Solanine
Solanine is a toxic glycoalkaloid known to accumulate under certain conditions in potato plant, sprouts and tuber in levels which, if ingested, may cause poisoning in humans and farm animals. However, ingested solanine is relatively less toxic than the parenterally administered compound, probably because of its poor absorption, rapid excretion and hydrolysis to less toxic solanine in stomach. Nevertheless, solanine poisoning may cause a gastrointestinal, nervous and exanthematous syndrome severe enough to be fatal.
Pharmacology of solanine - Fate and distribution studies using tritiated solanine in rats showed that the compound (1) is poorly absorbed from the gastrointestinal tract, (2) is rapidly eliminated in the urine and feces, and (3) reaches peak tissue concentrations in 12 hr. The descending order of tissue concentration in various organs was: spleen, kidney, liver, lung, fat, heart, brain, and blood. When administered ip, fecal and urinary excretion rates were comparable over a dose range of 5–15 mg/kg. However, at a dose of 25 mg/kg, there was an abrupt decrease in urinary and fecal excretion with a corresponding rise in concentration in liver, spleen, kidneys, and intestines. There was no proportionate increase in tissue concentration of solanine in lung, heart, blood, and brain over a dose range of 5–25 mg/kg. Solanine was very toxic to the chick embryo (yolk sac injection) and to mice, rats, and rabbits when administered parenterally.
Oral administration of the compound produced no toxic effects in mice at a dose of 1 g/kg. The aglycon solanidine was considerably less toxic than the glycoside. In unanesthetized rabbits, solanine produced tachycardia, tachypnea, and terminal bradypnea. There was an initial slight activation of the EEG followed by delta waves which were associated with bradypnea and cyanosis. Death resulting from solanine intoxication appeared to be caused by central nervous system depression because of the initial disappearance of EEG signals followed by cessation of respiration and terminal loss of ECG signals. Solanine and solanidine are very similar to cardiac glycosides with respect to effect on the heart. They produce positive inotropic action in the isolated frog ventricle. Toxic doses administered iv in rabbits produced ventricular extrasystoles and terminal ventricular fibrillation. Solanine had roughly the potency of the reference compound, K-strophanthoside, whereas solanidine was about one-fifth as active. Chromatographic evidence showed that there were at least 2 metabolites of solanine in addition to solanidine which possessed polarity intermediate to solanine and solanidine (aglycon).
An investigation of solanine poisoning
Induction of apoptosis in HepG2 cells by solanine and Bcl-2 protein
The protective and therapeutic effects of alpha-solanine on mice breast cancer
Interactive antifungal activity of the glycoalkaloids α-solanine and α-chaconine
Antitumor efficacy of α-solanine against pancreatic cancer in vitro and in vivo