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Low doses of nitrite, close to physiological levels, increase blood flow in normal and ischemic tissues through a nitric oxide (NO) dependent mechanism. Given that nitrite therapy and dietary supplementation with vegetables high in nitrate (e.g. beets) are gaining popularity we decided to determine if low doses of nitrite impact the development of choroidal neovascularization (CNV), a key feature of wet age related macular degeneration (AMD). Sodium nitrite (at 50 mg/L, 150 mg/L, and 300 mg/L), nitrate (1 g/L) or water alone were provided in the drinking water of C57BL/6J mice aged 2 or 12 months. Mice were allowed to drink ad libitum for 1 week at which time laser-induced choroidal neovascularization (L-CNV) was induced. The mice continued to drink the supplemented water ad libitum for a further 14 days at which point optical coherence tomography (OCT) was performed to determine the volume of the CNV lesion. Blood was drawn to determine nitrite and nitrate levels and eyes taken for histology. CNV volume was 2.86 × 10(7) μm(3) (±0.4×10(7)) in young mice on water alone but CNV volume more than doubled to >6.9 × 10(7) μm(3) (±0.8×10(7)) in mice receiving 300 mg/L nitrite or 7.34 × 10(7) μm(3) (±1.4×10(7)) in 1 g/L nitrate (p

The present study was conducted to investigate the protective effects of selenium on the oxidative damage of kidney cells (CIK) caused by nitrite exposure in grass carp (Ctenopharyngodon idella). Cells were pre-incubated by Na2SeO3 (10 μmol/L) for 12 h and then exposed to NaNO2 (25 mg/L) for 24 h, the cell viability, apoptosis, gene expression, and antioxidant enzyme activity were assayed. The results show that nitrite reduced cell viability and induced apoptosis, and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) as well as the sod, cat, and gpx genes reduced (p

Sodium nitrite is a common practice additive in meat products for enhancing color, flavor, and microbial quality; however, several studies link its post-procession to the formation of carcinogenic N-nitrosamines. The aim of this study was to fabricate and validate a portable, rapid, and accurate microfluidic polydimethylsiloxane (PDMS) analytical device to determine the nitrite concentration in meat products. The colorimetric determination of nitrite using PDMS is based on Griess reaction. The proposed PDMS method was validated and the uncertainty evaluated according to Eurachem guidelines. Results demonstrated that PDMS device’s detection and quantification limits for nitrite were 0.1 and 0.4 mg L−1, respectively. A complete correlation (R2 = 0.99) and RSD value was 1.3–2.1% (inter-day precision) and 1.5–2.4% (intra-day precision). The PDMS method is highly robust, accurate 98.8%, and uncertainty measurement 3.5%. No significant differences between PDMS device and spectrophotometry were found during the determination of nitrite in examined processed meat products. The overall analysis of the PDMS device could be completed within 10 min. The PDMS-based device has potential applications for rapid detection and routinely screen the nitrite concentration of meat products and guarantee food safety.

The application of plant extracts (PEs) could be a promising option to satisfy consumers' demand for natural additives to inhibit growth of variable pathogenic bacteria. Thus, the aim of this study was to develop a standardized microdilution method to examine the antimicrobial effects of 10 hydrophilic PEs against two strains of Clostridium perfringens facing various food-relevant influencing factors. Because of the high opacity of PEs, resazurin was used as an indicator for bacterial growth instead of pellet formation. The highest value of the MIC of the replications of each PE was defined as effective plant extract concentration (EPC), whereas the next concentration beneath the lowest MIC was defined as the ineffective plant extract concentration (IEPC). The EPCs of seven PEs, allspice, cardamom, cinnamon, clove, coriander, ginger, and mace, were between 0.625 and 10 g/kg, whereas extracts of caraway, nutmeg, and thyme showed no antimicrobial activity up to the maximum concentration tested (10 g/kg) against C. perfringens in vitro. Two intrinsic factors, sodium chloride (NaCl) and sodium nitrite (NaNO2), displayed either synergistic or additive effects or no interaction with most PEs. By combination with PEs at their IEPC (0.08 to 1.25 g/kg), MIC of NaCl and NaNO2 decreased from between 25 and 50 g/kg to between 6 and 25 g/kg and from more than 200 mg/kg to between 0.2 and 100 mg/kg, respectively. In contrast, lipid (sunflower oil) at a low concentration inhibited the antimicrobial effects of all tested PEs. For extrinsic factors, only allspice, ginger, and coriander could maintain their antimicrobial effects after being heated to 78°C for 30 min. The synergistic effect between PEs and pH values (5.0 and 5.5) was also found for all PEs. The established screening method with resazurin and defining EPC and IEPC values allows the verification of antimicrobial effects of PEs under various food-relevant influencing factors in a fast and reproducible way. HIGHLIGHTS

The aim of this study was to investigate the effects of dietary sodium nitrite and meat on human health. Sodium nitrite in processed meat is known to be one of the main precursors of carcinogens, such as N-nitroso compounds. However, we previously found that processed meat is not the primary source of sodium nitrite; nitrate or the conversion of nitrate in vegetables are contribute to generate more than 70% Sodium nitrite or nitrate containing compounds in body. Although the heavy consumption of meat is likely to cause various diseases, meat intake is not the only cause of colorectal cancer. Our review indicates that sodium nitrite derived from foods and endogenous nitric oxide may exhibit positive effects on human health, such as preventing cardiovascular disease or improving reproductive function. Therefore, further epidemiological studies considering various factors, such as cigarette consumption, alcohol consumption, stress index, salt intake, and genetic factors, are required to reliably elucidate the effects of dietary sodium nitrite and meat on the incidence of diseases, such as colorectal cancer.

Vegetables, drinking water, and preserved meats may contain sodium nitrite (NaNO2), which causes liver disease by inducing oxidative stress. Phytochemicals are highly recommended as an alternative to synthetic drugs and affordable medicines to treat liver disease because they have fewer or no side effects. Therefore, this study aims to determine the antioxidant and hepatoprotective potential of red okra fruit ethanol extract against NaNO2-induced liver damage. Thirty-six male mice were separated into six groups. The normal control group (WA) was given distilled water only, and the NaNO2 (SN) group was given only 50 mg/kg BW NaNO2. The other four groups (P1, P2, P3, and P4) were given NaNO2 and red okra ethanol extract at doses of 25, 50, 75, and 100 mg/kg BW, respectively. Gavage was administered orally for 21 consecutive days. Commercial kits define all biochemical parameters according to the manufacturer’s instructions. Liver tissue staining followed standard protocols using hematoxylin and eosin. The study revealed that NaNO2 induction causes oxidative stress and damages the liver. The activity of antioxidant enzymes (superoxide dismutase and catalase) significantly increased in the groups treated (P2–P4) with ethanol extract of red okra ( p < 0.05 ). Besides, the oxidants (malondialdehyde, F2-isoprostanes, and nitric oxide) in the liver homogenate significantly decreased in the P4 group, which were given red okra ethanol extract ( p < 0.05 ). Likewise, red okra pods decreased significantly for the serum biochemical parameters of liver damage (aspartate aminotransferase, alkaline phosphatase, and alanine aminotransferase) in the P3 and P4 groups ( p < 0.05 ). Then, it led to a restoration of the histological structure compared to exposed mice (SN), as the pathological scores decreased significantly in the P3 and P4 groups ( p < 0.05 ), as well as the number of the necrotic and swollen liver cells was reduced. Hepatocytes returned to normal. The results showed that the ethanol extract of red okra fruit could be helpful as an affordable medicine. It is an antioxidant and hepatoprotective agent to protect the liver from damage caused by NaNO2.

The use of sodium nitrite in suicide has become more common among young adults in the Republic of Korea. This report details the case of a 28-year-old man; the man had posted on a social network service detailing his attempt at suicide at 13:45. In the posted article, he stated that he had ingested 84 g of sodium nitrite. A post-mortem (PM) inspection was performed at 21:00, and peripheral blood (PB) was collected. An autopsy was performed approximately 44 h after death. The victim's face was dark brown in color, but the color of his oral mucosa was bright red. Toxicological analyses revealed 33% and 26% methemoglobinemia in the PB collected during PM inspection and autopsy, respectively. The concentration of nitrate in the PB collected during PM inspection, and PB and cardiac blood collected during the autopsy were 220.6 mg/L, 220.0 mg/L, and 218.5 mg/L, respectively. Nitrate was also detected in the pericardial fluid and cerebrospinal fluid at levels of 91.7 mg/L and 50.5 mg/L, respectively. The cause of death was determined to be methemoglobinemia-induced hypoxia due to sodium nitrite ingestion. This intoxication case informs some novel points about nitrite intoxication; the concentration of methemoglobin decreased during the PM period, while the concentration of nitrate was stable. There was no difference in the concentration of nitrate between cardiac and peripheral blood. Nitrate could be detected in the pericardial fluid and cerebrospinal fluid. This new information is helpful for better identifying future cases of nitrite intoxication.

The objective of this study was to evaluate quality characteristics of pork emulsified-sausage (ES) containing paprika oleoresin solution (POS) as a replacement for sodium nitrite (NaNO2) during refrigerated storage. ESs were prepared with four treatments: 1) REF, 150 ppm NaNO2; 2) CTL, 75 ppm NaNO2; 3) TRT1, 75 ppm NaNO2+0.1% POS (1% paprika oleoresin+99% sunflower seed oil); and 4) TRT2, 75 ppm NaNO2+0.1% POS (5% paprika oleoresin+95% sunflower seed oil). The addition of POS into ES increased redness and yellowness but decreased lightness (p

Inorganic nitrite is a source of nitric oxide (NO) and is considered as a potential therapy in settings where endogenous NO bioactivity is reduced and left ventricular (LV) function impaired. However, the effects of nitrite on human cardiac contractile function, and the extent to which these are direct or indirect, are unclear. We studied 40 patients undergoing diagnostic cardiac catheterization who had normal LV systolic function and were not found to have obstructive coronary disease. They received either an intracoronary sodium nitrite infusion (8.7–26 µmol/min, n = 20) or an intravenous sodium nitrite infusion (50 µg/kg/min, n = 20). LV pressure-volume relations were recorded. The primary end point was LV end-diastolic pressure (LVEDP). Secondary end points included indices of LV systolic and diastolic function. Intracoronary nitrite infusion induced a significant reduction in LVEDP, LV end-diastolic pressure-volume relationship (EDPVR), and the time to LV end-systole (LVEST) but had no significant effect on LV systolic function or systemic hemodynamics. Intravenous nitrite infusion induced greater effects, with significant decreases in LVEDP, EDPVR, LVEST, LV dP/dtmin, tau, and mean arterial pressure. Inorganic nitrite has modest direct effects on human LV diastolic function, independent of LV loading conditions and without affecting LV systolic properties. However, the systemic administration of nitrite has larger effects on LV diastolic function, which are related to reduction in both preload and afterload. These contractile effects of inorganic nitrite may indicate a favorable profile for conditions characterized by LV diastolic dysfunction. NEW & NOTEWORTHY This is the first study to assess the direct and indirect effects of inorganic nitrite on invasive measures of left ventricular function in humans in vivo. Inorganic nitrite has a modest direct myocardial effect, improving diastolic function. Systemic administration of nitrite has larger effects related to alterations in cardiac preload and afterload. The changes induced by nitrite appear favorable for potential use in conditions characterized by LV diastolic dysfunction.

Sodium nitrite (NaNO2) found in vegetables, drinking water, and cured meats, can damage tissue because it is an oxidant. Plant phytochemicals such as quercetin are antioxidants. This study aimed to determine the potential of red okra pods ethanol extract (ROE) to repair kidney damage in mice (Mus musculus) induced by NaNO2. The red okra pods were extracted three times with saturated ethanol. The experiment used 36 male BALB/c mice aged 6-8 weeks and body weight of about 28 g. There are six research groups, namely, normal control, negative control (exposure to NaNO2 50 mg/kg BW), treatment of exposure to NaNO2 and administration of ROE at doses of 25, 50, 75, and 100 mg/kg BW. Sodium nitrite and ROE were given daily for 23 days by gavage. On day 24, the serum was isolated. Blood urea nitrogen (BUN) and creatinine (Cre) levels are measured to assess kidney function, as well as measuring the oxidant malondialdehyde (MDA) and the antioxidant enzyme of superoxide dismutase (SOD). The kidneys were made histological preparations and analyzed on the proximal convoluted tubule (PCT). All data were statistically analyzed (α=0.05). This study indicated that the administration of ROE at a 100 mg/kg BW dose is the most optimal in repairing damage to the PCT with increased normal cells and reduced necrosis. Besides, it degraded BUN, Cre, and MDA levels in the serum of mice exposed to NaNO2 compared to the other treatments. All doses of ROE promoted the SOD level. ROE restore kidney tissue, especially on PCT to normal. Kidney damage due to exposure to NaNO2 preservatives can be reduced by administering ROE. ROE prevents kidney damage through an increase in antioxidant enzymes. ROE can be used as a food ingredient as a source of antioxidants, thereby reducing the impact of oxidant compounds.

The corrosion inhibition behavior of sodium nitrite (NaNO2) towards pure copper (99.95%) in simulated cooling water (SCW) was investigated by means of electrochemical impedance spectroscopy (EIS) and dynamic electrochemical impedance spectroscopy (DEIS). NaNO2 interferes with metal dissolution and reduce the corrosion rate through the formation or maintenance of inhibitive film on the metal surface. Surface morphologies illustrated that the surface homogeneity increased on adding sodium nitrite. Sodium nitrite’s adsorption on copper surface followed the modified form of Langmuir, Freundlich and Frumkin isotherms. Physiosorption mode was involved in the corrosion protection. Electrochemical results revealed an corrosion resistance of copper increases on increasing the inhibitor concentration. The DEIS results indicated that copper corrosion mechanism could be hindered by 50% even after interval of 24 h by optimum concentration of sodium nitrite. The maximum inhibition was achieved with 2000 ppm of NaNO2. With this concentration, inhibition efficiency of up to 61.8% was achievable.

[Figure not available: see fulltext.] Isotope-labeled antiviral drug Triazavirin containing 2H, 13C, and 15N atoms in its structure has been synthesized. 13C2H3I and KS13CN served as donors of 13C isotopes. The use of 13С-MeI containing 2H atoms made it possible to additionally incorporate deuterium labels into the structure of the compound. The 15N atoms were incorporated using 15N-enriched sodium nitrite, aminoguanidine carbonate, and ethyl nitroacetate. The resulting 2H3,13C2,15N3-Triazavirin was characterized by NMR spectroscopy. © 2021, Springer Science+Business Media, LLC, part of Springer Nature. This work was supported by the Russian Foundation for Basic Research (grant 20-03-00842) and the Ministry of Science and Higher Education of the Russian Federation (project No. FEUZ-2020-0058 (N687.42B.223/20)).

To determine the efficacy of inorganic nitrite supplementation on endothelial function in humans and mechanisms of action, we performed (1) a randomized, placebo-controlled, parallel-group clinical trial with sodium nitrite (80 mg/day, 12 weeks) in older adults (N=49, 68±1 year) and (2) reverse-translation experiments in young (6 months) and old (27 months) c57BL/6 mice. In the clinical trial, sodium nitrite increased plasma nitrite ( P P P P P P P Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02393742.

Nitric oxide (NO) has the potential to modulate myofibroblast differentiation. In this study, we investigated the effect of exogenous NO on the myofibroblast differentiation of human keratocytes using sodium nitrite as a NO donor. Myofibroblasts were induced by exposing resting keratocytes to transforming growth factor (TGF)-β1. N-cadherin and α-smooth muscle actin (αSMA) were used as myofibroblast markers. Both resting keratocytes and -stimulated keratocytes were exposed to various concentrations of sodium nitrite (1 μM to 1000 mM) for 24 to 72 h. Exposure to sodium nitrite did not alter keratocytes’ viability up to a 10 mM concentration for 72 h. However, significant cytotoxicity was observed in higher concentrations of sodium nitrite (over 100 mM). The expression of αSMA and N-cadherin was significantly increased in keratocytes by TGF-β1 stimulation after 72 h incubation. The addition of sodium nitrite (1 mM) to TGF-β1-stimulated keratocytes significantly decreased αSMA and N cadherin expression. Smad3 phosphorylation decreased after sodium nitrite (1 mM) exposure in TGF-β1-stimulated keratocytes. The effect of NO was reversed when NO scavenger, 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) was added in the culture medium. Application of sodium nitrite resulted in significant decrease of corneal opacity when measured at 2 weeks after the chemical burn in the mouse. These results verified the potential therapeutic effect of NO to decrease myofibroblast differentiation of human keratocytes and corneal opacity after injury.

Sodium nitrite is an oxidizing agent capable of producing profound methemoglobinemia. Large quantities of sodium nitrite can be purchased online, and recent literature has identified several cases ...

Aims: Sodium nitrite is a food preservative that can endanger human health. This study aimed to investigate the perinatal and neonatal effects of sodium nitrite on the functional and tissue structure of rats’ offspring kidneys. Methods & Materials: In this experimental study, 56 female rats were divided into seven groups (n=8): control, perinatal and neonatal control groups, experimental groups 1 and 2 perinatal and neonatal (under oral treatment of doses of 90 and 180 mg/kg sodium nitrite during pregnancy and lactation). At the end of infancy, 8 offspring of rats were randomly selected from each group. After blood sampling, creatinine, urea, and uric acid levels were measured, and by extracting their kidneys, histopathological evaluation was performed. Findings: Perinatal and neonatal administration of 90 and 180 mg/kg sodium nitrite impaired renal tissue structure and significantly increased serum levels of creatinine, urea, and uric acid levels (P

The widespread industrial use of nitrite in preservatives, colorants, and manufacturing rubber products and dyes increases the possibilities of organ toxicity. Lithium borate (LB) is known as an antioxidant and an oxidative stress reliever. Therefore, this study is aimed at examining the effect of LB on nitrite-induced hepatorenal dysfunction. Twenty-eight male Swiss mice were divided into four equal groups. Group 1, the control group, received saline. Group 2 received LB orally for 5 consecutive days at a dose of 15 mg/kg bw. Group 3, the nitrite group, received sodium nitrite (NaNO2) on Day 5 (60 mg/kg bw intraperitoneally). Group 4, the protective group (LB + NaNO2 group), received LB for 5 days and then a single dose of NaNO2 intraperitoneally on Day 5, the same as in Groups 2 and 3, respectively. Samples of blood and kidney were taken for serum analysis of hepatorenal biomarkers, levels of antioxidants and cytokines, and the expression of genes associated with oxidative stress and inflammation. NaNO2 intoxication increased markers of liver and kidney functions yet decreased reduced glutathione (GSH), superoxide dismutase (SOD), and catalase activities in blood. NaNO2 also increased the expression of tumor necrosis factor (TNF-α), interleukin-1β and interleukin-6 (IL-1β and IL-6). Pre-administration of LB protected mice from oxidative stress, lipid peroxidation, and the decrease in antioxidant enzyme activity. Moreover, LB protected mice from cytokine changes, which remained within normal levels. LB ameliorated the changes induced by NaNO2 on the mRNA of nuclear factor erythroid 2-related factor 2 (Nfr2), heme oxygenase-1 (HO-1), nuclear factor-kappa B (NF-κB), transforming growth factor-beta 2 (TGF-β2), and glutathione-S-transferase (GST) as determined using quantitative real-time PCR (qRT-PCR). These results collectively demonstrate that LB ameliorated NaNO2-induced oxidative stress by controlling the oxidative stress biomarkers and the oxidant/antioxidant state through the involvement of the Nrf2/HO-1 and NF-κB signaling pathways.

Nitric oxide (NO) is a gaseous signaling molecule that plays an important role in myriad physiological processes, including the regulation of vascular tone, neurotransmission, mitochondrial respiration, and skeletal muscle contractile function. NO may be produced via the canonical NO synthase-catalyzed oxidation of l-arginine and also by the sequential reduction of nitrate to nitrite and then NO. The body's nitrate stores can be augmented by the ingestion of nitrate-rich foods (primarily green leafy vegetables). NO bioavailability is greatly enhanced by the activity of bacteria residing in the mouth, which reduce nitrate to nitrite, thereby increasing the concentration of circulating nitrite, which can be reduced further to NO in regions of low oxygen availability. Recent investigations have focused on promoting this nitrate-nitrite-NO pathway to positively affect indices of cardiovascular health and exercise tolerance. It has been reported that dietary nitrate supplementation with beetroot juice lowers blood pressure in hypertensive patients, and sodium nitrite supplementation improves vascular endothelial function and reduces the stiffening of large elastic arteries in older humans. Nitrate supplementation has also been shown to enhance skeletal muscle function and to improve exercise performance in some circumstances. Recently, it has been established that nitrate concentration in skeletal muscle is much higher than that in blood and that muscle nitrate stores are exquisitely sensitive to dietary nitrate supplementation and deprivation. In this review, we consider the possibility that nitrate represents an essential storage form of NO and discuss the integrated function of the oral microbiome, circulation, and skeletal muscle in nitrate-nitrite-NO metabolism, as well as the practical relevance for health and performance.

Aims To determine whether inorganic nitrite improves peripheral and pulmonary oxygen (O2 ) transport during exercise in heart failure with preserved ejection fraction (HFpEF). Methods and results Data from two invasive, randomized, double-blind, placebo-controlled trials with matched workload exercise of inhaled and intravenous sodium nitrite were pooled for this analysis (n = 51). Directly measured O2 consumption (VO2 ) and blood gas data were used to evaluate the effect of nitrite on skeletal muscle O2 conductance (Dm), VO2 kinetics, alveolar capillary membrane O2 conductance (DL ), and O2 utilization during submaximal exercise. As compared to placebo, treatment with nitrite resulted in an improvement in Dm (+4.9 ± 6.5 vs. -0.9 ± 4.3 mL/mmHg*min, P = 0.0008) as well as VO2 kinetics measured by mean response time (-5.0 ± 6.9 vs. -0.6 ± 6.0 s, P = 0.03), with preserved O2 utilization despite increased convective O2 delivery through cardiac output (+0.4 ± 0.7 vs. -0.3 ± 0.9 L/min, P = 0.02). Nitrite improved DL (+2.5 ± 6.3 vs. -2.0 ± 9.0 mL/mmHg*min, P = 0.05) with exercise, which was associated with lower pulmonary capillary pressures (r = -0.34, P = 0.02), and reduced pulmonary dead space ventilation fraction (-0.01 ± 0.05 vs. +0.02 ± 0.05, P = 0.02). Conclusion Sodium nitrite enhances skeletal muscle Dm during exercise as well as pulmonary O2 diffusion, optimizing O2 kinetics in tandem with increased convective O2 delivery through cardiac output augmentation. The favourable combined pulmonary, cardiac and peripheral effects of nitrite may improve exercise tolerance in people with HFpEF and requires further investigation. Clinical trial registration ClinicalTrials.gov ID NCT01932606 and NCT02262078.

Aneurysmal subarachnoid haemorrhage (SAH) is a devastating subset of stroke. One of the major determinates of morbidity is the development of delayed cerebral ischemia (DCI). Disruption of the nitric oxide (NO) pathway and consequently the control of cerebral blood flow (CBF), known as cerebral autoregulation, is believed to play a role in its pathophysiology. Through the pharmacological manipulation of in vivo NO levels using an exogenous NO donor we sought to explore this relationship.Phase synchronisation index (PSI), an expression of the interdependence between CBF and arterial blood pressure (ABP) and thus cerebral autoregulation, was calculated before and during sodium nitrite administration in 10 high-grade SAH patients acutely postrupture. In patients that did not develop DCI, there was a significant increase in PSI around 0.1 Hz during the administration of sodium nitrite (33%; p-value 0.006). In patients that developed DCI, PSI did not change significantly.Synchronisation between ABP and CBF at 0.1 Hz has been proposed as a mechanism by which organ perfusion is maintained, during periods of physiological stress. These findings suggest that functional NO depletion plays a role in impaired cerebral autoregulation following SAH, but the development of DCI may have a distinct pathophysiological aetiology.

Meat industries utilize plant material such as celery in cured meat products. Extraction of valuable bioactive compounds, nitrates and nitrites often involves processes that increase cost or lack sustainability. Thus, this study investigated the effect of ball-milled celery powders (CP) on the physicochemical, antioxidant, and antimicrobial properties along with curing efficiency in comminuted meat product. Pork sausages loaded with CPs with different average particle sizes: 265 μm (T1), 68 μm (T2) and 7 μm (T3) were compared to those added without and with sodium nitrite (150 ppm). The a* values were increased for sausages with larger particle size. The L* values decreased for all CPs. Residual nitrite for all particle sizes increased in the earlier stages and decreased at the end of storage period. The curing efficiency also increased for larger size particles with an increase until day 9 followed by a gradual decrease. Superfine CP had a tendency to improve the antioxidant activities. The antimicrobial activity of CPs was not comparable with nitrite added sausages. The textural parameters remained unaffected by particle size. Thus, instead of extracts or juices, micronized CPs could be used to improve the antioxidant activities and curing efficiency of label friendly reformulated meat products.

Objective: The objective of the study was to assess the neuroprotective effect of azilsartan as a memory enhancer against scopolamine-induced amnesia in rats. Methods: Albino Swiss male rats in equal numbers per group (n=6) were taken. Scopolamine hydrobromide was administered to induce amnesia within the rats. Control group rats were administered normal, negative control groups were administered with scopolamine to induce amnesia and nitrite during trials, positive control group rats were administered piracetam+ scopolamine and piracetam nitrite during trials, and test control group rats were administered azilsartan +sodium nitrite and azilsartan nitrite. Exteroceptive behavioral models just like the elevated plus-maze model, Morris water maze model, acquisition trials, and retrieval trial were wont to evaluate the neuroprotective effect of azilsartan. Results: The scopolamine and azilsartan have a significantly decreasing effect on time spent within the target quadrant (TSTQ) but piracetam has an increasing effect. The effect of azilsartan on transfer latency time (TLT) was observed against scopolamine-induced amnesia in rats using the elevated plus-maze test. Piracetam was found to decrease the TLT and restore memory function at a better dose. Within the case of scopolamine treated rats, a big increase in TLT was noted. Azilsartan treated group also increased TLT within the elevated plus maze. It is noted that the scopolamine features a significantly increasing effect on escape latency time (ELT). Piracetam features a decreasing effect on ELT. A rise in ELT was seen because of azilsartan. Conclusion: This study suggested that the azilsartan features a significant decreasing effect on TSTQ, azilsartan treated group also increased TLT and ELT.

The current was conducted to evaluate the ameliorating effect of Chlorella vulgaris (CV) extract against sodium nitrite-induced hepatotoxicity in rats. Forty-five rats were allocated randomly into 5 groups (n = 9). Group I (GI), control group: orally gavaged with normal saline daily. Group II (GII): orally gavaged with CV extract (70 mg/kg BW) for 3 months. Group III (GIII): orally gavaged with sodium nitrite (80 mg/kg BW) for 3 months. Group IV (GIV): received sodium nitrite as GIII and CV extract as GII simultaneously for 3 months. Group V (GV): received CV extract as GII and then, sodium nitrite as in GIII from the end of first month until the end of the experiment. Sodium nitrite significantly increased the activities of serum alanine aminotransferase, aspartate aminotransferase, and serum concentrations of tumor interleukin 1-β and necrosis factor α. In addition, it increased concentrations of malondialdehyde and nitric oxide and expression level of caspase-3 in the hepatic tissue. However, it decreased activities of hepatic glutathione peroxidase, catalase, and superoxide dismutase and induced degenerative and necrotic changes in hepatic tissues. In contrast, CV extract administration modulated sodium nitrite-induced inflammation, oxidative stress, and alteration in hepatic tissue function and architecture. This study indicated that CV extract modulated sodium nitrite-induced hepatic toxicity through decreasing oxidative stress and inflammation and enhancing antioxidant enzyme activities in hepatic tissue of rats.

Sodium nitrite is a powerful oxidizing agent that causes hypotension and limits oxygen transport and delivery in the body through the formation of methemoglobin. Clinical manifestations can include cyanosis, hypoxia, altered consciousness, dysrhythmias, and death. The majority of reports on sodium nitrite poisonings have been the result of unintentional exposures. We report a case of an intentional fatal overdose of sodium nitrite. A 17-year-old female reportedly drank approximately one tablespoon of sodium nitrite in a self-harm attempt. The patient was hypotensive and cyanotic upon EMS arrival. The patient decompensated rapidly into a bradycardic arrest during transport despite intubation, push-dose epinephrine, and intravenous fluid resuscitation. In the Emergency Department (ED), she received methylene blue and packed red cells but could not be resuscitated despite a prolonged effort. EMS professionals should consider sodium nitrite toxicity in patients with a suspected overdose who present with a cyanotic appearance, pulse oximetry that remains around 85% despite oxygen, and dark brown blood seen on venipuncture. Early prehospital contact with the Poison Control Center and ED prenotification in poisoned patients is encouraged.

Dimethylamine (DMA) and sodium nitrite (NaNO2) are present in numerous foods, food additive and environmental factors, which enhance chemical driven liver damage by inducing oxidative stress and cellular injury. Therefore, this study evaluated the possible therapeutic and protective effects of selected plant extracts on dimethylamine (DMA) and sodium nitrite (NaNO2)-induced hepatotoxicity in mice. The selected plants (Morinda lucida, Securine gavirosa, Xylopia aethiopica, Piper guineense and Calotropis procera) were extracted by maceration in distilled water and concentrated using freeze dryer. Swiss male albino mice were divided into Group I (control group) received distilled water; group II were administered orally with DMA (150 mg/kg body weight) and NaNO2 (100 mg/kg body weight) twice every week for 4 weeks, group III were treated orally with extract every 48 hrs simultaneously with DMA and NaNO2 and continued until the end of the experiment, group IV were treated orally with extract and fractions (150 mg/kg body weight) every 48 hrs for four weeks after the administration of DMA and NaNO2 and continued until the end of the experiment (4 weeks) and group V were given 5-flourouracil every 48 hours after induction of liver toxicity in mice. Liver function (alanine amino transferase, aspartate amino transferase, gamma glutamyl transferase and alkaline phosphatase) tests were done in the serum of mice using standard method. Extract of P. guineense exhibited the best activity and was fractionated for further hepatoprotective studies. Liver sections of the mice treated with fractions of P. guineense were used for immuno-histochemical studies for p53, BCl-2, COX-2 and Ki-67 expression, and liver histological analysis. The antioxidant status of the mice treated with fractions of P. guineense was determined by measuring the catalase activity, sodium dismutase activity, reduced glutathione and malondialdehyde concentrations in the liver homogenates. Data were expressed as mean and considered significant at p

This study aims to investigate the mechanisms through which fructose diphosphate (FDP) causes anti-hypoxia and anti-fatigue effects and improves learning and memory. Mice were divided into three groups: low-dose FDP (FDP-L), high-dose FDP (FDP-H), and a control group. Acute toxic hypoxia induced by carbon monoxide, sodium nitrite, and potassium cyanide and acute cerebral ischemic hypoxia were used to investigate the anti-hypoxia ability of FDP. The tests of rod-rotating, mouse tail suspension, and swimming endurance were used to explore the anti-fatigue effects of FDP. The Morris water maze experiment was used to determine the impact of FDP on learning and memory ability. Poisoning-induced hypoxic tests showed that mouse survival time was significantly prolonged in the FDP-L and FDP-H groups compared with the control group (p < 0.05). In the exhaustive swimming test, FDP significantly shortened struggling time and prolonged the time of mass-loaded swimming; the rod-rotating test showed that endurance time was significantly prolonged by using FDP (p < 0.05). FDP significantly decreased lactate and urea nitrogen levels and increased hepatic and muscle glycogen and glucose transporter-4 and Na+-K+-ATPase (p < 0.05). To conclude, FDP enhances hypoxia tolerance and fatigue resistance and improves learning and memory ability through regulating glucose and energy metabolism.

The study of Rosela Leaf Extract As A Protective Agent Against The Damage Of Liver Tissue OfMale Mice Strain DDW that has been Induced By Sodium Nitrite was conducted. The experiment used Completely Randomized Design. The treatment given was three different dosages of rosella leaf extract, namely 14 mg / ml, 28 mg / ml and 42 mg / ml and without any extract as a control. All mice have been induced by sodium nitrite for 18 days followed by healing process through injection of 0.3 ml of rosella leaf extract at different concentration per day during 14 days. The result showed that he control, treatment of 14 mg / ml and 42 mg / ml affected the color change of liver tissue. However, the control increased liver tissue weight compared to all treatments. The damage levels of hepatocyte tissue treated by all different dosages of fresh rosella leaf extract decreased compared to the damage level of control. It could be concluded that fresh rosella leaf extract showed potential agent to protect liver mice from damage caused by sodium nitrite induction.

A simple, fast, and sensitive spectrophotometric method was suggested for the determination of Bromhexine Hydrochloride (BHH) in its pharmaceutical formulations. The method depends on the diazotization of BHH by sodium nitrite in acidic medium to produce the corresponding diazonium salt. The latter is coupled with phloroglucinol reagent in alkali medium to form a yellow water soluble azo-dye which has a maximum absorption at 405 nm with a molar absorptivity of 2.7×104 l.mol-1.cm-1 and Sandellʼs sensitivity of 0.01517 µg.cm-1. Beerʼs low is obeyed within a concentration range of 0.25-15 µg.mL-1 of BHH. The LOD and LOQ values of the proposed method were 0.087 µg.mL-1 and 0.293 µg.ml-1, respectively. The proposed method was validated with standard methods and successfully applied to the determination of Bromhexine in its pharmaceutical formulations as tablets, syrup, and injections.

Background Sodium nitrite is known to induce methemoglobinemia and hypotension when ingested, but reports of intentional ingestion remain rare. Case Series We report five cases of severe methemoglobinemia secondary to large sodium nitrite ingestion that were reported to and managed by the California Poison Control System in 2019, resulting in three fatalities. The estimated doses ingested ranged from 15 grams to 113 grams, with one patient surviving after an ingestion of 60 grams. The highest documented methemoglobin level was 73%. The 2 patients who survived received methylene blue early in their clinical course. One patient required higher doses of methylene blue compared with other cases of nitrite-associated methemoglobinemia. In the patients who survived, all symptoms resolved within 24 h. Why Should an Emergency Physician Be Aware of This? These cases highlight the severe toxicity associated with intentional large sodium nitrite ingestion. In management, consideration should be given to administering higher initial or more frequent doses of methylene blue compared with standard practice. Given that sodium nitrite is readily accessible through online vendors, and is being circulated through various suicide forums, it has the potential to be more commonly encountered in the emergency department.

Background The severity of pulmonary hypertension (PH) is monitored by measuring pulmonary vascular resistance, which is a steady-state measurement and ignores the pulsatile load encountered by the right ventricle (RV). Pulmonary vascular impedance (PVZ) can depict both steady-state and pulsatile forces, and thus may better predict clinical outcomes. We sought to calculate PVZ in patients with PH associated with heart failure with preserved ejection fraction who were administered inhaled sodium nitrite to better understand the acute effects on afterload. Methods and Results Fourteen patients with PH associated with heart failure with preserved ejection fraction underwent right heart catherization and were administered inhaled sodium nitrite. A Fourier transform was used to calculate PVZ for both before and after nitrite for comparison. Inhaled sodium nitrite decreased characteristic impedance (inversely related to proximal pulmonary artery compliance) and total work performed by the RV. RV efficiency improved, defined by a reduction in the total work divided by cardiac output. There was a mild decrease in pulmonary steady-state resistance after the administration of inhaled sodium nitrite, but this effect was not significant. Conclusions PVZ analysis showed administration of inhaled sodium nitrite was associated with an improvement in pulmonary vascular compliance via a decrease in characteristic impedance, more so than pulmonary steady-state resistance. This effect was associated with improved RV efficiency and total work.

Background: Food additives are a substance added to food to enhance its flavor or appearance or to preserve it. They are widely used nowadays. Objectives: The aim of the current work was to determine the hazardous effects of sodium nitrate, fast green and glycine on some physiological parameters such as liver enzymes, lipid profile , hormonal assays …etc. Materials and methods: This study has been done on forty male albino rats. The Animals were divided into four groups: Group I (Control untreated group), Group II (fast green-treated group), Group III (glycine-treated group) and Group IV (sodium nitrate-treated group). Estimation of some biochemical parameters (liver enzymes, kidney function tests, glucose, protein profile and lipid profile) and hormonal assays [testosterone, T3 (triiodothyronine), T4 (thyroxine) and insulin were done. Results: body weight was increased in fast green-treated group and decreased in sodium nitrate group. There was an increase in the activities of AST and ALT as well as urea and creatinine, in both sodium nitrate and fast green groups. There was a decrease in plasma proteins in both fast green and sodium nitrate groups. Lipid profile [total cholesterol (TC), triglycerides (TG), very low-density lipoprotein-cholesterol (VLDL-chol) and low-density lipoprotein-cholesterol (LDL-chol)] were decreased in fast green-treated groups while high-density lipoprotein-cholesterol (HDL-chol) was increased. In sodium nitrate group, the lipid profile (TC, TG, VLDL and LDL) were increased while HDL was decreased. Serum glucose, insulin, and HOMA-IR (insulin resistance) were decreased in fast green-treated group and increased in sodium nitrate-treated group. There was a decrease in T3 and T4 in fast green-treated group while were increased in sodium nitrate-treated group. Testosterone decreased in fast green-, glycine- and sodium nitrate-treated groups. While glycine-treated group showed the same results as the control group. Conclusion: It could be concluded that minimizing the use of food additives protects young children and mature people from their destructive effects.

Objective: Potential combined nephrotoxic effect following simultaneous administration of two food additives: potassium bromate (PBR) (20 mg/kg of body weight, twice weekly) and sodium nitrite (SNT) (60mg/kg of body weight as a single dose) orally was investigated. Methods: Nephrotoxicity was assessed by determining urea, creatinine and electrolyte concentrations in the serum. In addition, concentrations of nitric oxide, reduced glutathione, total thiol, malondialdehyde and activities of arginase, adenosine deaminase, catalase, superoxide dismutase, and glutathione perioxidase in the kidney were investigated. Results: The results revealed that individual exposure to PBR or SNT significantly induced nephrotoxicity and oxidative stress in rats however, this was enhanced by co-exposure as evidenced by significant alteration in these kidney markers when compared with the control. Conclusion: This study accentuates the risk of enhanced nephrotoxicity in food containing both additives. Key words: Potassium bromate, sodium nitrite, renal markers.

Erythrocytes exhibit high susceptibility to hemolysis in several pathologies due to the oxidation of cellular components. We hypothesized that annatto carotenoids improve the redox status of erythrocyte plasma membranes and promote a consequent increase in human erythrocyte resistance to hemolysis. The objective of this study was to evaluate whether food-grade annatto carotenoids can increase human erythrocyte resistance to hemolysis in vitro and ex vivo. For the in vitro experiment, erythrocytes from healthy volunteers were isolated and coincubated with bixin (BIX) or norbixin (NBIX) and 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH), glucose, or sodium nitrite (NaNO2) as hemolysis inducers. In the ex vivo study, healthy volunteers consumed a capsule containing BIX or NBIX (0.05 mg/kg body weight per day) or placebo for 7 days before blood sample collection. Their erythrocytes were isolated and incubated with AAPH, glucose, or NaNO2. In both the ex vivo and in vitro studies, erythrocytes were subjected to osmotic fragility tests. The activity of antioxidant enzymes, and reduced glutathione and lipid peroxidation levels in erythrocytes were also evaluated ex vivo. In vitro BIX and NBIX not only reduced erythrocyte membrane fragility induced by AAPH, glucose, or NaNO2 but also improved basal osmotic resistance in the micromole-per-liter range (P

Milicia excelsa (Moraceae) is used to treat mental illnesses, among other traditional uses in Africa, but no scientific supports for its use. Hence, this study investigated the antihypoxic potential of the ethanol leaf extract of Milicia excelsa in mice, as well as determined quantitatively the phytoconstituents present in the extract. Hypoxia was induced by sodium nitrite (360 mg/kg, i.p., a haemic hypoxic model) and sodium fluoride (150 mg/kg, i.p., a circulatory hypoxic model) in mice. The phytocompounds were estimated using standard methods. The extract at 500 and 1000 mg/kg, per oral significantly (p

The present study investigated the unsafe impacts of sodium nitrite, sodium benzoate and their mixture which is utilized in fabricating of the food on some biochemical parameters in male albino rats. Rats (40) were divided into four groups as follows: group 1 used as the control, group II and III were treated orally with sodium nitrite nano2 (80 mg/kg BW) and sodium benzoate (SB) (200 mg/kg BW), respectively. Group IV was treated orally with a mixture of sodium nitrite and sodium benzoate. Rats took their respective doses every day for 8 weeks. The obtained results showed that sodium nitrite, sodium benzoate and their mixture (nano2 and SB) initiated a diminished within in the activity of antioxidant enzymes (SOD, CAT, and GSH) within the kidney, while, MDA recorded a highly significant activity level within experimental groups. Urea and creatinine mean levels were were expanded within plasma of the experimental rats. In the histology of the kidney, sections appeared edema with few mononuclear leukocyte cellular infiltrations, shrinkage of glomeruli. The severity of these changes increased in the experimental group which treated by the mixture of sodium nitrite and sodium benzoate. Overexpression in p53 occurred in experimental groups that were treated by nano2, SB and their mixture. The present study concluded that the mixture of food additives can induce toxicity in the kidney of rats. It is obvious that food additives induced nephrotoxicity within the kidney. It decreased the antioxidant enzymes (GSH, CAT, and SOD) and increased MDA. Increase tumor suppressor gene p53 in kidney tissue. Food added substances caused changes in biochemical parameters as in creatinine and urea. The utilization of food additives must be decreased. The presence of more than one type of food additives on our food and the usage of the mixture of sodium nitrite and sodium benzoate initiated changes in biochemical parameters and immune-histopathological changes.

This paper experimentally investigated the effect of nitrite-based corrosion inhibitor and cation type namely Na+, Mg2+ and Ca2+ associated with chloride ions on free chloride (CF) and total chloride (CT) ion concentrations of concrete exposed to composite chloride-sulfate ( C l - + S O 4 2 - ) environment. Concrete cubes were prepared using Portland pozzolana cement and w/c ratio of 0.55. Sodium nitrite (NaNO2) was used as a corrosion inhibitor at an admixed dosage of 3% by weight of cement. After curing, the cubes were subjected to composite C l - + S O 4 2 - solutions such as NaCl + MgSO4, MgCl2 + MgSO4, and CaCl2 + MgSO4. Powder samples were collected at different depth intervals from the cubes to determine the CF and CT concentrations. Fourier transform infrared (FTIR) spectroscopy and Field emission scanning electron microscope (FESEM) analyses were carried to examine the microstructure of concrete. The experimental results indicated that addition of NaNO2 in concrete reduced the penetration of chloride ions. Concrete exposed to CaCl2 + MgSO4 solution mostly showed higher CF and CT concentrations than NaCl + MgSO4 solution followed by MgCl2 + MgSO4 solution. Results of microstructure study indicated the formation of different compounds in concrete exposed to composite C l - + S O 4 2 - solutions.

Methemoglobin (metHb) arises from the oxidation of ferrous hemoglobin (HbFe2+, Hb) to ferric hemoglobin (HbFe3+, metHb), which is unable to bind gaseous ligands such as oxygen (O2) and carbon monoxide (CO), and binds to nitric oxide (NO) significantly slower compared to Hb. Therefore, metHb does not elicit vasoconstriction and systemic hypertension in vivo due to its extremely slow NO scavenging rate in comparison to cell-free Hb, but will induce oxidative tissue injury, demonstrating the potential of using metHb as a control material when studying the toxicity of cell-free Hb. Hence, the goal of this work was to develop a novel manufacturing strategy for production of metHb that is amenable to scale-up. In this study, small scale (e.g. 1 mL reaction volume) screening experiments were initially conducted to determine the optimal molar ratio of Hb to the oxidization agents hydrogen peroxide (H2O2) or sodium nitrite (NaNO2) to achieve the highest conversion of Hb into metHb. A spectral deconvolution program was employed to determine the molar fraction of various species (hemichrome, metHb, oxyHb, metHb-NO2−, and NaNO2) in solution during the oxidation reaction. From this analysis, either a 1:1 or 1:5 molar ratio was identified as optimal molar ratios of Hb:NaNO2 (heme basis) that yielded the highest conversion of Hb into metHb with negligible amounts of side products. Hence in order to reduce the reaction time, a 1:5 molar ratio was chosen for large scale (i.e. 1.5 L reaction volume) synthesis of bovine metHb (metbHb) and human metHb (methHb). The biophysical properties of metHb were then characterized to elucidate the potential of using the synthesized metHb as a non-O2 carrying control material. The haptoglobin binding kinetics of metHb were found to be similar to Hb. Additionally, the synthesized metHb was stable in phosphate buffered saline (PBS, 50 mM, pH 7.4) at 4°C for approximately one week, indicating the high stability of the material.

Objective: The present study intended to explore the anti-fatigue and anti-hypoxia efficacy of Tremella extract in mouse model. Methods: Kunming mice were randomized into 5 groups randomly (n = 12/group; half male and female), and given 0.9%Nacl (10 mL/Kg Serving as blank control group)orally, 0.6 g/kg rhodiola capsule (Serving as positive group) and Tremella extract at doses of high (3.0 g/kg), middle (1.5 g/kg) and low (0.5 g/kg) once a day for 14 days. At the end of drug intragastric gavage, following endurance running test, rotating rod test, normobarie hypoxia test and sodium nitrite poisoning test were performed. Result: 14-day Tremella extract administration fails to influence mouse horizontal and vertical movement indicating little neurotoxicity at chosen doses. Through rotating rod, forced running test, the anti-fatigue activity of Tremella extract was demonstrated. Via normobarie hypoxia test, sodium nitrite poisoning test, Tremella extract was confirmed to possess anti-hypoxia effect. Tremella extract treatment significantly enhanced the liver levels of superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), increased the expressions of ATP and hepatic glycogen, muscle glycogen in tissue. Conclusion: We conclude that Tremella extract efficiently enhances mouse fatigue endurance and anti-hypoxia capability partly through energy reserves and antioxidant enzyme activity. Keywords: Tremella, Anti-fatigue, Anti-hypoxia, Antioxidant

Inhaled sodium nitrite has been reported to decrease pulmonary artery pressure in hemoglobin E/β-thalassemia (HbE/β-thal) patients with pulmonary hypertension. This study investigated the pharmacokinetics and pharmacodynamics of inhaled nebulized sodium nitrite in 10 healthy subjects and 8 HbE/β-thal patients with high estimated pulmonary artery pressure. Nitrite pharmacokinetics, fraction exhaled nitric oxide (FENO), estimated right ventricular systolic pressure (eRVSP) measured by echocardiography, and platelet activation were determined. Nebulized sodium nitrite at doses used in this study (37.5 and 75 mg for healthy subjects and 15 mg for HbE/β-thal patients) was well tolerated and did not cause changes in methemoglobin levels and systemic blood pressure. Absorption of inhaled nitrite was rapid with the absolute bioavailability of 18%. In whole blood, nitrite exhibited the dose-independent pharmacokinetics with clearance (CL) of 1.5 l/h/kg, volume of distribution (Vd) of 1.3 l/kg and half-life (t1/2) of 0.6 h. CL and Vd of nitrite was higher in red blood cells (RBC) than whole blood and plasma. HbE/β-thal patients had lower nitrite CL and longer t1/2 in RBC than healthy subjects. FENO increased immediately after inhalation. Following nitrite inhalation, eRVSP remained unchanged but platelet activation was suppressed as evidenced by inhibition of adenosine diphosphate (ADP)-induced P-selectin expression and increase in phosphorylated vasodilator-stimulated phosphoprotein (P-VASPSer239) in platelets. There were no changes in markers of oxidative and nitrosative stress after inhalation. Our results support further development of inhaled nebulized sodium nitrite for treatment of pulmonary hypertension in β-thalassemia.