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| Names | |||
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| IUPAC name 2,6-Diamino-4,5-dihydroxypyrimidine | |||
| Other names 2,6-Diamino-4,5-pyrimidinediol; 2,6-diamine-5-hydroxy-4(3H)-pyrimidinone; 2,4-diamino-5,6-dihydroxypyrimidine | |||
| Identifiers | |||
3D model (JSmol) |
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| ChemSpider |
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| UNII | |||
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| Properties | |||
| C4H6N4O2 | |||
| Molar mass | 142.118 g·mol−1 | ||
| Appearance | Brownish needles | ||
| Solubility in 10% KOH | Soluble[vague] | ||
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |||
Divicine (2,6-diamino-4,5-dihydroxypyrimidine) is an oxidant and a base with alkaloidal properties found infava beans andLathyrus sativus. It is anaglycone ofvicine. A common derivative is the diacetate form (2,6-diamino-1,6-dihydro-4,5-pyrimidinedione).[1]
Divicine is found infava beans and in the legumeLathyrus sativus, also known as khesari, which is a cheap and robust food source commonly grown in Asia and East Africa.[citation needed]
In plants, reduced divicine is formed from the hydrolysis of the inactive β–glucoside,vicine.[2]
A simplified three-step process for artificial divicine synthesis:
Some chemical characteristics of divicine have been examined. It is known that it vigorously reducesalkaline solutions of 2,6-dichlorophenolindophenol, phosphomolybdate or phosphotungstate and produces an intense blue colour when reacting with an ammoniacal ferric chloride solution, which is used for the identification and proof of the presence of an enolichydroxyl group.
Divicine is very unstable if oxygen is present and the oxidation is most rapid at alkaline pH levels. The half-life of divicine, at room temperature and neutral pH, is around half an hour. Both compounds are almost immediately destroyed by boiling, and breakdown in regular conditions can be accelerated by the presence of heavy metal ions, especially Cu2+.[4]
Divicine has been deemed ahemotoxic component offava beans and plays a role in the development offavism, a disorder that involves a hemolytic response to the consumption of broad beans due toglucose-6-phosphate dehydrogenase (G6PD or G6PDH) deficiency. This deficiency, an X-linked recessive hereditary disease, is the most common enzyme deficiency worldwide. It is particularly common in those of African, Asian, Mediterranean, and Middle-Eastern descent. Symptoms offavism includehemolysis, prolongedjaundice,kernicterus, and evenacute renal failure in extreme cases.[5]
Divicine reacts with oxygen in red blood cells, which createsreactive oxygen species such ashydrogen peroxide andsuperoxide anion. These molecules are strong oxidizers ofNADPH andglutathione.[6] G6PD deficient individuals cannot regenerate NADPH quickly enough to prevent depletion of glutathione. This depletion results in the cells having no protection against oxidative stress caused by the aglycones. Oxidative stress leads to damage of haemoglobin and disulphide bond aggregates (Heinz bodies), which result in haemolytic anaemia, called favism.[7]
Divicine is also present in and at least partially responsible for the poisonous action ofLathyrus sativus - a legume commonly grown in drought- and famine-prone regions of Asia and East Africa as an ‘insurance crop’ for human consumption and livestock feed when other crops fail to grow, despite their known health hazards.[citation needed]
In vitro studies in rats showed that a hemotoxic dose of divicine of 1.5 mM, when added to a suspension of red blood cells, resulted in a rapid decline in cellular glutathione, formation ofechinocytes and damage to the membrane skeleton. This resulted in a decrease inhaematocrit.[8]
