Serum Nitrite Levels Research Articles

Impact of spinal anesthesia on myocardial damage, ultrastructure and cellular mechanisms in rats undergoing thoracic incision surgery.

Impact of spinal anesthesia on myocardial damage, ultrastructure and cellular mechanisms in rats undergoing thoracic incision surgery.

Pelargonidin improves functional recovery and attenuates neuropathic pain following spinal cord injury in rats: relevance to its neuroprotective, antioxidant, and anti-inflammatory effects.

Spinal cord injury (SCI) significantly impairs individuals' sensorimotor functions, hindering daily activities. Current therapeutic options often demonstrate limited efficacy and lead to undesirable side effects. Emerging research highlights the potential of anthocyanins, especially pelargonidin, which possess neuroprotective, anti-inflammatory, and antioxidant properties beneficial for neurological conditions. This study sought to explore the impact of intrathecal administration of pelargonidin on the recovery of sensory-motor functions and associated disorders in a rat model of SCI through neuroprotective effects and regulating inflammatory/oxidative stress mediators. In total, 35 male Wistar rats were divided into five groups: sham, SCI, and three treatment groups receiving different intrathecal concentrations of pelargonidin (1, 2, and 4mM) once on day 0 after surgery/injury. Weight changes were assessed and behavioral analyses were done, including hot plate tests, acetone drop tests, von Frey tests, inclined plane tests, as well as Basso, Beattie, and Bresnahan (BBB) scores, weekly up to day 28 post-injury. On day 28, serum levels of nitrite, catalase, and glutathione as well as matrix metalloproteinase (MMP) assays and histological evaluations were done. Pelargonidin significantly attenuated neuropathic pain, improved motor performance, and reduced weight loss in rats with SCI. Biochemical assays demonstrated increased serum catalase/glutathione level, and MMP2 activity, while decreased serum nitrite level and MMP9 activity. Histological analyses showed an enhancement in the number of motor neurons in the ventral horn of the spinal cord after treatment with pelargonidin, highlighting its neuroprotective and neurogenic effects. Pelargonidin makes substantial therapeutic benefits following SCI by accelerating sensorimotor recovery. This effect is likely due to its strong antioxidant, anti-inflammatory, and neuroprotective properties.

Galbanic acid delays the development of seizures by modulating the expression of TNFα, IL1β, and TLR4 genes and reducing hippocampal nitrite levels and may be useful in the treatment of epilepsy.

Galbanic acid delays the development of seizures by modulating the expression of TNFα, IL1β, and TLR4 genes and reducing hippocampal nitrite levels and may be useful in the treatment of epilepsy.

Unveiling the effects of Rosa canina oligosaccharide liposome on neuropathic pain and motor dysfunction following spinal cord injury in rats: relevance to its antioxidative effects.

Spinal cord injury (SCI) is a leading cause of sensorimotor disorders, impacting millions of people globally. The absence of effective treatments and the side effects of existing medications highlight the need for innovative research into new therapeutic compounds. Given the critical role of oxidative stress in the development of SCI and the antioxidant properties of oligosaccharides in other neurological disorders, this study focuses on the role of oxidative stress in SCI and explores the potential of a novel oligosaccharide nanoformulation derived from Rosa canina (Oligo-L). Oligo-L was formulated using soy lecithin as the phospholipid and the characterization included size, zeta potential, morphology, and drug loading efficiency. Then 35 Wistar male rats were divided into five groups of Sham, SCI, and Oligo-L (10μL intrathecal injection of 15, 30, and 45mg/mL). An aneurysm clip was used to induce compression injury of the SCI and Oligo-L groups. Sensory-motor functions were evaluated weekly for 4weeks using tests such as the BBB scale, inclined plane, acetone drop, hot plate, von Frey, and monitoring of weight changes. Additionally, oxidative stress markers and histological changes were examined to evaluate changes in nitrite, glutathione, catalase, and neuronal survival. The findings indicated that Oligo-L treatment led to significant improvements in neuropathic pain, and motor function performance and weight of the animals from the first week post-SCI. Oligo-L also enhanced catalase and glutathione levels while reducing serum nitrite levels, contributing to neuronal preservation. Additionally, Oligo-L increased neuronal survival in the both ventral (motor neurons) and dorsal (sensory neurons) horns of the spinal cord. Overall, Oligo-L, characterized by its beneficial physicochemical properties, showed promising potential as a neuroprotective agent and facilitated the recovery of sensory and motor functions after SCI.

Tadalafil Ameliorates Chronic Ischemia-Associated Bladder Overactivity in Fructose-Fed Rats by Exerting Pelvic Angiogenesis and Enhancing p-eNOS Expression.

Metabolic syndrome (MetS) can contribute to a chronic ischemia-relative overactive bladder (OAB). Using fructose-fed rats (FFRs), a rat model of MetS, we investigated the effects of tadalafil (a phosphodiesterase-5 inhibitor) on MetS-associated chronic bladder ischemia and bladder overactivity. Phenotypes of the OAB, including increased micturition frequency and a shortened intercontractile interval in cystometry, were observed in FFRs, together with reduced bladder blood perfusion (in empty bladders) via laser color Doppler imaging and elevated serum nitrite levels, suggesting chronic ischemia-related bladder dysfunction. Treatment with tadalafil (2 mg/kg) promoted pelvic angiogenesis, as shown by magnetic resonance imaging, and increased VEGF and p-eNOS overexpression in the bladder. This treatment restored bladder perfusion and alleviated bladder overactivity without significantly altering most MetS parameters. At the molecular level, FFRs exhibited increased ischemia markers (NGF, HIF-2α, and AMPK-α2) and decreased p-AMPK-α2, along with elevated proinflammatory mediators (ICAM-1, nuclear NF-κB, COX-2, IL-1β, IL-6, and TNF-α), enhanced mitochondria biogenesis (PGC-1α, TFAM, and mitochondria DNA copy number), oxidative stress (decreased nuclear NRF2, increase MnSOD and 8-OHdG staining), and tissue fibrosis (increased TGF-β1, collagen I, and fibronectin). Tadalafil treatment improved these effects. Together, these findings suggest that tadalafil may promote VEGF-associated angiogenesis, enhance p-eNOS staining in the bladder vasculature, normalize bladder perfusion in microcirculation, and reduce serum nitrite levels. Consequently, tadalafil mitigates the adverse effects of chronic ischemia/hypoxia, improving bladder overactivity. We elucidated the mechanisms underlying the tadalafil-mediated amelioration of MetS-associated OAB symptoms.

Rutin engages opioid/benzodiazepine receptors towards anti-neuropathic potential in a rat model of chronic constriction injury: relevance to its antioxidant and anti-inflammatory effects.

Neuropathic pain is a chronic type of pain caused by damage or dysfunction in the nervous system. It can be quite bothersome and often doesn't well respond to common painkillers. Among natural compounds, rutin (Rut) stands out for its remarkable antioxidant, and anti-inflammatory properties. In this research, our objective is to investigate the impact of Rut on an animal model of chronic constriction injury (CCI). A total of 54 adult Wistar rats were divided randomly into nine separate groups. Groups included sham, CCI, gabapentin (GBP, 100 mg/kg), Rut (10, 25 mg/kg), flumazenil (FLU, 0.5 mg/kg), naloxone (NAL, 0.1 mg/kg), Rut (10 mg/kg) + FLU (0.5 mg/kg), and Rut (10 mg/kg) + NAL (0.1 mg/kg). The aforementioned drug injection (intraperitoneal, i.p.) and sensorimotor behavioral tests were performed on days 1, 3, 5, 7, 9, 11, and 14. Biochemical (e.g., nitrite, catalase, glutathione), zymography (matrix-metalloproteinase 2 and 9), and histopathological tests were performed on day 14 after surgery. The findings demonstrated that Rut administration effectively alleviated symptoms of allodynia/hyperalgesia, and improved locomotor activity following CCI. Additionally, Rut administration resulted in increased catalase and glutathione activity, while reducing serum nitrite levels, as well as matrix metalloproteinase 2 and 9 activity. Additionally, histological results indicated that Rut improved sciatic nerve regeneration. Since the aforementioned effects of Rut were reversed by using opioid and benzodiazepine receptor antagonists (i.e., NAL and FLU, respectively), the receptors' involvement was revealed in the anti-neuropathic effects of Rut. In conclusion,Rut emerged as a potentially effective candidate for treating neuropathic pain and improving motor function by increasing antioxidant mediators, suppressing inflammation, and activating opioid/benzodiazepine receptors.

Association of over-the-counter mouthwash use with markers of nitric oxide metabolism, inflammation, and endothelial function-a cross-sectional study.

Regular use of mouthwash can disrupt nitrate reduction by oral bacteria and may affect systemic nitric oxide (NO) levels, which are important for inflammation and endothelial function. We aim to assess the association between over-the-counter (OTC) mouthwash use and nitrate/nitrite, markers of inflammation (IL-6, TNF-α, CRP) and endothelial function (sICAM-1, sVCAM-1) in serum and saliva, and to assess the relationship between nitrate/nitrite levels and these biomarkers, as well as how OTC mouthwash modulated this relationship. We hypothesize that nitrates/nitrites are associated with these biomarkers, and that their associations would vary with the frequency of mouthwash use. Our cross-sectional study used data and specimen from the baseline of the San Juan Overweight Adult Longitudinal Study (SOALS). Robust Gamma regression with log-link function, Spearman correlations and partial correlations adjusted for covariates were used for the analysis. Using OTC mouthwash twice a day or more was significantly associated with lower serum nitrite levels compared to less frequent use (β = -0.357, 95% CI: -0.650, -0.064), but not with other markers of inflammation and endothelial function. Mouthwash use differentially impacted the relationship between nitrate/nitrite and TNF-α, sICAM-1 and sVCAM-1. Specifically, in the participants who used mouthwash less than twice a day or no use, TNF-α (β = -0.35, 95% CI: -0.52, -0.18), and sICAM-1 (β = -0.21, 95% CI: -0.32, -0.09) were negatively associated with serum nitrite. In the participants who used mouthwash twice a day or more use, TNF-α was positively associated with serum nitrate (β = 3.36, 95% CI: 2.07, 4.65), salivary nitrite (β = 1.04, 95% CI: 0.39, 1.69) and salivary nitrate (β = 0.48, 95% CI: 0.25, 0.71); sICAM-1 was positively associated with serum nitrate (β = 1.58, 95% CI: 0.86, 2.29). In both subgroups of mouthwash users, sVCAM-1 was positively correlated with serum nitrate and salivary nitrate. In addition, sVCAM-1 was positively correlated with serum nitrite in participants who used mouthwash frequently (ρ_S = 0.18, p = 0.045). Regular use of OTC mouthwash was associated with systemic nitric oxide. This raises concerns about its potential effects on the levels of inflammatory and endothelial biomarkers associated with cardiometabolic diseases.

Protective effects of polydatin amphiphilic chitosan nanocarriers against an aluminum chloride-induced model of Alzheimer's disease in rats: relevance to its anti-inflammatory and antioxidant effects.

Alzheimer's disease (AD) is the most frequent cause of dementia. Since there are complex pathophysiological mechanisms behind AD, and there is no effective treatment strategy, it is necessary to introduce novel multi-targeting agents with fewer side effects and higher efficacy. Polydatin (PD) is a naturally occurring resveratrol glucoside employing multiple mechanisms toward neuroprotection. In the current study, the anti-AD mechanisms of a novel amphiphilic chitosan nanocarrier formulation (ACN) of PD (NPD) were studied. After preparing the amphiphilic chitosan nanoformulation (i.e., NPD), physicochemical properties were assessed, including particle size, zeta potential, drug loading, drug release, MTT, Fourier transform infrared spectroscopy (FT-IR), and scanning electron microscopy (SEM). For in vivo analysis, aluminum chloride (AlCl3) was injected intraperitoneally for 14 days to induce AD in male Albino Wistar rats. To examine the anti-AD mechanisms of NPD, a total of 36 rats were divided into six groups of six. Behavioral tests, including open field, Y-maze, elevated plus maze, and shuttle box were done on days 7, 8, 14, and 15. Additionally, zymography, biochemical analysis, and histological studies were done. NPD, as a newly synthesized formulation for PD, potentially improved memory and cognitive behavioral parameters and reduced the activity ofinflammatory matrix metalloproteinase 9 (MMP9) and serum nitrite levels, while increasing anti-inflammatory MMP2, antioxidant catalase, and glutathione. NPD also prevented morphological changes and increased neuronal survival in the CA2, CA4, and DG regions of the rat hippocampus. In conclusion,NPD is a novel formulation against AD through anti-inflammatory, antioxidant, and neuroprotective mechanisms.

Polydatin attenuates Alzheimer's disease induced by aluminum chloride in rats: evidence for its antioxidant and anti-inflammatory effects.

Considering the complex pathophysiological mechanisms behind Alzheimer's disease (AD), a few drugs for managing related cognitive symptoms have been approved. The phytochemical resveratrol has shown promising anti-inflammatory and antioxidant effects in AD, but it has low bioavailability. Chemical modification of resveratrol to its glycosylated form, polydatin (PD), significantly increases its bioavailability and bioactivity. The study aimed to investigate the therapeutic potential and mechanisms of action of PD against AD in rats. AD was caused by an intraperitoneal (i.p.) administration of aluminum chloride (AlCl3). Six groups of six rats each were defined as sham, negative control (AlCl3), positive control (Donepezil), and treatments (PD 5, 10, and 20mg/kg, i.p.). On days 7, 8, 14, and 15, the rats' behavioral changes were assessed by the open field, Y-maze test, passive avoidance test, and elevated plus maze tests. At the end of the study, the blood samples were collected to assess the levels of glutathione (GSH), catalase (CAT), and nitrite, as well as the activity of matrix metalloproteinases (MMPs). Furthermore, hippocampal brain tissue was removed and used for histological investigations. The findings revealed that PD injections at three different doses (5, 10, and 20mg/kg) improved cognitive and other behavioral impairments. Furthermore, PD improved the antioxidant capacity by increasing GSH and CAT while decreasing serum nitrite levels. PD showed anti-inflammatory effects by reducing the activity of inflammatory MMP-9, while elevating the activity of anti-inflammatory MMP-2. PD also modulated pathogenic changes in the hippocampal brain tissue. PD alleviated cognitive and other behavioral impairments in AD rats by enhancing antioxidant defenses and reducing neuroinflammation.

Organic vs. inorganic nitrates: Metabolic and vascular outcomes in STZ-induced diabetes in mice

Organic vs. inorganic nitrates: Metabolic and vascular outcomes in STZ-induced diabetes in mice

Protective effects of astaxanthin solid lipid nanoparticle as a promising candidate against acute kidney injury in rats.

Acute kidney injury (AKI) is a sudden onset of renal injury that occurs within a few hours or days. Ischemia-reperfusion (IR) is a major cause of AKI. There are multiple dysregulated mechanisms behind the pathogenesis of AKI and IR which urges the need for finding multi-targeting therapies. Natural products are multi-targeting agents with promising sources of anti-inflammation, antioxidant, and antiapoptosis. Among them, astaxanthin (AST) is a keto-carotenoid with a high antioxidant potential. Using solid lipid nanoparticles (SLNs) as a novel formulation of AST helps to increase its efficacy and reduce side effects against AKI. After SLN preparation and loading of AST, the physicochemical properties were evaluated, using scanning electron microscopy (SEM) and dynamic light scattering (DLS) tests. For the in vivo study, 28 rats were divided into four groups, including sham, ischemia/reperfusion (I/R), and groups receiving protective and daily doses of AST-SLN (5 and 10 mg/kg, i.p.) during all 5 days before ischemia. Exactly 24 h after ischemia, kidneys were isolated for histological studies, and also, serum levels of catalase (CAT), glutathione (GSH), nitrite, blood urea, and creatinine were measured. The results indicated that intraperitoneal administration of SLN-AST reduced oxidative stress by decreasing serum nitrite levels, while increasing CAT and GSH. SLN-AST also improved renal function by decreasing serum urea and creatinine and preventing tissue damage. Therefore, SLN-AST could be a hopeful adjuvant candidate to prevent AKI by modulating renal function, preventing tissue damage, and through antioxidant mechanisms.

Sinapinic acid as a potential therapeutic agent for epilepsy through targeting NMDA receptors and nitrite level

Epilepsy, a widespread neural ailment considered by prolonged neuronal depolarization and repetitive discharge, has been linked to extreme stimulus of N-methyl-D-aspartate receptors (NMDARs). Despite the availability of approved anti-seizure medications (ASMs) in many developed nations, approximately 30% of epilepsy patients continue to experience drug-resistant seizures. Thus, a growing interest in discovering natural compounds as potential sources for new medications is growing. Sinapinic acid, a natural derivative of cinnamic acid found in food sources, is known for its neuroprotective properties. This study investigated how sinapinic acid interacts with NMDA receptors and its potential role in providing anticonvulsant effects. Male mice were randomly allocated into nine groups: a control group receiving normal saline (1 ml/kg), groups treated with sinapinic acid at doses of 1, 3, and 10 mg/kg, a group treated with diazepam at 10 mg/kg, a group treated with an NMDA agonist at 75 mg/kg, a group treated with an NMDA antagonist at 0.5 mg/kg, a group receiving the ineffective dose of sinapinic acid (1 mg/kg) along with the NMDA antagonist, and a group receiving the effective dose of sinapinic acid (10 mg/kg) along with the NMDA agonist. Sinapinic acid and other treatments were administered intraperitoneally 30 min prior to inducing seizures with PTZ injection. Seizure onset time was recorded following PTZ injection. Blood and brain samples were collected after anesthesia to determine serum and brain nitrite levels. Real-time PCR assessed NMDAR gene expression in the prefrontal cortex (PFC). Data were analyzed using Prism software. The time seizures began was notably extended in groups treated with sinapinic acid at doses of 3 and 10 mg/kg compared to those treated with saline (P < 0.05). Additionally, in the receiving group of an ineffective dose of sinapinic acid alongside ketamine, the beginning of seizure time was significantly prolonged compared to the group that received the ineffective dose of sinapinic acid alone (P < 0.05). Serum and prefrontal cortex (PFC) nitrite levels were significantly lower in mice treated with sinapinic acid at doses of 1, 3, and 10 mg/kg compared to the saline-treated group (P < 0.05). The gene expression of the NMDAR NR2B subunit in the PFC was decreased in groups treated with sinapinic acid at 1 and 10 mg/kg compared to the saline-treated group. Furthermore, co-administration of sinapinic acid (10 mg/kg) with NMDA resulted in significantly lower NR2A gene expression than the group treated with 10 mg/kg of sinapinic acid alone. Conversely, co-administration of ketamine with sinapinic acid (1 mg/kg) significantly increased NR2B subunit gene expression compared to the group treated with sinapinic acid at 1 mg/kg alone. Sinapinic acid showed anticonvulsant effects through reduced serum and PFC nitrite and modulation of glutamatergic signaling.

Polydatin attenuated neuropathic pain and motor dysfunction following spinal cord injury in rats by employing its anti-inflammatory and antioxidant effects.

Considering the complex pathological mechanisms behind spinal cord injury (SCI) and the adverse effects of present non-approved drugs against SCI, new studies are needed to introduce novel multi-target active ingredients with higher efficacy and lower side effects. Polydatin (PLD) is a naturally occurring stilbenoid glucoside recognized for its antioxidative and anti-inflammatory properties. This study aimed to assess the effects of PLD on sensory-motor function following SCI in rats. Following laminectomy and clip compression injury at the thoracic 8 (T8)-T9 level of the spinal cord, rats were randomly assigned to five groups: Sham, SCI, and three groups receiving different doses of PLD treatment (1, 2, and 3mg/kg). Over 4weeks, behavioral tests were done such as von Frey, acetone drop, hot plate, Basso-Beattie-Bresnahan, and inclined plane test. At the end of the study, changes in catalase and glutathione activity, nitrite level, activity of matrix metalloproteinase 2 (MMP2) and MMP9 as well as spinal tissue remyelination/neurogenesis, were evaluated. The results revealed that PLD treatment significantly improved the behavioral performance of the animals starting from the first week after SCI. Additionally, PLD increased catalase, and glutathione levels, and MMP2 activity while reduced serum nitrite levels and MMP9. These positive effects were accompanied by a reduction in the size of the lesion and preservation of neuronal count. In conclusion, PLD showed neuroprotective effects in SCI rats by employing anti-inflammatory and antioxidant effects, through which improve sensory and motor function.

Sequential Administration of Febuxostat, Amlodipine and Vitamin E Attenuate Oxidative Stress and Improve Spermatogenesis in Testicular Ischemia Reperfusion Injury in Wistar Rats

This study investigated the effects of sequential administration of febuxostat, amlodipine, and vitamin E on oxidative stress and spermatogenesis following testicular ischemia-reperfusion injury (TIRI) in Wistar rats. Ninety male rats (120-150 g) were divided into 9 groups (n=10 each): sham operation (SO), torsion-detorsion (TD), and seven treatment groups receiving different combinations of the drugs. The treatment groups included torsion + febuxostat + detorsion (TFD), torsion + detorsion + amlodipine (TDA), torsion + detorsion + vitamin E (TDV), and combinations thereof (TFDA, TFDV, TDAV, TFDAV). TIRI was induced by 720° clockwise testicular torsion for 1 hour followed by detorsion. Febuxostat (5 mg/kg) was administered 30 minutes after torsion, amlodipine (2.5 mg/kg) immediately upon detorsion, and vitamin E (10 mg/kg) 30 minutes after detorsion. Rats were sacrificed 56 days post-reperfusion. Testicular tissue was analyzed for antioxidant enzymes (superoxide dismutase, catalase), lipid peroxidation (malondialdehyde), total protein, inflammatory markers (serum nitrite, IL-1β), and spermatogenesis indices (testicular biopsy score, Leydig cell count). Results showed that TIRI significantly decreased antioxidant enzymes, significantly increased lipid peroxidation and inflammatory markers, and impaired spermatogenesis. In the TD group, superoxide dismutase (SOD) and catalase (CAT) activities were significantly decreased, while malondialdehyde (MDA) increased significantly compared to the SO group (p&lt;0.01). Serum nitrite and IL-1β levels in the TD group were also increased (p&lt;0.001). Furthermore, the testicular biopsy score and Leydig cell count in the TD group were significantly decreased in this study (p&lt;0.01). Sequential administration of febuxostat, amlodipine and vitamin E, particularly when all three were used (TFDAV group), significantly attenuated these changes. In the TFDAV group, SOD and CAT activities were improved, while MDA decreased compared to the TD group (p&lt;0.05). Serum nitrite and IL-1β levels in the TFDAV group were also decreased (p&lt;0.001). In addition, the testicular biopsy score and Leydig cell count in the TFDAV group increased in comparison with the TD group (p&lt;0.001). The study concludes that this sequential multi-drug approach shows promise in mitigating the long-term detrimental effects of TIRI on testicular function and fertility. The combination of febuxostat (a xanthine oxidase inhibitor), amlodipine (a calcium channel blocker), and vitamin E (an antioxidant) appears to provide protection against oxidative stress and inflammation induced by TIRI, thereby preserving spermatogenesis.

An Electroanalytical Enzymeless α-Fe2O3-ZnO Hybrid Nanostructure-Based Sensor for Sensitive Quantification of Nitrite Ions.

Nitrite monitoring serves as a fundamental practice for protecting public health, preserving environmental quality, ensuring food safety, maintaining industrial safety standards, and optimizing agricultural practices. Although many nitrite sensing methods have been recently developed, the quantification of nitrite remains challenging due to sensitivity and selectivity limitations. In this context, we present the fabrication of enzymeless iron oxide nanoparticle-modified zinc oxide nanorod (α-Fe2O3-ZnO NR) hybrid nanostructure-based nitrite sensor fabrication. The α-Fe2O3-ZnO NR hybrid nanostructure was synthesized using a two-step hydrothermal method and characterized in detail utilizing x-ray diffraction (XRD), field emission scanning electron microscopy (FESEM), transmission electron microscopy (TEM), and X-ray photoelectron spectroscopy (XPS). These analyses confirm the successful synthesis of an α-Fe2O3-ZnO NR hybrid nanostructure, highlighting its morphology, purity, crystallinity, and elemental constituents. The α-Fe2O3-ZnO NR hybrid nanostructure was used to modify the SPCE (screen-printed carbon electrode) for enzymeless nitrite sensor fabrication. The voltammetric methods (i.e., cyclic voltammetry (CV) and differential pulse voltammetry (DPV)) were employed to explore the electrochemical characteristics of α-Fe2O3-ZnO NR/SPCE sensors for nitrite. Upon examination of the sensor's electrochemical behavior across a range of nitrite concentrations (0 to 500 µM), it is evident that the α-Fe2O3-ZnO NR hybrid nanostructure shows an increased response with increasing nitrite concentration. The sensor demonstrates a linear response to nitrite concentrations up to 400 µM, a remarkable sensitivity of 18.10 µA µM-1 cm-2, and a notably low detection threshold of 0.16 µM. Furthermore, its exceptional selectivity, stability, and reproducibility make it an ideal tool for accurately measuring nitrite levels in serum, yielding reliable outcomes. This advancement heralds a significant step forward in the field of environmental monitoring, offering a potent solution for the precise assessment of nitrite pollution.

Montelukast Ameliorates 2K1C-Hypertension Induced Endothelial Dysfunction and Associated Vascular Dementia.

Declined kidney function associated with hypertension is a danger for cognitive deficits, dementia, and brain injury. Cognitive decline and vascular dementia (VaD) are serious public health concerns, which highlights the urgent need for study on the risk factors for cognitive decline. Cysteinyl leukotriene (CysLT1) receptors are concerned with regulating cognition, motivation, inflammatory processes, and neurogenesis. This research aims to examine the consequence of montelukast (specific CysLT1 antagonist) in renovascular hypertension 2-kidney-1-clip-2K1C model-triggered VaD in experimental animals. 2K1C tactics were made to prompt renovascular hypertension in mature male rats. Morris water maze was employed to measure cognition. Mean arterial pressure (MAP), serum nitrite levels, aortic superoxide content, vascular endothelial activity, brain's oxidative stress (diminished glutathione, raised lipid peroxides), inflammatory markers (IL-10, IL-6, TNF-α), cholinergic activity (raised acetylcholinesterase), and cerebral injury (staining of 2, 3, 5- triphenylterazolium chloride) were also examined. Montelukast in doses of 5.0 and 10.0 mg kg-1 was used intraperitoneally as the treatment drug. Along with cognitive deficits, 2K1C-operated rats showed elevated MAP, endothelial dysfunction, brain oxidative stress, inflammation, and cerebral damage with diminished serum nitrite/nitrate. Montelukast therapy significantly and dose-dependently mitigated the 2K1Chypertension- provoked impaired behaviors, biochemistry, endothelial functions, and cerebral infarction. The 2K1C tactic caused renovascular hypertension and associated VaD, which was mitigated via targeted regulation of CysLT1 receptors by montelukast administration. Therefore, montelukast may be taken into consideration for the evaluation of its complete potential in renovascular-hypertension-induced VaD.

Safety of dietary nitrate supplementation by calcium nitrate for finishing pigs as measured by methemoglobin and serum and tissue nitrate levels.

Nitrate supplementation has been studied as a beneficial constituent of the human diet, particularly for its effects on vascular health through vasodilation. Recent studies have focused on the benefits of nitrate supplementation in animals, especially in swine. Up to 1,200 mg/kg dietary nitrate supplementation from Ca nitrate was beneficial in farrowing and lactating sows and their offspring, and up to 6,000 mg/kg supplemental nitrate showed no adverse health effects in sows or piglets. Controlled study data evaluating the safety of nitrate supplementation to growing swine of any weight class is scant. Therefore, an experiment was conducted to test the hypothesis that increased inclusion rates of dietary nitrate through the addition of Ca nitrate in diets would not influence concentrations of nitrate or nitrite in serum and tissue, nor blood hemoglobin and methemoglobin. Forty-eight individually housed pigs (initial weight 119.1 ± 5.3 kg) were randomly allotted to four dietary treatments containing 0, 500, 1,000, or 2,000 mg/kg dietary nitrate and fed experimental diets for 28 d. Growth performance was not influenced (P > 0.10) by dietary treatment. The most sensitive safety endpoint, methemoglobin, did not change (P > 0.10) with dietary nitrate exposure up to 2,000 mg/kg. Serum and tissue nitrate and nitrite levels, myoglobin, and hemoglobin were not adversely affected (P > 0.10). Total myoglobin in the loin linearly increased (P < 0.05) with greater dietary nitrate in the diet, which is correlated with the red color of meat. This work established the safety of up to 2,000 mg/kg dietary nitrate from Ca nitrate as an ingredient in food for finishing pigs.

SOCIAL COGNITION AND OXIDATIVE STRESS IN SCHIZOPHRENIA PATIENTS AND FIRST-DEGREE RELATIVES OF PATIENTS.

Misattribution of motivational salience to non-salient (neutral) stimuli could be viewed as a hallmark of psychosis in schizophrenia. Studies have recently revealed increased subjective experience of emotional arousal (EA) to neutral social stimuli in paranoid schizophrenia psychosis, suggesting a misattribution of emotional salience to them. We examined this phenomenon directly by quantifying the level of EA subjectively attributed to low-arousal, neutral-valenced faces. Patients with remitted schizophrenia (PG) (n=26), first-degree relatives of schizophrenic patients (RG) (n=25), and healthy controls (HCG) (n=36) were compared in terms of oxidative stress parameters -serum Superoxide Dismutase, Catalase, Glutathione Peroxidase (GPx), Nitrite, Nitrate, Malondialdehyde, and Total Glutathione levels-, social cognition measured by the Reading the Mind in the Eyes Test and working memory measured by the N-back Task. Groups were compared, assuming that HCG had a genetically lower risk of schizophrenia compared to PG and RG. HCG performed significantly better than PG and RG, who were genetically at high risk, in terms of social cognition (respectively p=0.000, p=0.014), working memory (respectively p=0.001, p=0.003), and had statistically lower Glutathione Peroxidase (GPX) level than the PG and RG (both p:0.000). After controlling for the effect of the general intellectual abilities measured by the Raven Standard Progressive Matrices Test and working memory the differences between groups on the Eyes Test disappeared (p=0.057). However, this value tended to be significant. It was concluded that social cognition and working memory and GPx level may be used as endophenotypes and social cognition, working memory, and general intellectual skills are different but strongly related constructs. Endophenotypes guide treatment targets even after the disease has developed. The results of our study showed that in addition to psychopharmacological treatments, interventions to reduce oxidative stress and approaches to improve cognitive skills will have a positive impact on the disease's progression.

Chronic red laser treatment induces hypotensive effect in two-kidney one-clip model of renovascular hypertension in rat.

To evaluate whether the chronic effect of photobiomodulation therapy (PBM) onsystolic arterial pressure (SAP)from two kidneys one clip (2K-1C) hypertension animal models can cause a hypotensive effect. Serum levels of nitric oxide were also analyzed and the assessment of lipid peroxidation of the thoracic aorta artery. Male Wistar rats were used. Hypertensive animals (2K-1C) with Systolic arterial pressure (SAP) greater than or equal to 160mmHg were used. Systolic arterial pressure (SAP) was determined by the tail plethysmography technique. Normotensive (2K) and hypertensive (2K-1C) rats were treated to PBM for 4weeks using a laser whose irradiation parameters were: red wavelength (λ) = 660nm: operating continuously; 56s per point (3 points) spot size = 0.0295 cm2; average optical power of 100 mW; energy of 5.6J per point; irradiance of 3.40 W/cm2; fluency of 190J/cm2 per point. The application was on the animals tails, at 3 different points simultaneously, in contact with the skin. To assess serum nitrite and nitrate (NOx) levels, blood collection was performed after chronic PBM treatment, 24h after the last laser application. The evaluation of the lipid peroxidation of the thoracic aorta artery was performed by measuring the concentration of hydroperoxide by the FOX method. Chronic photobiomodulation therapy (PBM) by red laser (660nm) can induce a hypotensive effect in 64% of 2K-1C hypertensive animals, which we say responsive animals. There was no difference in serum NO levels 24h after the last red laser application, between treated and non-treated groups. Aortic rings from 2K-1C hypertensive animals present a higher lipid peroxidation. The chronic PBM treatment by red laser decreased aortic rings lipid peroxidation in hypertensive responsive groups, compared to control. our results indicate that chronic PBM made by red laser has an important hypotensive effect in renovascular hypertensivemodels, by a mechanism that involves decrease in oxidative stress from vascular beds.

Dietary nitrate accelerates the healing of infected skin wounds in mice by increasing microvascular density

Dietary nitrate accelerates the healing of infected skin wounds in mice by increasing microvascular density