Hydroxidooxidonitrogen
Hydroxidooxidonitrogen Uses, Dosage, Side Effects, Food Interaction and all others data.
Hydroxidooxidonitrogen (as sodium nitrite) is used as part of an intravenous mixture with sodium thiosulfate to treat cyanide poisoning. It is on the World Health Organization's List of Essential Medicines, a list of the most important medications needed in a basic health system. There is also research to investigate its applicability towards treatments for heart attacks, brain aneurysms, pulmonary hypertension in infants, and Pseudomonas aeruginosa infections.
Sodium nitrite reverses cyanide toxicity and produces blood vessel dilation .
| Trade Name | Hydroxidooxidonitrogen |
| Generic | Nitrous acid |
| Nitrous acid Other Names | dioxonitric acid, hydroxidooxidonitrogen, nitrosyl hydroxide |
| Type | |
| Formula | HNO2 |
| Weight | Average: 47.0134 Monoisotopic: 47.000728281 |
| Groups | Approved, Investigational |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Hydroxidooxidonitrogen is an iron binder used to reverse life-threatening acute cyanide poisoning.
For sequential use with sodium thiosulfate for the treatment of acute cyanide poisoning that is judged to be life-threatening .
Hydroxidooxidonitrogen is also used to associated treatment for these conditions: Toxic effect of hydrocyanic acid and cyanides
How Hydroxidooxidonitrogen works
Cyanide has a high affinity for the oxidized form of iron (Fe3+) such as that found in cytochrome oxidase a3 . Cyanide binds to and inhibits cytochrome oxidase a3, preventing oxidative phophorylation from occuring. The resultant lack of ATP cannot support normal cellular processes, particularly in the brain. Compensatory increases in anaerobic respiration result in rising levels of lactic acid and subsequent acidosis.
Nitrite primarily acts by oxidizing hemoglobin to methemoglobin . The now oxidized Fe3+ in methemoglobin also binds cyanide with high affinity and accepts cyanide from cytochrome a3. This leaves cytochrome a3 free to resume its function in oxidative phosphorylation. The slow dissociation of cyanide from methemoglobin allows hepatic enzymes such as rhodanese to detoxify the compound without further systemic toxicity occuring. Methemoglobin is reduced back to hemoglobin by methemoglobin reductase allowing the affected blood cells to resume normal functioning.
The reduction of nitrite by hemoglobin results in the formation of nitric oxide . Nitric oxide acts as a powerful vasodilator, producing vascular smooth muscle relaxation through activation of soluble guanylate cyclase and the subsequent cyclic guanylyl triphosphate mediated signalling cascade .
Toxicity
Oral LD50 of 157.9mg/kg observed in rats and 175mg/kg observed in mice . Estimated oral LD50 of 35mg/kg in humans . Sodium nitrite toxicity manifests as cardiovascular collapse following severe hypotension due to nitrite's vasodilatory action.
Food Interaction
No interactions found.Half Life
Half life of 0.4-0.78h .
Innovators Monograph
You find simplified version here Hydroxidooxidonitrogen
