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α-Solanine
Names
IUPAC name
(2S,3R,4S,5S,6R)-2-(((2R,3S,4S,5R,6R)-3-hydroxy-2-(hydroxymethyl)-5-(((2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl)oxy)-6-(((4S,6aR,6bS,8aS,8bR,9S,9aR,14aS,15aS,15bS)-6a,8a,9-trimethyl-3,4,5,6,6a,6b,7,8,8a,8b,9,9a,10,11,12,13,14a,15,15a,15b-icosahydro-1H-naphtho[2',1':4,5]indeno[1,2-b]indolizin-4-yl)oxy)tetrahydro-2H-pyran-4-yl)oxy)-6-(hydroxymethyl)tetrahydro-2H-pyran-3,4,5-triol
Other names
α-Solanine; Solanin; Solatunine
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
UNII
  • InChI=1S/C45H73NO15/c1-19-6-9-27-20(2)31-28(46(27)16-19)15-26-24-8-7-22-14-23(10-12-44(22,4)25(24)11-13-45(26,31)5)57-43-40(61-41-37(54)35(52)32(49)21(3)56-41)39(34(51)30(18-48)59-43)60-42-38(55)36(53)33(50)29(17-47)58-42/h7,19-21,23-43,47-55H,6,8-18H2,1-5H3/t19-,20+,21-,23-,24+,25-,26-,27+,28-,29+,30+,31-,32-,33+,34-,35+,36-,37+,38+,39-,40+,41+,42-,43+,44-,45-/m0/s1 ☒N
    Key: ZGVSETXHNHBTRK-OTYSSXIJSA-N ☒N
  • InChI=1/C45H73NO15/c1-19-6-9-27-20(2)31-28(46(27)16-19)15-26-24-8-7-22-14-23(10-12-44(22,4)25(24)11-13-45(26,31)5)57-43-40(61-41-37(54)35(52)32(49)21(3)56-41)39(34(51)30(18-48)59-43)60-42-38(55)36(53)33(50)29(17-47)58-42/h7,19-21,23-43,47-55H,6,8-18H2,1-5H3/t19-,20+,21-,23-,24+,25-,26-,27+,28-,29+,30+,31-,32-,33+,34-,35+,36-,37+,38+,39-,40+,41+,42-,43+,44-,45-/m0/s1
    Key: ZGVSETXHNHBTRK-OTYSSXIJBP
  • C[C@H]1CC[C@@H]2[C@H]([C@H]3[C@@H](N2C1)C[C@@H]4[C@@]3(CC[C@H]5[C@H]4CC=C6[C@@]5(CC[C@@H](C6)O[C@H]7[C@@H]([C@H]([C@H]([C@H](O7)CO)O)O[C@H]8[C@@H]([C@H]([C@@H]([C@H](O8)CO)O)O)O)O[C@@H]9[C@@H]([C@@H]([C@H]([C@@H](O9)C)O)O)O)C)C)C
Properties
C45H73NO15
Molar mass 868.06
Appearance white crystalline solid
Melting point 271 to 273 °C (520 to 523 °F; 544 to 546 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)
Tracking categories (test):

Solanine is a glycoalkaloid and Steroidal alkaloid poison found in species of the nightshade family within the genus Solanum, such as the potato (Solanum tuberosum), the tomato (Solanum lycopersicum), and the eggplant (Solanum melongena). It can occur naturally in any part of the plant, including the leaves, fruit, and tubers. Solanine has pesticidal properties, and it is one of the plant's natural defenses. Solanine was first isolated in 1820 from the berries of the European black nightshade (Solanum nigrum), after which it was named.[1] It belongs to the chemical family of saponins.

Solanine Poisoning edit

Symptoms edit

Solanine poisoning is primarily displayed by gastrointestinal and neurological disorders. Symptoms include nausea, diarrhea, vomiting, stomach cramps, burning of the throat, cardiac dysrhythmia, nightmares, headache, dizziness, itching, eczema, thyroid problems, inflammation and pain in the joints. In more severe cases, hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils, hypothermia, and death have been reported.[2][3][4] Gaffield and Keeler (1996) reported the instance of craniofacial birth defects when ingested by pregnant Syrian hamsters. [5] In addition, Renwick et al. (1984) found similar malformations in Syrian hamsters.[6]

Ingestion of solanine in moderate amounts can cause death. One study suggests that doses of 2 to 5 mg/kg of body weight can cause toxic symptoms, and doses of 3 to 6 mg/kg of body weight can be fatal.[7]

Symptoms usually occur 8 to 12 hours after ingestion, but may occur as rapidly as 10 minutes after eating high-solanine foods.

Treatment of these symptoms consist of electrolyte and fluid replacement along with anticonvulsants.[8] The California Poison Control System generally recommends oral administration of activated charcoal and gastric lavage, if necessary.[9]

Mechanism of action edit

Solanum glycoalkaloids can inhibit cholinesterase, disrupt cell membranes, and cause birth defects.[10] The anticholinergic activity of solanine causes the gastrointestinal side effects of nausea, vomiting, diarrhea and abdominal pain along with the cardiovascular impacts.[9] One study suggests that the toxic mechanism of solanine is caused by the chemical's interaction with mitochondrial membranes. Experiments show that solanine exposure opens the potassium channels of mitochondria, decreasing their membrane potential. This, in turn, leads to K+ being transported from the mitochondria into the cytoplasm, and this increased concentration of K+ in the cytoplasm triggers cell damage and apoptosis.[11]

Correlation with birth defects edit

Some studies show a correlation between the consumption of potatoes suffering from late blight (which increases solanine and other glycoalkaloid levels) and the incidence of birth defects like exencephaly, encephalocele, anophthalmia, and congenital spina bifida in humans. However, other studies have shown no statistically significant correlation between solanine intake and the incidence of birth defects.[12] Currently, the connection betweeen human birth defects and solanine is circumstantial, mostly based on high rates of spina bifida in Ireland which uses potatoes as a dietary staple and during Spring when potatoes would be harvested.[13] Gaffield and Keeler (1996) found that 0.24 g/kg of solanine intake causes birth defects in Syrian hamsters, which are considered to have similar genetic makeup to humans.[14] Meanwhile Renwick et al. (1984) found the same side effects in just 0.2 g/kg.[6] Potatoes, on average, contain 11.25 mg of solanine. With the average adult weighing 70 kg, the dose would be require the intake of over 300 potatoes. Meanwhile, Nishie et al. (1975) concluded that there is no statistically significant correlation between solanine and birth defects in chicken embryos for doses of 0, 1, and 1.5 mg/kg.[15] John Sever's review of solanine studies also hypothesizes that genetic, immediate, and intergenerational factors may predominantly influence the instance of these birth defects rather than solanine intake.[16] There is still debate on the impact of solanine on birth defects.

Presence in Nature edit

Solanine, along with other glycoalkaloids like chaconine are used by potatoes to protect their tubers from consumption by animals. Each potato has about 0.75 mg/g. It is widely accepted that potatoes contain solanine, while there is some debate over its presence in tomatoes.

In Potatoes edit

 
Green potatoes usually have elevated levels of solanine and should not be eaten.

Potatoes naturally produce solanine and chaconine, a related glycoalkaloid, as a defense mechanism against insects, disease, and herbivores. Potato leaves, stems, and shoots are naturally high in glycoalkaloids.

When potato tubers are exposed to light, they turn green and increase glycoalkaloid production. This is a natural defense to help prevent the uncovered tuber from being eaten. The green colour is from chlorophyll, and is itself harmless. However, it is an indication that increased level of solanine and chaconine may be present. In potato tubers, 30–80% of the solanine develops in and close to the skin, and some potato varieties have high levels of solanine.

Some potato diseases, such as late blight, can dramatically increase the levels of glycoalkaloids present in potatoes. Tubers damaged in harvesting and/or transport also produce increased levels of glycoalkaloids; this is believed to be a natural reaction of the plant in response to disease and damage.

In the 1970s, solanine poisoning affected 78 schoolboys in Britain. Due to immediate and effective treatments, no one died.[8]

Green colouring under the skin strongly suggests solanine build-up in potatoes, although each process can occur without the other. A bitter taste in a potato is another, potentially more reliable indicator of toxicity. Because of the bitter taste and appearance of such potatoes, solanine poisoning is rare outside conditions of food shortage. The symptoms are mainly vomiting and diarrhea, and the condition may be misdiagnosed as gastroenteritis. Most potato poisoning victims recover fully, although fatalities are known, especially when victims are undernourished or do not receive suitable treatment.[8] Fatalities are also known from solanine poisoning from other plants in the nightshade family, such as the berries of Solanum dulcamara (woody nightshade).[17]

The United States National Institutes of Health's information on solanine strongly advises against eating potatoes that are green below the skin.[18] Meanwhile, the California Poison Control System's publication, Poisoning and Drug Overdose lists unripe potatoes as Group 1 toxic plants. These "contain systemically active poisons that may cause serious poisoning."[9]

Home processing methods (boiling, cooking, frying, and microwaving) have small and variable effects on glycoalkaloids. For example, boiling potatoes reduces the α-chaconine and α-solanine levels by only 3.5% and 1.2%, respectively; the corresponding loss during microwaving is 15%. Deep-frying at 150 °C (302 °F) does not result in any measurable change; significant degradation starts at ∼170 °C (338 °F), and deep-frying at 210 °C (410 °F) for 10 min causes a loss of ∼40%.[19] Freeze-drying or dehydration has little effect.[20]

Biosynthesis edit

 
The biosynthesis of solanine from cholesterol in Solanaceae plants.

SGT1 has been found to have both glucosyltransferase and galactosyltransferase activity.[21] In doing so, it is utilized in two of the last three steps, adding the first chain of carbohydrates to the solanidine aglycone. These two steps add the glucose and galactose to the molecule, while the final step of the biosynthesis adds rhamnose. The solanidine molecule along with the cholesterol starting material lacks toxicity, making them unable to keep off predators. As a result, when the tuber is exposed to the sunlight the biosynthesis increases in rate, spurring the production of solanine and chaconine.

In Tomatoes edit

Some, such as the California Poison Control System, have claimed that tomatoes and tomato leaves contain solanine. However, Mendel Friedman of the United States Department of Agriculture contradicts this claim, stating that tomatine, a relatively benign alkaloid, is the tomato alkaloid while solanine is found in potatoes. Food science writer Harold McGee has found scant evidence for tomato toxicity in the medical and veterinary literature.[22] Like in potatoes, the California Poison Control System reports in Poisoning and Drug Overdose that the tomatoes are a Group 1 toxic plant. Tomatine is not mentioned as a poisonous compound in the California Poison Control System's publication. [9]

 
The biosynthesis of tomatine in tomatoes.

In its biosynthesis, tomatine remains similar to solanine, differing in its pentane cyclization step.[23] According to Nishie (1975) in mice, the glycoalkaloid shares a relatively similar LD50 with solanine at 32.4 uM/kg.[15] It also acts as an inhibitor of cholinesterase, causing similar side effects. It does lack, however, the toxicity of solanine with doses of 30, 50, and 100 mg/kg not producing any deaths in rabbits. Meanwhile, solanine caused death at 40 mg/kg. In terms of teratogenicity, tomatine is comparable at high levels with Nishie (1975) also reporting the presence of abnormalities at 12, 20, and 25 mg/kg when injected into chick embryos [15].

See also edit

References edit

  1. ^ Desfosses, M. (1820): Extrait d'une lettre à M. Robiquet. In: J. de Pharmacie. Bd. 6, S. 374–376.
  2. ^ http://msue.anr.msu.edu/news/solanine_poisoning_how_does_it_happen
  3. ^ https://medlineplus.gov/ency/article/002875.htm
  4. ^ http://www.smithsonianmag.com/arts-culture/horrific-tales-of-potatoes-that-caused-mass-sickness-and-even-death-3162870/
  5. ^ Gaffield, William, and Richard F. Keeler. “Induction of Terata in Hamsters by Solanidane Alkaloids Derived FromSolanumtuberosum.” Chemical Research in Toxicology, vol. 9, no. 2, 1996, pp. 426–433., doi:10.1021/tx950091r.
  6. ^ a b Renwick, J. H., et al. “Neural-Tube Defects Produced in Syrian Hamsters by Potato Glycoalkaloids.” Teratology, vol. 30, no. 3, 1984, pp. 371–381., doi:10.1002/tera.1420300309.
  7. ^ Executive Summary of Chaconine & Solanine Archived 15 August 2006 at the Wayback Machine
  8. ^ a b c "Solanine poisoning". BMJ. 2 (6203): 1458–9. 1979. doi:10.1136/bmj.2.6203.1458-a. PMC 1597169. PMID 526812.
  9. ^ a b c d Olson, Kent; Anderson, Ilene; Benowitz, Neal; Blanc, Paul; Clark, Richard; Keaerney, Thomas; Osterloh, John (2007). Poisoning and Drug Overdose (5 ed.). New York: The McGraw-Hill Companies. pp. 312, 317, 318, 320. ISBN 978-0-07-144333-3. {{cite book}}: |access-date= requires |url= (help)
  10. ^ Friedman, Mendel; McDonald, Gary M. (1999). "Postharvest Changes in Glycoalkaloid Content of Potatoes". In Jackson, Lauren S.; Knize, Mark G.; Morgan, Jeffrey N. (eds.). Impact of Processing on Food Safety. Advances in Experimental Medicine and Biology. Vol. 459. pp. 121–43. doi:10.1007/978-1-4615-4853-9_9. ISBN 978-1-4615-4853-9. PMID 10335373.
  11. ^ Gao, Shi-Yong; Wang, Qiu-Juan; Ji, Yu-Bin (2006). "Effect of solanine on the membrane potential of mitochondria in HepG2 cells and [Ca2+]i in the cells". World Journal of Gastroenterology. 12 (21): 3359–67. doi:10.3748/wjg.v12.i21.3359. PMC 4087866. PMID 16733852.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ "Solanine and Chaconine". Retrieved 31 May 2009.
  13. ^ Renwick, John (December 1973). "Prevention of Anencephaly and Spina Bifida in Man". Teratology. 8 (3): 321–323. doi:10.1002/tera.1420080314. {{cite journal}}: |access-date= requires |url= (help)
  14. ^ Gaffield, William; Keeler, Richard (1 March 1996). "Introduction of Terata in Hamsters by Solanidane Alkaloids Derived from Solanum tuberosum". Chemical Research in Toxicology. 9 (2): 426–433. doi:10.1021/tx950091r. PMID 8839045. {{cite journal}}: |access-date= requires |url= (help)
  15. ^ a b c Nishie, K., et al. “Pharmacology and Toxicology of Chaconine and Tomatine.” Research Communications in Chemical Pathology and Pharmacology, vol. 12, no. 4, Dec. 1975, pp. 657–668.
  16. ^ Sever, John (December 1973). "Potatoes and Birth Defects: Summary". Teratology. 8 (3): 319–320. doi:10.1002/tera.1420080313. {{cite journal}}: |access-date= requires |url= (help)
  17. ^ Alexander, R. F.; Forbes, G. B.; Hawkins, E. S. (1948). "A Fatal Case of Solanine Poisoning". BMJ. 2 (4575): 518. doi:10.1136/bmj.2.4575.518. PMC 2091497. PMID 18881287.
  18. ^ MedlinePlus Encyclopedia: Potato plant poisoning - green tubers and sprouts
  19. ^ Friedman, Mendel (2006). "Potato Glycoalkaloids and Metabolites:  Roles in the Plant and in the Diet". J. Agric. Food Chem. 54 (23): 8655–8681. doi:10.1021/jf061471t. PMID 17090106.
  20. ^ "Review of Toxicological Literature prepared for Errol Zeiger, PhD, National Institute of Environmental Health Sciences, Submitted by Raymond Tice". Testing Status of Agents at NTP (National Toxicology Program). February 1998. Archived from the original on 18 January 2013. {{cite web}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  21. ^ Mccue, Kent F., et al. “Metabolic Compensation of Steroidal Glycoalkaloid Biosynthesis in Transgenic Potato Tubers: Using Reverse Genetics to Confirm the in Vivo Enzyme Function of a Steroidal Alkaloid Galactosyltransferase.” Plant Science, vol. 168, no. 1, 2005, pp. 267–273., doi:10.1016/j.plantsci.2004.08.006.
  22. ^ McGee, Harold (29 July 2009). "Accused, Yes, but Probably Not a Killer". The New York Times. Retrieved 23 May 2010.
  23. ^ Ohyama, K, et al. “Biosynthesis of Steroidal Alkaloids in Solanaceae Plants: Involvement of an Aldehyde Intermediate during C-26 Amination.” Phytochemistry., U.S. National Library of Medicine, May 2013, www.ncbi.nlm.nih.gov/pubmed/23473422.

External links edit

Category:Steroidal alkaloids Category:Alkaloid glycosides Category:Steroidal alkaloids found in Solanaceae Category:Nitrogen heterocycles Category:Saponins

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