Acute Toxicity of High Doses of the Glycoalkaloids, α-Solanine and α-Chaconine, in the Syrian Golden Hamster

Abstract

Sprouted, stressed, or spoiled potato tubers have reportedly led to human acute intoxication, coma, and death when consumed in high amounts. These effects have been attributed to glycoalkaloids (GAs), primarily alpha-solanine and alpha-chaconine, naturally present in all potatoes. The level of GAs in potato tubers has previously been shown to increase substantially as a result of improper handling and postharvest storage. A short-term study was performed to investigate the dose-response profile of alpha-solanine and alpha-chaconine alone or in combination, administered daily by oral gavage to Syrian Golden hamsters. Daily doses of 100 mg of alpha-solanine [kg body weight (BW)] (-1) induced death in two of four hamsters within 4 days, when administered by gavage to female Syrian hamsters. Doses of 100 mg of alpha-chaconine alone or alpha-solanine and alpha-chaconine combined in a ratio of 1:2.5, in doses of 75 or 100 mg (kg BW) (-1), induced death in one of four hamsters within the same period. Animals dosed with alpha-solanine alone or in combination with alpha-chaconine suffered from fluid-filled and dilated small intestines. The GA administration had no effect on acetyl cholinesterase (AChE) or butyryl cholinesterase (BuChE) activity in plasma or brain. Liquid chromatography-mass spectrometry-based metabolomics showed that there was a specific accumulation of alpha-chaconine in the liver tissues. In addition, metabolomics gave direct evidence of glycolytic metabolism of the GA with the beta 1, beta 2, and gamma-GAs detected in the urine and, to a lesser extent, the feces. Doses from 75 mg (kg BW) (-1) of alpha-chaconine, alpha-solanine, or the two compounds combined were potentially lethal within 4-5 days in the Syrian Golden hamster. However, the cause of death in these studies could not be established. No synergistic effects of alpha-solanine combined with alpha-chaconine were evident.

Compositional and toxicological analysis of a GM potato line with reduced α-solanine content – A 90-day feeding study in the Syrian Golden hamster

“…Previous studies have reported cell lysing properties of GAs, e.g. severe gastric and intestinal mucosal necrosis in hamsters receiving up to 33 mg alkaloid extracts/kg body weight/day (Baker et al, 1987), as well as distended, gas and fluid filled intestines and stomach (Langkilde et al, 2008(Langkilde et al, , 2009. However, in the present study no effects were observed on any organs in hamsters, either macroscopically or histologically, after feeding diets with either Desirée wild-type or GM SGT 9-2 FDPP.…”

“…In that study, the equivalent dose of total GA in the ratio 1:3.7 had no influence on the brain AChE activity. An acute study on the effects of GA (75 and 100 mg/kg body weight) in Syrian Golden hamsters did not exhibit any significant effects on AChE or BuChE (Langkilde et al, 2008). The intake of FDPP in the present study led to doses of total GA from 7-33 mg/kg body weight/day, based on a feed intake of 10 g/animal/day and an average body weight of 100 g.…”

“…Hamsters were randomly sorted into nine experimental groups, ten animals per group. Female hamsters were chosen as these have been used in previous studies investigating the toxicity of GA's (Langkilde et al, 2008(Langkilde et al, , 2009.…”

Therapeutic value of steroidal alkaloids in cancer: Current trends and future perspectives

“…spina bifida and other deformities) . According to Chaube et al ., 1976, Smith et al ., 1996, and Langkilde et al ., 2008, the inhibition of cholinesterase enzyme activity in the human central nervous system (CNS) and cell membrane disruption in the gastrointestinal tract (GIT) may be attributed to the toxic effects of α ‐chaconine and α ‐solanine . In hamsters, the teratogenic effects of solasodine may be attributed to the induction of spina bifida, exencephaly and cranial blebbing .…”

Solanaceae Juss.

“…Although atropine is apparently somewhat protective (Patil et al 1972), acetylcholinesterase inhibition, which may contribute to signs such as salivation, is not typically a major factor in toxicity (Bushway et al 1987). However, high, near lethal dosage of GAs did not affect plasma or brain acetylchoinesterase and butyryl cholinesterase in Syrian Golden hamsters (Langkilde et al 2008). However, high, near lethal dosage of GAs did not affect plasma or brain acetylchoinesterase and butyryl cholinesterase in Syrian Golden hamsters (Langkilde et al 2008).…”