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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. It belongs to the chemical family of saponins.

Symptoms
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. Gaffield and Keeler (1996) reported the instance of craniofacial birth defects when ingested by pregnant Syrian hamsters. In addition, Renwick et al. (1984) found similar malformations in Syrian hamsters.

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.

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. The California Poison Control System generally recommends oral administration of activated charcoal and gastric lavage, if necessary.

Mechanism of action
Solanum glycoalkaloids can inhibit cholinesterase, disrupt cell membranes, and cause birth defects. The anticholinergic activity of solanine causes the gastrointestinal side effects of nausea, vomiting, diarrhea and abdominal pain along with the cardiovascular impacts. 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.

Correlation with birth defects
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. 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. 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. Meanwhile Renwick et al. (1984) found the same side effects in just 0.2 g/kg. 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. 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. There is still debate on the impact of solanine on birth defects.

Presence in Nature
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


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.

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

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

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 does not result in any measurable change; significant degradation starts at ∼170 C, and deep-frying at 210 C for 10 min causes a loss of ∼40%. Freeze-drying or dehydration has little effect.

Biosynthesis
SGT1 has been found to have both glucosyltransferase and galactosyltransferase activity. 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
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. 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.

In its biosynthesis, tomatine remains similar to solanine, differing in its pentane cyclization step. According to Nishie (1975) in mice, the glycoalkaloid shares a relatively similar LD50 with solanine at 32.4 uM/kg. 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.