Glycoalkaloids occur in solanaceous plants such as potatoes, tomatoes, or melanzani, although no data are available on the occurrence of tomato and melanzani glycoalkaloids.
The major glycoalkaloids in potatoes are α-solanine and α-chaconine, with 100 g of potatoes containing an average of 1-15 mg of glycoalkaloids, much of which is found in the skin of potato tubers. High concentrations are also found in the shoots and shoot buds ("eyes"), as well as in greenish colored areas.
The lowest dose with observed adverse effect is 1 mg of potato glycoalkaloids (potato TGA) per kg of body weight. After ingestion of this dose, gastrointestinal symptoms of varying severity such as vomiting, diarrhea and abdominal pain may occur. Other poisoning symptoms such as drowsiness, apathy, confusion, weakness, visual disturbances, rapid and weak pulse and low blood pressure may appear as a result of dehydration after vomiting and diarrhea. In severe cases, glycoalkaloids can cause paralysis, respiratory failure, heart failure and coma. For humans, doses in the range of 3-6 mg of potato glycoalkaloids per kg body weight are considered potentially lethal.
Situation in Austria
In Austria, no maximum content has been set, but there are minimum requirements for the marketing of table potatoes in the Table Potato Marketing Ordinance to avoid a high glycoalkaloids content. For example, potatoes must be free of conspicuous green tubers. For Class I potatoes, a slight green coloration of no more than 1/8 of the surface is allowed. For Class II potatoes, a slight green coloration that can be removed by normal peeling is allowed.
- Store potato in a cool, dark and dry place
- Do not eat old, dried, green or sprouting potatoes
- Generously remove green spots and eyes (sprout buds)
- Peel the potato before eating
- If eating the potato skin is desired, use only fresh uninjured tubers
- Do not consume snacks made from potato peelings
- Young children should eat only peeled potatoes
- Do not eat potatoes and potato dishes with a bitter taste, as this is an indication of a high glycoalkaloids content
- Do not reuse potato cooking water, as some of the glycoalkaloids are transferred to the cooking water.
- Change frying fat for potatoes and potato products regularly
- Reduction of glycoalkaloids content by processing and preparation:
- By peeling by 25% to 75%By boiling or blanching peeled potatoes by 5% to 65%.
- By frying peeled potatoes in oil by 20% to 90%.
- By baking unpeeled potatoes in the microwave or in the oven by 3 % to 45 % and by 20 to 50 %, respectively
Uptake, distribution, degradation, and excretion.
The potato glycoalkaloids α-solanine and α-chaconine show relatively low oral bioavailability with differences between species. Hamsters show higher absorption and slower excretion rates for both compounds compared to rats. Limited information is available on the absorption, distribution, degradation, and excretion of potato glycoalkaloids in experimental animals. In humans, α-solanine and α-chaconine are absorbed systemically after ingestion. Relatively long serum half-lives have been reported for both substances, suggesting possible accumulation. No further information is available on the degradation and excretion of glycoalkaloids in humans.
Data on the uptake, distribution, degradation, and excretion of glycoalkaloids from tomatoes and melanzani in experimental animals and in humans are still lacking.
Mode of action of glycoalkaloids
Glycoalkaloids can form complexes with 3b-hydroxysterols in the cell membrane. This complex formation results in membrane disruption and loss of membrane integrity. After oral ingestion of glycoalkaloids, these effects affect the mucosa of the gastrointestinal tract, causing nausea, vomiting, and diarrhea. Glycoalkaloids also reversibly and competitively inhibit acetylcholinesterase (AChE) and serum butrylylcholinesterase (BuChE), two enzymes involved in the breakdown of the neurotransmitter acetylcholine. Inhibition of these two enzymes results in an excess of acetylcholine, which can contribute to the symptoms of glycoalkaloid poisoning. At high doses, α-tomatin can form a nonabsorbable complex with cholesterol and other sterols in the intestinal lumen, which can impair the absorption of cholesterol. As a result, blood cholesterol levels were lowered in rodents.
In acute oral toxicity studies in experimental animals, no adverse effects of α-solanine were observed at doses of 250 mg/kg body weight (bw) per day in rats and 1000 mg/kg bw per day in mice. Data on other glycoalkaloids from potato, tomato, and melanzani are lacking. In studies with repeated oral administration of potato glycoalkaloids, rodents showed nonspecific effects, such as reduced body weight and relative liver weight, with evidence of similar potency of α-solanine and α-chaconine. In contrast, the aglycone solanidine increased absolute and relative liver weight in mice, indicating a different effect of the aglycone compared with the glycoalkaloids.
α-Tomatine and its aglycone tomatidine showed no effect in rats when applied at 20 mg/kg bw per day for a period of 200 days. In mice, one to two weeks of treatment with α-solasonin resulted in body weight gain, while its aglycone solasodine decreased body weight gain and caused gastric gland degeneration and liver toxicity.
Developmental studies in hamsters showed that administration of potato glycoalkaloids and their aglycones during pregnancy can lead to effects on the central nervous system of embryos in the form of malformations of the brain (exencephaly, encephalocele, and anophthalmia). In rats, decreased postnatal survival of pups due to inadequate milk production has been reported after treatment with α-solanine. Male fertility in dogs and rhesus monkeys was reduced by administration of the aglycone solasodine from melanzani, and decreased epididymal weight and sperm-depleted epididymal lumen were observed.
There is no evidence of genotoxicity of the glycoalkaloids α-solanine and α-chaconine and the aglycone solanidine and the Melanzani glycoalkaloid α-solamargine, but insufficient information is available for a conclusive evaluation. No long-term chronic toxicity and carcinogenicity study could be identified for glycoalkaloids or for the respective aglycones.
Effects in humans
In humans, acute toxic effects following ingestion of potato glycoalkaloids include gastrointestinal symptoms of varying severity, such as vomiting, diarrhea, and abdominal pain, which may occur at an intake of the sum of potato glycoalkaloids (potato TGA) of 1 mg/kg bw or more. Other symptoms such as drowsiness, apathy, confusion, weakness, visual disturbances, rapid and weak pulse, and low blood pressure may result from dehydration following vomiting and diarrhea.
In severe cases, paralysis, respiratory failure, cardiac failure, coma, and death have been reported. Doses in the range of 3-6 mg potato TGAs per kg body weight are considered potentially lethal to humans. Results of studies in volunteers suggest possible differences in the human population with respect to individual susceptibility to glycoalkaloids.
Rodent acute toxicity data were not adequate to establish a reference point for evaluating acute exposure to potato glycoalkaloids in humans. Based on human data from case reports, outbreaks, and studies in volunteers, a LOAEL (Lowest Observed Adverse Effect Level - lowest dose at which adverse health effects are already observed) of 1 mg potato TGA per kg bw per day was chosen as the reference point for acute risk assessment. Available data were insufficient to derive a health-based guideline value. Instead, the margin of exposure (MOE) approach was used to assess potential health risks due to acute exposure to potato TGAs via food.
It was assumed that symptoms were mainly due to local irritation of the gastrointestinal mucosa rather than inhibition of AChE activity. To assess risk, an MOE of 10 is considered sufficient considering extrapolation from a LOAEL to a NOAEL by a factor of 3 and interindividual variability in sensitivities by a factor of 3.2. Accordingly, an MOE greater than 10 indicates that there is no health concern.
The experimental data available for repeated-dose toxicity are insufficient to identify a reference point for chronic exposure to potato glycoalkaloids. No evidence of health problems associated with repeated or long-term ingestion of glycoalkaloids via potatoes has been found in humans.
With respect to glycoalkaloids or aglycones occurring in edible parts of food crops other than S. tuberosum, no appropriate study has been identified to determine a reference point for glycoalkaloids or aglycones from tomato or melanzani.
Data on the occurrence of glycoalkaloids were available only for α-solanine and α-chaconine and mainly in the categories of "main potatoes" (conventional potato varieties) and "new potatoes" (new potato varieties that have lower glycoalkaloid content). Few data were available for processed foods. No data were available on the occurrence of tomato and melanzani glycoalkaloids and their aglycones.
Because data on the occurrence of potato glycoalkaloids do not cover all potato-containing food categories in the Comprehensive Food Consumption Database, it was decided to use raw primary commodities (RPC) data from the main potato and new potato categories and the RPC consumer database for the exposure assessment. The data from the new potato category were combined with those from the main potato category, and the average concentration in the Upperbound (UB: all values below the detection and quantification limits were set equal to the respective limit) for the sum of α-solanine and α-chaconine was 51.2 mg/kg, and the 95th percentile (P95) was 116.8 mg/kg. The minimum and maximum concentrations were 1.1 and 276.6 mg/kg, respectively.
Acute dietary exposure to potato TGAs was estimated using a probabilistic approach that included only days on which potatoes were consumed. Because no data were available on the occurrence of glycoalkaloids in tomatoes and melanzani, these foods were not included in the exposure estimate.
Processing of potatoes reduces the glycoalkaloids content in the final processed product. In general, and according to the literature, peeling potatoes reduces glycoalkaloids content by 25-75%, boiling in water and blanching peeled potatoes reduces glycoalkaloids content by 5-65%, and frying peeled potatoes in oil reduces glycoalkaloids content by 20-90%. Microwave and oven baking of unpeeled potatoes may result in a 3-45% and 20-50% reduction in glycoalkaloid content, respectively. No information is available on the chemical nature of glycoalkaloid degradation products. For exposure estimation, processing factors for the major food processing steps, including peeling and heat processing (boiling, frying, baking), were applied to the occurrence data as follows: Processing factors between 0.25 and 0.75 were assigned to peeling potatoes; between 0.1 and 0.8 to frying and deep-frying; and between 0.35 and 0.95 for all other cooking methods.
Information on peeling of potatoes was not available in the consumer database, but it was assumed that 90% of potatoes are consumed peeled. When cooking method information was not available, a cooking method was randomly assigned to the eating event based on the relative frequency of cooking methods reported.
The average UB exposure to potato TGAs in all surveys ranged from 23.3 µg/kg bw per day in adults to 174.0 µg/kg bw per day in young children. Exposure at the 95th percentile ranged from 78.3 µg/kg bw per day in adults to 535.1 µg/kg bw per day in young children (up to 822.9 µg/kg bw per day at the upper limit of the 95% confidence interval).
Comparing the LOAEL for potato TGAs of 1 mg/kg bw per day with the acute exposure estimates, the MOEs indicate health concerns for the younger age groups, on the one hand for the consumption surveys with the highest average consumption, and on the other hand for the high intake in the 95th percentile in all surveys. For adults, MOEs indicate health concerns only for those consumption surveys with the highest intake in the 95th percentile. The average percentage of days with potato consumption across all surveys per age group where potato TGA intake is below the MOE of 10 was calculated. The highest number of days with potato consumption below an MOE of 10 was estimated for infants at 56% followed by children at 50%. For the other age groups, estimated TGA intake was below the MOE of 10 in up to 22-40% of survey days.
For tomato and melanzani glycoalkaloids, the risk to human health could not be characterized because of the lack of data on occurrence in food and limited information on adverse effects in experimental animals and humans. The impact of the uncertainties on the risk assessment of acute exposure to potato glycoalkaloids in food was rated as moderate by EFSA. Overall, the identified uncertainties may lead to either an overestimation or an underestimation of risk.
EFSA Journal 2020;18(8):6222 Risk assessment of glycoalkaloids in feed and food, in particular in potatoes and potato-derived products.
Last updated: 29.09.2022