Metabolism of Saponins From Narthecium Ossifragum - a Plant Implicated in the Aetiology of Alveld,a Hepatogenous Photosensitization of Sheep

One sheep was dosed over 4 consecutive days with 2.1 kg of leaves and flower stems of Narthecium ossifragum before it was killed. Sarsasapogenin and smilagenin glycosides, in the ratio 9:1, were the dominant saponins present in the dosed plant material. GC-MS analyses of the free and conjugated sapogenin content of samples recovered from the sheep identified three distinct regions of metabolic activity. In the first metabolic region, in the rumen and omasum, the ingested plant saponins were hydrolysed to the parent sapogenins, before being oxidized at C-3 and reduced to give the epi analogues of the ingested sapogenins. The second metabolic region consisted of the duodenum, jejunum, the liver and associated ducts. Sapogenins appear to be absorbed in the jejunum and may be transported via the portal vein to the liver, where 3-OH-5-H sapogenins (epismilagenin and episarsasapogenin), but not 3-OH-5-H sapogenins (smilagenin and sarsasapogenin), are conjugated and excreted into the bile as episarsasapogenin and epismilagenin conjugates in the ratio 4:1. In the third metabolic region, in the caecum and the colon, the epi-sapogenin conjugates were hydrolysed to free epi-sapogenins. The absence of free and/or conjugated sapogenins in urine, collected 24 h after dosing commenced, indicates that saponins and their metabolites are not likely to be implicated in the kidney disease occurring in ruminants ingesting N. ossifragum.     

Alveld-Producing Saponins: II. Toxicological Studies

The phototoxic lamb disease alveld, prevalent in South-Western Norway, is caused by ingestion of Narthecium ossifragum. Earlier studies have shown that peroral administration of large amounts of crude saponins from this plant elicits the disease. Such saponins have now been purified further by 2 different methods (A and B). Two A type preparations resulted in alveld when fed to 2 lambs. The most highly purified preparation (type B) did not cause alveld in the 2 lambs tested. Lambs vary, however, in their susceptibility to the disease. Both types of preparations led to increases in serum aspartate aminotransferase, bilirubin and 5′-nucleotidase in rats when injected intraperitoneally in amounts of 50 or 100 mg/kg body Weight. Cannulation of the bile duct showed that injected saponins reduced both the volume of bile and the amounts of bilirubin and bile acids excreted. Histological changes seen in the light microscope were, except for the most peripheral parts of the liver, hardly noticable. These observations support the view that saponins are the liver-toxic agents responsible for alveld. The possibility is discussed that the effect arises through a change in the lipid environment of carrier-mediated transport systems.