From Wikipedia, the free encyclopedia
Jump to: navigation, search
Not to be confused with Solanin.
Solanine 3d structure.png
IUPAC name
20562-02-1 N
ChemSpider 28033 N
ECHA InfoCard 100.039.875
Jmol 3D model Interactive image
PubChem 6537493
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 YesYN ?)
Infobox references

Solanine is a glycoalkaloid poison found in species of the nightshade family (Solanaceae), 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]

Solanine poisoning[edit]


Solanine poisoning is primarily displayed by gastrointestinal and neurological disorders. Symptoms include nausea, diarrhea, vomiting, stomach cramps, burning of the throat, cardiac dysrhythmia, nightmare, headache and dizziness. In more severe cases, hallucinations, loss of sensation, paralysis, fever, jaundice, dilated pupils, hypothermia, and death have been reported.[citation needed]

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.[2]

Symptoms usually occur 8 to 12 hours after ingestion, but may occur as rapidly as 30 minutes after eating high-solanine foods.

Mechanism of action[edit]

Solanum glycoalkaloids can inhibit cholinesterase, disrupt cell membranes, and cause birth defects.[3] 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.[4]

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 congenital spina bifida in humans.[citation needed] However, other studies have shown no correlation between potato consumption and the incidence of birth defects.[5]

In potatoes[edit]

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

Solanine occurs naturally in many species of the genus Solanum, including the potato (Solanum tuberosum), tomato (Solanum lycopersicum), eggplant (Solanum melongena), and bittersweet nightshade (Solanum dulcamara).

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.[6]

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.[6] Fatalities are also known from solanine poisoning from other plants in the nightshade family, such as the berries of Solanum dulcamara (woody nightshade).[7]

The United States National Institutes of Health's information on solanine strongly advises against eating potatoes that are green below the skin.[8]

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%.[9] Freeze-drying or dehydration has little effect.[10]

In tomatoes[edit]

Some, such as the California Poison Control System, have claimed that tomatoes and tomato leaves contain solanine.[citation needed] However, Mendel Friedman of the federal 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.[11]

See also[edit]


  1. ^ Desfosses, M. (1820): Extrait d'une lettre à M. Robiquet. In: J. de Pharmacie. Bd. 6, S. 374–376.
  2. ^ Executive Summary of Chaconine & Solanine Archived 15 August 2006 at the Wayback Machine.
  3. ^ Friedman, Mendel; McDonald, Gary M. (1999). "Postharvest Changes in Glycoalkaloid Content of Potatoes". In Jackson, Lauren S.; Knize, Mark G.; Morgan, Jeffrey N. Impact of Processing on Food Safety. Advances in Experimental Medicine and Biology. 459. pp. 121–43. doi:10.1007/978-1-4615-4853-9_9. ISBN 978-1-4615-4853-9. PMID 10335373. 
  4. ^ 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 (inactive August 17, 2015). PMC 4087866free to read. PMID 16733852. 
  5. ^ "Solanine and Chaconine". Retrieved 31 May 2009. 
  6. ^ a b "Solanine poisoning". BMJ. 2 (6203): 1458–9. 1979. doi:10.1136/bmj.2.6203.1458-a. PMC 1597169free to read. PMID 526812. 
  7. ^ 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 2091497free to read. PMID 18881287. 
  8. ^ MedlinePlus Encyclopedia Potato plant poisoning - green tubers and sprouts
  9. ^ 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. 
  10. ^ "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 2013-01-18. 
  11. ^ McGee, Harold (2009-07-29). "Accused, Yes, but Probably Not a Killer". The New York Times. Retrieved 2010-05-23. 

External links[edit]