Severe Methemoglobinemia due to Sodium Nitrite Poisoning

Katabami, Kenichi; Hayakawa, Mineji; Gando, Satoshi

doi:10.1155/2016/9013816

Cited by 49 publications

(54 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our previous work showed that erythrocytes treated with 5 mM NaNO 2 exhibit significant and quantifiable alterations in stress parameters at this concentration (Ansari et al, ). It has also been reported that accidental or intentional (suicidal) ingestion of sodium nitrite results in high MetHb levels (>50%) in blood of affected persons, similar to those obtained by us using 5 mM NaNO 2 (Chui et al, ; Katabami et al, ). Our results show for the first time that crocin significantly protected erythrocytes from NaNO 2 ‐induced cell damage and can be an effective agent in mitigating oxidative stress and other damaging effects of nitrite on human tissues.…”

Section: Introductionsupporting

confidence: 81%

Crocin protects human erythrocytes from nitrite‐induced methemoglobin formation and oxidative damage

Ansari

Ali

Mahmood

2016

Cell Biology International

View full text Add to dashboard Cite

Sodium nitrite (NaNO ) is a common contaminant of drinking water and food and feed chain. Nitrite induces oxidative damage in humans and animals. In this work, we studied the protective effect of crocin, the active constituent of Crocus sativus (saffron), on NaNO -induced oxidative damage in human erythrocytes. Changes in oxidative stress parameters following NaNO incubation of erythrocytes in presence and absence of crocin were determined. It was found that crocin pre-treatment significantly attenuated NaNO -induced oxidative damage of proteins, lipids, and plasma membrane. Crocin reduced the level of methemoglobin, the primary acute effect of nitrite intoxication. It also improved the antioxidant capacity of cells and NaNO -induced morphological changes in erythrocytes. Crocin is thus a potent protective agent against nitrite-induced cytotoxicity.

show abstract

Section: Introductionsupporting

confidence: 81%

Crocin protects human erythrocytes from nitrite‐induced methemoglobin formation and oxidative damage

Ansari

Ali

Mahmood

2016

Cell Biology International

View full text Add to dashboard Cite

show abstract

“…Ozen et al [21] have reported degenerative changes in organs of nitrite-treated mice. Although chronic exposure of humans to low doses of nitrite is common world-wide, many cases of intentional or accidental exposure to high doses of nitrite have also been documented [22,23]. However, reports on the mechanistic details of nitrite-induced oxidative stress in mammals are lacking in literature.…”

Section: Introductionmentioning

confidence: 99%

Acute oral dose of sodium nitrite induces redox imbalance, DNA damage, metabolic and histological changes in rat intestine

Ansari¹,

Ali²,

Arif³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Industrialization and unchecked use of nitrate/nitrite salts for various purposes has increased human exposure to high levels of sodium nitrite (NaNO2) which can act as a pro-oxidant and pro-carcinogen. Oral exposure makes the gastrointestinal tract particularly susceptible to nitrite toxicity. In this work, the effect of administration of a single acute oral dose of NaNO2 on rat intestine was studied. Animals were randomly divided into four groups and given single doses of 20, 40, 60 and 75 mg NaNO2/kg body weight. Untreated animals served as the control group. An NaNO2 dose-dependent decline in the activities of brush border membrane enzymes, increase in lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased thiol content was observed in all treated groups. The activities of various metabolic and antioxidant defense enzymes were also altered. NaNO2 induced a dose-dependent increase in DNA damage and DNA-protein crosslinking. Histopathological studies showed marked morphological damage in intestinal cells. The intestinal damage might be due to nitrite-induced oxidative stress, direct action of nitrite anion or chemical modification by reaction intermediates.

show abstract

“…Previously reported cases of methemoglobinemia secondary to sodium nitrate ingestion include individuals inadvertently using sodium nitrate in place of table salt due to inappropriate or non-existent labeling [6][7][8]. Our patient survived after a MetHb level of 92.7% on co-oximetry, which is among the highest recorded MetHb levels [9,10]. Katabami et al describe a case of methemoglobinemia after intentional ingestion of sodium nitrite with a MetHb level of 92.5% [9].…”

Section: Discussionmentioning

confidence: 70%

“…Methemoglobinemia occurs when MetHb levels in the circulation are greater than 1.5%. Notably, sodium nitrite is a very similar substance to sodium nitrate, and may also cause methemoglobinemia; such toxicity is treated in a similar fashion [9][10][11][12][13].…”

Section: Discussionmentioning

confidence: 99%

Survival after severe methemoglobinemia secondary to sodium nitrate ingestion

Cruz

Glick

Merker

et al. 2018

Toxicology Communications

View full text Add to dashboard Cite

Sodium nitrate is used as a food preservative and color fixative. Sodium nitrate poisoning has occurred in the setting of well water contamination with nitrogenous waste runoff. Most clinically significant exposures result from improper labeling or unintentional use. We describe a case of severe methemoglobinemia associated with intentional sodium nitrate ingestion. A 23-year-old female presented to the emergency department (ED) for an intentional ingestion of sodium nitrate obtained from an online distributor. On arrival, blood pressure was 89/42 mmHg and oxygen saturation was 74% on pulse oximetry. Due to clinical decline, the patient underwent endotracheal intubation in the ED. Co-oximetry demonstrated a methemoglobin (MetHb) level of 92.7%, which is among the highest recorded MetHb levels. The patient received two doses of 1 mg/kg methylene blue and experienced dramatic clinical improvement and subsequent successful extubation. Healthy erythrocytes undergo oxidative stress from normal metabolism resulting in spontaneous formation of MetHb. Reduction of MetHb to hemoglobin occurs via the protective enzymes cytochrome-b5 reductase and nicotinamide adenine dinucleotide phosphate (NADPH) MetHb reductase. Sodium nitrate acts as an oxidizing agent causing methemoglobinemia. Treatment includes methylene blue, which acts as a cofactor for NADPH MetHb reductase. KEYWORDS Methemoglobinemia; sodium nitrate, methylene blueCONTACT Maricel Dela Cruz

show abstract

Severe Methemoglobinemia due to Sodium Nitrite Poisoning

Cited by 49 publications

References 7 publications

Crocin protects human erythrocytes from nitrite‐induced methemoglobin formation and oxidative damage

Crocin protects human erythrocytes from nitrite‐induced methemoglobin formation and oxidative damage

Acute oral dose of sodium nitrite induces redox imbalance, DNA damage, metabolic and histological changes in rat intestine

Survival after severe methemoglobinemia secondary to sodium nitrate ingestion

Contact Info

Product

Resources

About