Nitrite Toxicity Research Articles

Integrated physiological, energy metabolism, and metabonomic responses indicate the stress response in the hepatopancreas of Litopenaeus vannamei to nitrite stress

Nitrite is a toxic substance found in rearing water that affects shrimp health. The hepatopancreas is an important digestive, immune, and metabolic organ in the shrimp. In this study, shrimps (Litopenaeus vannamei) were separately exposed to 1 and 5 mg/L nitrite stress for 48 h, and the toxicity of nitrite in the hepatopancreas was explored by integrating histology, physiological indicators, energy metabolism, and metabolomics. Nitrite stress induced morphological changes and stress responses in the hepatopancreas. Specifically, physiology-related indices, such as the relative gene expression levels of antioxidants (ROMO1, Nrf2, GPx), endoplasmic reticulum stress (Bip, IRE1 and XBP1), and immune genes (ALF, Pen-3, Lys) were decreased, whereas the gene expression of apoptosis (Casp-3), detoxification (CYP450), and glutamic oxaloacetic transaminase (GOT) activity were increased. The activities of osmotic adjustment-related enzymes (NKA, CMA, and ATPase) also decreased. Energy metabolism-related indices, such as pyruvate and hepatic glycogen contents, increased, whereas glucose, lactic acid, triglyceride, and ATP contents and ATPase activity decreased, and the relative gene expression levels of carbohydrate metabolism (PDH, HK, and LDH) and electron-transport chain genes (CytC, COI and CCO) decreased, and the expressions of lipid metabolism (AMPK, SREBP, and FAS), tricarboxylic acid cycle (MDH, CS, IDH and FH) genes were also disturbed. The metabolic pattern of the hepatopancreas was affected by nitrite stress. Glycine, serine, and threonine metabolism were highly affected, and more functional amino acids varied in the 5 mg/L nitrite stress group. These results reveal the toxic effects of nitrite stress on the stress response, physiology, energy metabolism, and metabolite homeostasis in the hepatopancreas of shrimp. Several potential metabolite biomarker candidates were identified for toxicological evaluation.

Temporal and tissue-specific regulation of energy metabolism in the swimming crab Portunus trituberculatus during nitrite stress and recovery

Nitrite is a common pollutant in aquaculture systems that poses a significant threat to aquatic animals. Energy metabolism is critical in ensuring survival of animals under environmental stressors. However, regulation of energy metabolism in crustaceans under nitrite stress has not been well understood. Here we investigated energy metabolism regulation during nitrite stress and recovery in different tissues of the swimming crab Portunus trituberculatus, an important aquaculture species in China. Our results revealed that nitrite can cause tissue hypoxia and impair energy homeostasis, and energy balance cannot be restored even after a 96-hour recovery. Following exposure, mobilization of glycogen and lipids exhibited different temporal patterns. In response to energy imbalance, AMPK signaling was activated to counter energy imbalance. However, prolonged nitrite stress impaired AMPK signaling, leading to a further decline in energy supply. The findings improve our understanding for nitrite toxicity in P. trituberculatus, and provide valuable information for aquaculture management.

Repeated dose, 28-day oral toxicity study of curcumin, anthocyanins, and sodium nitrite in Wistar rats

ObjectiveThe goal of the present study was to examine the repeated dose 28-day oral toxicity of curcumin, anthocyanins, and sodium nitrite in Wistar rats. MethodsFor this purpose, forty-eight male Wistar rats were randomly divided into 8 groups (n = 6 each), encompassing untreated controls and experimental groups treated with curcumin, anthocyanins, and sodium nitrite. Three rats from each group were sacrificed by cervical dislocation under di-ethyl ether anesthesia after 2 and 4 weeks of therapy, respectively. Blood samples were collected for serum chemistry. All of the animals' livers, hearts, and kidneys were removed and sent for histopathological examination. ResultsAfter two weeks of inquiry, certain groups displayed higher hematological values, while others had lower values compared to the control group. AST, CK, and LDH enzyme activity were higher in groups 2–8, but urea concentrations were higher in groups 6 and 8. After four weeks, the Hb, MCH, and MCHC values in group 4 were greater, as were the WBC levels in groups 4 and 6, whereas other groups had lower MCV and WBC values. The weekly body weight gain was insignificantly different between treatment groups. Throughout the experiment, none of the animals perished. Male rats' liver, kidney, and heart underwent histopathological changes after ingesting curcumin, sodium nitrite, and anthocyanin. ConclusionBased on the findings, rats were more detrimental when curcumin, sodium nitrite, and anthocyanin were ingested together than when they were consumed individually, as evidenced by histopathological abnormalities in the liver, kidneys, and heart.

Method Validation Study of Dipstick Urinalysis as a Screening Tool for Sodium Nitrite Toxicity.

The incidence of suicide by intentional nitrite ingestion has increased since 2017. Limited options exist for commercial laboratory analysis for nitrite/nitrate. This study investigates the use of urine dipsticks for screening at autopsy for potential toxicity with sodium nitrite and, less commonly, alkyl nitrite. Archived samples of blood, urine, vitreous fluid, and gastric contents from 4 sodium nitrite/nitrate cases, 3 alkyl nitrite cases, and 4 control cases were tested using dipsticks. A rapid, strong positive result for nitrite was in the vitreous fluid of all 4-sodium nitrite/nitrate cases, along with 2 positive urine and 1 positive gastric. The 2 alkyl nitrite inhalation toxicity cases had no positive results. One alkyl nitrite ingestion case had a positive urine. The 4 controls had negative urine: equivocal results in 2 vitreous, and 1 positive gastric. Urine dipsticks are a useful adjunct to laboratory testing for nitrite toxicity and provide a rapid, cost-effective tableside result that may guide the need for further testing. Vitreous fluid and urine appear to be the most reliable specimens, although testing of gastric liquid may be useful to corroborate oral ingestion. Dipsticks may not be a reliable adjunct for testing for alkyl nitrite toxicity via inhalation route, likely due to the much lower nitrite concentration compared to nitrite ingestion cases.

Electrochemical detection of nitrite in medical and environmental samples with oxidation modified carbon fiber electrode

The potential toxicity of nitrite to organisms and the environment makes it necessary to build a sensitive and accurate nitrite detection platform. The oxidation-modified carbon fiber electrode (OMCF) with a rougher surface and oxygen-containing functional groups is constructed by a simple high-temperature calcined treatment at 400 °C for 2 h for sensitive detection of nitrite. The amperometric test results exhibit that OMCF has two linear ranges of 1–1000 µM and 1000–6000 µM. Besides, its corresponding sensitivities are 988.57 and 668.51 µA mM−1 cm−2, respectively. The low detection limit is 0.1 µM. Importantly, the OMCF can be used to detect nitrite in a drop of water or medical samples. In addition, the OMCF with a length of 150 cm was successfully synthesized. The nine sections of the above OMCF are randomly selected to detect nitrite, which shows good reproducibility. Therefore, this work provides a facile method for preparing OMCFs with high sensitivity and wide linear range for the electrochemical detection of nitrite in urine and enables large-scale electrode production for medical applications.

RETRACTED: Systematic Review of Fatal Sodium Nitrite Ingestion Cases: Toxicological and Forensic Implications.

Documented cases of sodium nitrite toxicity are almost exclusively caused by accidental ingestion; however, self-poisoning with sodium nitrite represents an increasing trend in nitrate-related deaths. This systematic review summarizes the most crucial evidence regarding the fatal toxicity of sodium nitrite. It identifies gaps and differences in the diagnostic forensic approaches and the detection methods of sodium nitrite intoxication. A total of eleven research articles were selected for qualitative and quantitative data. Most of the studies (6/11) were case reports. Fifty-three cases of fatal intoxication with sodium nitrite were chosen for the review. More research is required to develop cost-effective techniques and uniform cutoffs for blood nitrite and nitrate levels in the event of deadly sodium nitrite poisoning. There is still a lack of critical information on other matrices and the impact of time since death on toxicological results in such situations. The available evidence provides useful recommendations for forensic pathologists and health practitioners engaged in instances of sodium nitrite poisoning or death. The data should also set off alarm bells in the public health system, in prosecutor's offices, and for policymakers so that they may undertake preventative measures to stop and restrict the unregulated market for these substances.

Evaluation of the Antioxidant Effects of Berberine against Sodium Nitriteinduced Oxidative Injury in the Rat Liver.

Berberine is a plant derived alkaloid present in many plants that may has ameliorating potential influences against inflammatory and oxidative conditions. The current study aimed to evaluate the possible protective activity of berberine and investigate its probable mechanisms against sodium nitrite toxicity in the liver. Forty male rats were divided into five groups. Group one, as the control group, received normal saline, group two received berberine (100 mg.kg-1), and group three received sodium nitrite (80 mg.kg-1). Groups four and five received berberine in doses of 50 and 100 mg.kg-1, respectively, and sodium nitrite (80 mg.kg-1) was given orally. All the doses were orally administrated for two months. Then, at the end of the 60th day, the animals were sacrificed, and the liver homogenate was prepared. For evaluating the oxidative injury the levels of albumin (ALB) and aspartate transaminase (AST) in the serum and oxidative stress parameters in the liver were analyzed. Treatment of rats with sodium nitrite considerably increased the levels of serum AST and liver superoxide anion and significantly reduced the levels of serum ALB, hepatic superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase (CAT) activity in the liver tissue. Berberine treatment could ameliorate all these parameters dose dependently. Berberine at a dose of 100 mg.kg-1 had the best impact and reached the values of oxidative stress parameters to the normal level. Our results demonstrated that berberine in a dose-dependent manner offered protection against sodium nitrite-induced oxidative injury in liver, which possibly reflects the antioxidant abilities of this alkaloid.

Navigating Methemoglobinemia: A Sodium Nitrite Poisoning Case Report and Therapeutic Considerations

Incidences of sodium nitrite poisoning have frequently increased in the last few years with the wide, easy availability of the drug and the increase in suicidal tendencies in the population. Sodium nitrite is widely used as a food preservative and in treating cyanide toxicity. It is a powerful oxidizing agent, which oxidizes hemoglobin to methemoglobin, reducing the oxygen-carrying capacity of erythrocytes and causing tissue hypoxia. Patients with sodium nitrite toxicity present to emergency with hypotension, cyanosis, hypoxia, altered consciousness, dysrhythmia, and cardiac arrest. We report a case of a suicide survivor who presented with an intentional fatal overdose of sodium nitrite in an 18-year-old female by drinking approximately one tablespoon of sodium nitrite in a suicidal attempt. Upon arrival at the emergency department (ED), the patient was hypotensive, cyanotic, and cyanosis non-responsive to oxygen therapy. Hospital professionals should consider sodium nitrite toxicity in patients with a suspected overdose who present with a cyanotic appearance and pulse oximetry that remains around 85% despite oxygen and dark brown blood seen on venipuncture. Prompt diagnosis is crucial to start early treatment.

Acute toxicity of ammonia and nitrite to Siamese fighting fish (Betta splendens)

The acute toxicity and sublethal effects of ammonia and nitrite on the air-beathing Siamese fighting fish, betta (Betta splendens) was studied for 96 h. The LC50 (50% Lethal Concentration) for 96 h for adult bettas to ammonia-N and nitrite-N was 123.4 mM (1.7 g/L, 95% confidence limits: 114.7–130.0 mM) and 24.6 mM (343.6 mg/L, 95% confidence limits: 22.7–26.4 mM) respectively. Exposure to 90 mM ammonia did not affect ammonia and urea excretion rates in bettas. There was no significant difference in values between control and ammonia-loaded (90 mM ammonia) individuals in either brain or liver activities of glutamine synthase, while plasma ammonia levels slightly increased. It appears unlikely that ammonia was converted to urea or amino acids for detoxification. Sublethal nitrite (24.6 mM nitrite) affected plasma nitrite, methemoglobin and hemoglobin. Plasma nitrite values remained much lower than ambient concentrations. Betta has a labyrinth organ and can breathe air. Bettas may temporarily reduce the entry of ammonia and nitrite into the body by increasing the rate of air respiration and reducing the contribution of the gill epithelium, which is highly permeable to these nitrogenous pollutants.

The bZIP Transcription Factor Family Orchestrates the Molecular Response to Nitrite Stress in the Largemouth Bass Spleen

Nitrite toxicity poses a significant threat to aquatic organisms, including largemouth bass (LMB) and Micropterus salmoides. This study aimed to elucidate the role of bZIP transcription factors in mediating the molecular responses to nitrite stress in the LMB spleen. We identified 120 bZIP genes in the LMB genome using bioinformatics analysis and divided them into 11 subgroups based on phylogenetic relationships. Under nitrite stress, the bZIP_XI subgroup was upregulated, suggesting the activation of the stress response in the LMB spleen. Cellular pathway analysis revealed enrichment of pathways related to stress response, DNA repair, apoptosis, and autophagy. Co-expression network analysis highlighted bZIP_XI members such as msabZIP_49, msabZIP_12, msabZIP_39, and msabZIP_116 as potential key regulators. These transcription factors likely modulated the expression of stress-related genes like VCAM1, POLE3, and BMP1. Conserved binding motifs in the promoters of these genes may support regulation by bZIP_XI. Furthermore, bZIP_XI members correlated with immune cell infiltration in the spleen, potentially regulating immune-related genes like BCL2L1 and SELE. Homologs of bZIP_XI in other fish species exhibited similar expression patterns under stress. Overall, this study implicates the bZIP transcription factor family, notably the bZIP_XI subgroup, in orchestrating the molecular response of the LMB spleen to nitrite toxicity by regulating stress response pathways and immune function. These findings provide insights into nitrite stress adaptation in fish.

Reduction of carcinogens in fermented fish (pla-ra and pla-som) by heating.

The risk factors for cholangiocarcinoma (CCA) are opisthorchiasis and the intake of a combination of nitroso compounds through the consumption of traditionally fermented fish, which is very popular in areas where liver flukes are endemic. The incidence of CCA remains high because this cultural habit of rural people has been altered. Therefore, decreasing nitrate and nitrite concentrations in fermented fish are an alternative approach to reducing the risk of CCA. Thus, this study aimed to reduce nitrate and nitrite concentrations in fermented foods by heating and investigated its effect on CCA development in a hamster model. We used Association of Official Analytical Chemists method 973.31 to measure the nitrate and nitrite concentrations in both fermented fish (pla-ra [PR]) and pickled fish (pla-som [PS]) before and after boiling for 5 and 30 min, respectively. The same samples were fed to Opisthorchis viverrini (OV)-infected or -uninfected hamsters for 3 months. Thereafter, the hamsters' liver and blood were collected for analysis. The levels of nitrates and nitrites in PS and PR significantly decreased following boiling for 5 and 30 min. The OV-PR and OV-PS groups showed dramatically increased numbers of inflammatory cells, fibrosis surrounding the bile duct, and focal fibrotic areas. However, after boiling the fermented dishes for 5 and 30 min, the extent of inflammatory cell infiltration and intensity of fibrosis in these groups were decreased. Our findings suggest that boiling reduces nitrate and nitrite toxicity in fermented dishes, as evidenced by reduced hepatic inflammation. However, regardless of heating, kidney tissues are adversely affected when fermented meals are consumed daily.

Microbial characteristics and potential mechanisms of souring control for a hypersaline oil reservoir

The production of hydrogen sulfide (H2S) had caused huge economic losses and security risks to oil fields, which had attracted the attention of many researchers. Studies focused on hypersaline oil reservoirs were scarce. Here, we simulated H2S inhibition by adding NO3 - and NO2 - in anaerobic bottles and up-flow sand-packed bioreactor in the laboratory using water samples from injection wells in the Jianghan reservoir. The microbial characteristics, pH, salinity, sulfate, sulfide, NO3 - and NO2 - were measured at every stage. The content of H2S and elemental sulfur (S0) gradually reduced to 0 mg/L with injected 400 mg/L of NO3 - and 300 mg/L of NO2 -. Halophilic nitrate-reducing bacteria (NRBs) related to Halomonas and Arcobacter could suppress the activity of sulfate-reducing bacteria (SRBs) through the accumulation of nitrite toxicity and the competition of organic substrates with SRBs. When SRBs activity could not be suppressed, the sulfur-oxidizing bacteria related to Sulfurimonas, Thiomicrospira and Acrobacter were accumulated for souring control through microbial sulfur cycle of H2S production and oxidation. Salinity could be a key parameter affecting microbial development and interactions. This study provides a fundamental data to souring control in the hypersaline oil reservoir by reinjection produced water amended with NO3 - and NO2 -.

Presumptive Identification of Nitrite by Griess Reagent Test Strips - Case reports of fatal poisoning with sodium nitrite.

The intentional ingestion of sodium nitrite causes toxicity by inducing methemoglobinemia which can lead to cyanosis, hypotension, and death. The number of reported suicide cases has significantly increased in the past ten years as sodium nitrite is readily available online. The traditional tests for nitrite and nitrate require specialized detection methods which are not typically available in a postmortem toxicology laboratory. This rise in sodium nitrite overdose cases indicates the need for a simple, quick test for suspected nitrite toxicity. In this study, a common Griess reagent color test (MQuant™ Nitrite Test Strips) was used as a presumptive method in cases where the ingestion of sodium nitrite was suspected. The test results were consistent between samples in all cases and vitreous humor was identified as a reliable matrix to be used in the cases of suspected sodium nitrite poisonings. Case reports of five patients who died of suicide by sodium nitrite in a six-month span are presented.

Nitrite decreases sickle hemoglobin polymerization in vitro independently of methemoglobin formation

The root cause of sickle cell disease (SCD) is the polymerization of sickle hemoglobin (HbS) leading to sickling of red blood cells (RBC). Earlier studies showed that in patients with SCD, high-dose nitrite inhibited sickling, an effect originally attributed to HbS oxidation to methemoglobin-S even though the anti-sickling effect did not correlate with methemoglobin-S levels. Here, we examined the effects of nitrite on HbS polymerization and on methemoglobin formation in a SCD mouse model. In vitro, at concentrations higher than physiologic (>1 μM), nitrite increased the delay time for polymerization of deoxygenated HbS independently of methemoglobin-S formation, which only occurred at much higher concentrations (>300 μM). In vitro, higher nitrite concentrations oxidized 100% of normal hemoglobin A (HbA), but only 70% of HbS. Dimethyl adipimidate, an anti-polymerization agent, increased the fraction of HbS oxidized by nitrite to 82%, suggesting that polymerized HbS partially contributed to the oxidation-resistant fraction of HbS. At low concentrations (10 μM-1 mM), nitrite did not increase the formation of reactive oxygen species but at high concentrations (10 mM) it decreased sickle RBC viability. In SCD mice, 4-week administration of nitrite yielded no significant changes in methemoglobin or nitrite levels in plasma and RBC, however, it further increased leukocytosis. Overall, these data suggest that nitrite at supra-physiologic concentrations has anti-polymerization properties in vitro and that leukocytosis is a potential nitrite toxicity in vivo. Therefore, to determine whether the anti-polymerization effect of nitrite observed in vitro underlies the decreases in sickling observed in patients with SCD, administration of higher nitrite doses is required.

Sodium nitrite poisoning: A series of 20 fatalities in which post-mortem blood nitrite and nitrate concentrations are reported

Sodium nitrite has several industrial applications however its accidental or intentional ingestion has been associated with severe toxicity and death. We present a series of 20 cases over 2 years in which evidence of sodium nitrite ingestion was found at the scene and supported by biochemical analysis of post-mortem blood nitrite and nitrate levels. Routine toxicological screening was performed on post-mortem blood samples received at University Hospitals of Leicester (UHL) NHS Trust, including ethanol analysis by headspace gas chromatography–flame ionisation detection (HS GC-FID), drug screening by high resolution accurate mass–mass spectrometry (HRAM-MS) and confirmatory drug quantitation by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Cases in which the history indicated the possibility of nitrite salts present at the scene, purchase of a suicide kit or a dusky-ash appearance of skin on post-mortem were referred to a specialist laboratory for nitrite and nitrate analysis. Analysis was based upon the gas-phase chemiluminescent reaction between nitric oxide (NO) and ozone; NO levels were determined using an NOA 280A, Sievers NO analyser. Twenty post-mortem cases in which sodium nitrite ingestion was the most probable cause of death were reported between January 2020 and February 2022; mean age was 31 years (range 14–49) with 9/20 (45%) female. 16/20 (80%) of cases had a history of depression and / or mental health issues. In half of the cases, anti-depressant / anti-psychotic drugs were prescribed; these drugs were detected in 8/20 (40%) cases. Ethanol was detected in 4/20 (20%) cases and anti-emetic drugs in 7/20 (35%) cases; anti-emetic drugs may be used to aid retention of sodium nitrite. Illicit drugs (amphetamine, cannabis and cocaine) were present in 3/20 cases (15%). Nitrite was found to be elevated in all but one case (95%), and nitrate was elevated in 17/20 (85%) cases. This paper highlights a surge in numbers of deaths across England and Wales due to sodium nitrite toxicity. Although, nitrite poisoning remains a rare cause of death, it is worthwhile considering its use in individuals with suicidal ideation given its unregulated availability online. The detection and quantitation of nitrite and nitrate requires specialised, highly reliable methodology currently only available in research laboratories. Implication of sodium nitrite ingestion also relies heavily upon circumstantial evidence combined with quantification. The provision of a quantitative nitrite / nitrate analytical service greatly assists in determining the cause of death in these cases.

Reproductive Toxicity of Sodium Nitrite and Its Modulation by Ascorbic Acid as An Antioxidant in Pregnant Female Mice

Reproductive Toxicity of Sodium Nitrite and Its Modulation by Ascorbic Acid as An Antioxidant in Pregnant Female Mice

Reproductive Toxicity of Sodium Nitrite and Its Modulation by Ascorbic Acid as An Antioxidant in Male Mice

Reproductive Toxicity of Sodium Nitrite and Its Modulation by Ascorbic Acid as An Antioxidant in Male Mice

Double-edged sword effects of dissimilatory nitrate reduction to ammonium (DNRA) bacteria on anammox bacteria performance in an MBR reactor

Dissimilatory nitrate reduction to ammonium (DNRA) bacteria imposing double-edged sword effects on anammox bacteria were investigated in an anammox-membrane bioreactor (MBR) experiencing an induced crash-recovery event. During the experiment, the anammox-MBR was loaded with NH4+-N:NO2−-N ratios (RatioNH4+-N: NO2−-N) of 1.20–1.60. Initially, the anammox-MBR removed over 95% of 100 mg/L NH4+-N and 132 mg/L NO2−-N (RatioNH4+-N: NO2−-N = 0.76, the well accepted stoichiometric RatioNH4+-N: NO2−-N for anammox) in the influent (Stage 0). Then, we induced a system crash-recovery event via nitrite shock loadings to better understand responses from different guilds of bacteria in anammox-MBR, loaded with 1.60 RatioNH4+-N: NO2−-N with 100 mg/L NO2−-N in the influent (Stage 1). Interestingly, the nitrogen removal by anammox bacteria was maintained for about 20 days before starting to decrease significantly. In Stage 2, we further increased influent nitrite concentration to 120 mg/L (1.33 RatioNH4+-N: NO2−-N) to simulate a high nitrite toxicity scenario for a short period of time. As expected, nitrogen removal efficiency dropped to only 16.8%. After the induced system crash, anammox-MBR performance recovered steadily to 93.2% nitrogen removal with a 1.25 RatioNH4+-N:NO2−-N and a low nitrite influent concentration of 80 mg/L NO2−-N. Metagenomics analysis revealed that a probable causality of the decreasing nitrogen removal efficiency in Stage 1 was the overgrowth of DNRA-capable bacteria. The results showed that the members within the Ignavibacteriales order (21.7%) out competed anammox bacteria (17.0%) in the anammox-MBR with elevated nitrite concentrations in the effluent. High NO2−-N loading (120 mg N/L) further caused the predominant Candidatus Kuenenia spp. were replaced by Candidatus Brocadia spp. Therefore, it was evident that DNRA bacteria posed negative effects on anammox with 1.60 RatioNH4+-N: NO2−-N. Also, when 120 mg/L NO2−-N fed to anammox-MBR (RatioNH4+-N: NO2−-N = 1.33), canonical denitrification became the primary nitrogen sink with both DNRA and anammox activities decreased. They probably fed on lysed microbial cells of anammox and DNRA. In Stage 3, a low RatioNH4+-N: NO2−-N (1.25) with 80 mg/L NO2−-N was used to rescue the system, which effectively promoted DNRA-capable bacteria growth. Although anammox bacteria's abundance was only 7.7% during this stage, they could be responsible for about 90% of the total nitrogen removal during this stage.

Sodium nitrite ingestion in Singapore – a case report

Sodium nitrite is a strong oxidising agent with multiple industrial uses. Ingestion of a small dose can cause death rapidly through the formation of methaemoglobin and nitric oxide. Globally, while deaths due to sodium nitrite ingestion have been sporadic and tended to be accidental, the frequency of deaths due to purposeful ingestions is increasing. Local incidences of sodium nitrite ingestion in Singapore remain rare. We present a case report of a death due to sodium nitrite ingestion in Singapore, the challenges faced, and the various diagnostic approaches to sodium nitrite toxicity.

Hierarchical porous carbon foam embedded with readily accessible atomic iron sites for efficient electrochemical nitrite sensing

A hierarchical porous carbon foam embedded with atomic iron sites is facilely synthesized and works as an efficient electrochemical nitrite sensor.