapeutic effect. The development of a formulation platform with integration of multiple therapeutic modalities using a simple and convenient method is still a challenge. Here, we report the facile construction of a ferritin-based nanosensitizer FCD by co-encapsulating chlorin e6 (Ce6) and dihydroartemisinin (DHA) in horse spleen ferritin, and was employed for synergistic ferroptosis and SPDT. Ferritin in FCD can release Fe3+ under acidic conditions and Fe3+ can be reduced to Fe2+ in the presence of glutathione (GSH). The Fe2+ can react with hydrogen peroxide (H2O2) to produce harmful hydroxyl radicals. Furthermore, a large amount of ROS can be generated via the reaction of Fe2+ with DHA and by simultaneously irradiation of FCD with both light and ultrasound. More importantly, the depletion of GSH by FCD could decrease glutathione peroxidase 4 (GPX4) and increase lipid peroxidation (LPO) levels, thereby inducing ferroptosis. Therefore, by integrating the advantageous GSH-depletion capacity, ROS generation ability, and ferroptosis induction capability into one single nanosystem, FCD can serve as a promising platform for combined chemo-sono-photodynamic therapy of cancer.

Intrauterine androgen exposure impairs gonadal adipose tissue functions of adult female rats

Prenatal androgen exposure induces fetal programming leading to alterations in offspring health and phenotypes that resemble those seen in women with Polycystic Ovary Syndrome. It has been described that prenatal androgenization affects the reproductive axis and leads to metabolic and endocrine disorders. Adipose tissue plays a crucial role in all these functions and is susceptible to programming effects. Particularly, gonadal adipose tissue is involved in reproductive functions, so dysfunctions in this tissue could be related to fertility alterations. We aimed to investigate the extent to which prenatal hyperandrogenization is able to alter the functionality of gonadal adipose tissue in female adult rats, including lipid metabolism, adipokines expression, and de novo synthesis of steroids. Pregnant rats were treated with 1 mg of testosterone from day 16 to day 19 of pregnancy, and female offspring were followed until 90 days of age, when they were euthanized. The prenatally hyperandrogenized (PH) female offspring displayed two phenotypes: irregular ovulatory (PHiov) and anovulatory (PHanov). Regarding lipid metabolism, both PH groups displayed disruptions in the main lipid pathways with altered levels of triglyceride and increased lipid peroxidation levels. In addition, we found that Peroxisome Proliferator-Activated Receptors (PPARs) alpha protein expression was decreased in both PH phenotypes (p < 0.05), but no changes were found in PPARγ protein levels. Furthermore, regarding adipokines, no changes were found in Leptin and Adiponectin protein levels, but Chemerin protein levels were decreased in the PHiov group (p < 0.05). Regarding de novo synthesis of steroids, the PHanov group showed increased protein levels of Cyp17a1 and Cyp19, while the PHiov group only showed decreased protein levels of Cyp19 (p < 0.05). These results suggest that prenatal androgen exposure affects females’ gonadal adipose tissue in adulthood, disturbing different lipid pathways, Chemerin expression, and de novo synthesis of steroids.

4-Hydroxynonenal Modulates Blood-Brain Barrier Permeability In Vitro through Changes in Lipid Composition and Oxidative Status of Endothelial Cells and Astrocytes.

Blood brain barrier (BBB) is a dynamic interface responsible for proper functioning of brain, but also a major obstacle for effective treatment of neurological diseases. Increased levels of free radicals, in high ferrous and high lipid content surrounding, induce lipid peroxidation, leading to production of 4-hydroxynonenal (HNE). HNE modifies all key proteins responsible for proper brain functioning thus playing a major role in the onset of neurological diseases. To investigate HNE effects on BBB permeability, we developed two in vitro BBB models-'physiological' and 'pathological'. The latter mimicked HNE modified extracellular matrix under oxidative stress conditions in brain pathologies. We showed that exogenous HNE induce activation of antioxidative defense systems by increasing catalase activity and glutathione content as well as reducing lipid peroxide levels in endothelial cells and astrocytes of 'physiological' model. While in 'pathological' model, exogenous HNE further increased lipid peroxidation levels of endothelial cells and astrocytes, followed by increase in Nrf2 and glutathione levels in endothelial cells. At lipid composition level, HNE caused increase in ω3 polyunsaturated fatty acid (PUFA) level in endothelial cells, followed by decrease in ω3 PUFA level and increase in monounsaturated fatty acid level in astrocytes. Using these models, we showed for the first time that HNE in 'pathological' model can reduce BBB permeability.

Effects of Eugenol on Water Quality and the Metabolism and Antioxidant Capacity of Juvenile Greater Amberjack (Seriola dumerili) under Simulated Transport Conditions.

Simple SummaryThe transportation of live fish is a very important part of the aquaculture system. The health status of fish can be affected in the closed-container transportation system. It has become very common to relieve the stress of fish in transport by adding anesthetics. With the food safety of fish having gained widespread attention, the addition of plant extracts as an alternative to anesthetics has become an important research topic. The objective of this study was to evaluate the effects of eugenol addition during simulated transport on water quality, and the metabolism and antioxidant capacity of liver and gills in the greater amberjack (Seriola dumerili). It was found that the addition of eugenol under simulated transport conditions had positive effects on water quality, and on liver and gill metabolism and antioxidant capacity in the greater amberjack. This study contributes to the healthy culture of the greater amberjack.This study investigated the effects of added eugenol on water quality and the metabolism and antioxidant capacity of the liver and gills of the greater amberjack (Seriola dumerili) during simulated transport. The juvenile fish (10.34 ± 1.33 g) were transported in sealed plastic bags containing different eugenol concentrations at a density of 24.79 kg/m3 for 8 h. The different eugenol concentrations were divided into five groups: 0 μL/mL (control group), 0.0125 μL/mL, 0.025 μL/mL, 0.0375 μL/mL, and 0.05 μL/mL, with three replicates of each. The results showed that 0.05 μL/mL of eugenol could significantly increase dissolved oxygen, but 0.025 μL/mL–0.0375 μL/mL resulted in a significant decrease in dissolved oxygen and significant increases in NH4+-N and NO2−-N. It was found that 0.05 μL/mL of eugenol caused significant up-regulation of the relative expression of CPT-1 in the liver, significant down-regulation of the relative expression of FAS and PK in the liver and gills, a significant increase in glycogen concentration, and a significant decrease in glucose concentration. This suggests that 0.05 μL/mL of eugenol could reduce the metabolic capacity of fish. In addition, 0.05 μL/mL of eugenol caused significant up-regulation of the relative expression of CAT and a significant decrease of MDA concentration in the liver. Meanwhile, the gills showed significant up-regulation of CAT relative expression, significant down-regulation of Keap1 relative expression, and a significant increase in GSH activity, resulting in a significant increase in MDA concentration when the concentration of eugenol reached or exceeded 0.025 μL/mL. This suggests that 0.05 μL/mL eugenol could improve the antioxidant capacity of fish and lipid peroxidation levels in the gills. In conclusion, the addition of 0.05 μL/mL eugenol could improve water quality, and the metabolic and antioxidant capacities of liver and gills, but it could also increase lipid peroxidation levels in the gills under transport conditions.

Combined Effects of Cadmium- and Cyanide-Contaminated Diet on Oxidative Stress Biomarkers in Different Tissues of Rats

Background. Several toxicants present simultaneously in the environment have combined toxicological effects. In addition, various xenobiotics have distinct effects on oxidative stress biomarkers in animal cells and tissues.&#x0D; The aim of this study was to analyze the effect of cadmium (Cd) and cyanide (CN) through the food chain on some antioxidant indices in the tissues (lungs, testes, heart, and brain) of male Wistar rats.&#x0D; Materials and Methods. The study included sixty African catfish allocated to four groups, each comprising fifteen fish, treated with potassium cyanide (KCN) and cadmium chloride (CdCl2), held at a temperature of 25°C in a 100-litre fish tank aquarium with water contaminated with 0.4 mg of both cyanide and cadmium/100 ml of water. All the fish were later killed, dried, and used to prepare diet for experimental animals. Twenty male rats divided into four groups, each comprising five rats, were used for this study as well, and fed for 28 days as follows: Group A - control diet; Group B - cyanide-contaminated diet; Group C - cadmium-contaminated diet; Group D - diet contaminated with cyanide + cadmium. Subsequently, they were sacrificed. Biochemical analysis of the tissues excised from the rats was done.&#x0D; Results. There was a significant (p &lt; 0.05) increase in lipid peroxidation level and a significant decrease in superoxide dismutase, catalase and reduced glutathione activities in the lungs, testes, heart, and brain of rats fed a catfish diet containing both cyanide and cadmium as compared to controls. In addition, contaminated diet altered acetylcholinesterase activity in the brain, glutathione peroxidase activity, glutathione-S-transferase activity, and glutathione reductase activity in the tissues of experimental rats.&#x0D; Conclusions. Cadmium and cyanide, via the food chain, induce oxidative stress in the lungs, testes, heart, and brain of rats.

Paradoxical Anxiety Level Reduction in Animal Chronic Stress: A Unique Role of Hippocampus Neurobiology.

A paradoxical reduction in anxiety levels in chronic predator stress paradigm (PS) in Sprague–Dawley rats has recently been shown in previous works. In this paper, we studied the possible neurobiological mechanism of this phenomenon. We segregated PS-exposed Sprague–Dawley rats into the high- and low-anxiety phenotypes. The long-lasting effects of PS on corticosterone levels, blood flow speed in the carotid arteries, diffusion coefficient, and 1H nuclear magnetic resonance spectra in the hippocampus were compared in the high-anxiety and low-anxiety rats. In addition, we evaluated the gene BDNF expression in the hippocampus which is considered to be a main factor of neuroplasticity. We demonstrated that in low-anxiety rats, the corticosterone level was decreased and carotid blood flow speed was increased. Moreover, in the hippocampus of low-anxiety rats compared to the control group and high-anxiety rats, the following changes were observed: (a) a decrease in N-acetyl aspartate levels with a simultaneous increase in phosphoryl ethanol amine levels; (b) an increase in lipid peroxidation levels; (c) a decrease in apparent diffusion coefficient value; (d) an increase in BDNF gene expression. Based on these findings, we proposed that stress-induced anxiety reduction is associated with the elevation of BDNF gene expression directly. Low corticosterone levels and a rise in carotid blood flow speed might facilitate BDNF gene expression. Meanwhile, the decrease in apparent diffusion coefficient value and decrease in N-acetyl aspartate levels, as well as an increase in the lipid peroxidation levels, in the hippocampus possibly reflected destructive changes in the hippocampus. We suggested that in Sprague–Dawley rats, these morphological alterations might be considered as an impetus for further increase in neuroplasticity in the hippocampus.

LUHMES Dopaminergic Neurons Are Uniquely Susceptible to Ferroptosis.

Ferroptosis is a necrotic cell death caused by lipid oxidation that may be responsible for neural degeneration in Parkinson's disease. We assessed whether three neuronal cell lines are sensitive to killing by ferroptosis. Ferroptosis inducer erastin killed LUHMES neurons at sub-micromolar concentrations, whereas neuronal cells derived from SH-SY5Y cells or neural stem cells were at least 50-fold less sensitive. LUHMES differentiated neurons were likewise sensitive to killing by RSL3 or ML210, inhibitors of the glutathione peroxidase 4 enzyme (GPX4) that consumes GSH to detoxify lipid peroxides. Additional assays showed that erastin, RSL3, and ML210 increased lipid peroxide levels, and that LUHMES neurons were protected from both peroxide accumulation and cell death by ferrostatin-1. A possible role of iron was assessed by evaluating the effects of five metal chelators on cytotoxicity of erastin and RSL3. LUHMES neurons were protected from RSL3 by three of the chelators, 2,3-dimercapto-1-propanesulfonic acid (DMPS), deferoxiprone (DFX), and deferiprone (DFP). Collectively, these results demonstrate the vulnerability of LUHMES neurons to ferroptosis by chemical treatments that disrupt glutathione synthesis, lipid peroxide detoxification, or iron metabolism. The same vulnerabilities may occur in CNS neurons, which reportedly generate low levels of GSH and metallothioneins, limiting their ability to neutralize oxidative stresses and toxic metals. These results suggest a rationale and methods to search for environmental toxicants that may exploit these vulnerabilities and promote neurodegenerative diseases.

Analysis of Physiological Status in Response to Water Deficit of Spelt (Triticum aestivum ssp. spelta) Cultivars in Reference to Common Wheat (Triticum aestivum ssp. vulgare)

Climate change, including decreasing rainfall, makes cultivating cereals more difficult. Drought stress reduces plant growth and most all yields. On the other hand, consumers’ interest in ancient wheat varieties, including spelt, is growing. The aim of this work is to compare the response to drought stress between spelt (Triticum aestivum ssp. spelta) and common wheat (Triticum aestivum ssp. vulgare). Six cultivars of spelt from different European countries and common wheat ‘Bogatka’ as a reference were chosen for research. The photosynthesis process, chlorophyll fluorescence, relative water content, and the content of free proline and anthocyanins in well-watered and drought-stressed plants were measured. It was shown that the spelt cultivars ‘Franckenkorn’ and ‘Badengold’ were much more resistant to water deficit than other cultivars and even common wheat. A slight reduction of CO2 assimilation (by 27%) and no reduction of transpiration rate, with simultaneous intensive proline (eighteen times fold increase) and anthocyanins accumulation (increase by 222%) along with a slight increase in lipid peroxidation level (1.9%) revealed in ‘Franckenkorn’ prove that this cultivar can cope with drought and can be effectively cultivated in areas with limited water abundance.