Isolation and structure determination of terminalin A toxic condensed tannin from Terminalia oblongata

Terminalia oblongata (yellow wood) is a small deciduous tree growing over an area of central Queensland that supports a large proportion of this state's cattle population. Cattle and sheep that consume yellow wood leaves are poisoned and die. Severe losses of these animals can occur, and this problem is considered the main cause of economic loss to the cattle industry in the area apart from drought. A new toxic condensed tannin, terminalin was isolated from Terminalia oblongata. Its structure was deduced following NMR, IR, UV, MS analyses and in the knowledge that these data show good correlations to those obtained from the related punicalagin molecule which is present in the plant. Terminalin has a high toxicity (20 mg/kg) to white Quackenbush male mice and produces a vascular renal necrosis with slight liver necrosis, unlike punicalagin, which produces liver lesions but not kidney lesions. Similar results were obtained with sheep. A most interesting aspect is that there are two different specific toxins in the plant. © 1994 wiley‐Liss, Inc

Isolation and characterisation of urushiol components from the Australian native cashew (Semecarpus australiensis)

Native cashew (Semecarpus australiensis) is a well-known food source for aboriginal people of northeastern Queensland and the Northern Territory. It is also well known that contact with the seeds at a certain stage of growth can cause severe dermatitis in susceptible individuals. To prepare the fruits for eating, they are commonly treated by leaching for 2-7 days with water followed by heating in bark, and this treatment apparently produces an edible cashew nut. Recently, attempts have been made to use this valuable source of food by a commercial company. It was necessary to identify the active principle(s) in the seeds to determine the most effective way of rendering the seed suitable for human consumption without altering the flavour. By using solvent extraction and silica-gel chromatography, a fraction containing one major urushiol was obtained, its structure was confirmed by comparison of its NMR and mass spectral (MS) data with that previously reported. This compound, which is found in high yield, is also found in poison ivy (Toxiodendron radicans) and is responsible for dermatitis in susceptible individuals. A method of removing the active principle from the seed has been suggested

Isolation and identification of a compound from avocado (Persea americana) leaves which causes necrosis of the acinar epithelium of the lactating mammary gland and the myocardium

It is well known that when lactating livestock eat avocado (Persea americana) leaves they may develop non‐infectious mastitis and agalactia. This is associated with extensive coagulative necrosis of the secretory acinar epithelium and interstitial oedema, congestion, and haemorrhage. Similar lesions have been produced in mammary glands of lactating mice fed a diet containing a small percentage of freeze‐dried avocado leaf. Tests using these animals have been used to isolate the active principle, termed persin, from avocado leaves. The purified persin was examined using IR, NMR, and UV spectroscopy and mass spectrometry, and identified as (Z,Z)‐1‐(acetyloxy)‐2‐hydroxy‐12,15‐heneicosadien‐4‐one. Persin has previously been isolated from avocado leaves and shown to have antifungal properties and to be toxic to silkworms. Our tests have shown that persin at the dose rate of 60‐100 mg/kg has the same effect on mammary glands in lactating mice as leaves from avocado. Enantioselective syntheses of the R and the S isomers of persin and related derivatives were carried out. These compounds were tested for activity required to induce widespread lactating mammary gland necrosis in mice, and only the R isomer was found active. At doses of persin above 100 mg/kg necrosis of myocardial fibres may occur and hydrothorax may be present in severely affected animals. The mechanism of action of persin on both the mammary gland and the myocardium remain to be resolved. © 1995 Wiley‐Liss, inc

Experimental intoxication by the leaves of Melia azedarach (Meliaceae) in cattle Intoxicação experimental pelas folhas de Melia azedarach (Meliaceae) em bovinos

Green leaves of Melia azedarach were administered at single doses ranging from 5 to 30 g/kg bw to 11 calves. Clinical signs were depression, ruminal stasis, dry feces with blood, ataxia, muscle tremors, sternal recumbency, hypothermia and abdominal pain. Serum AST and CPK were increased. Signs appeared from 8 to 24 hours after dosing, and the clinical course lasted from 2 to 72 hours. Three calves dosed with 30g/kg bw died. The macroscopic findings included intestinal congestion, yellow discoloration of the liver, brain congestion and dry feces with blood in the rectum. The liver showed swollen and vacuolated hepatocytes. Necrotic hepatocytes were scattered throughout the parenchyma or concentrated in the periacinar zone. Degenerative and necrotic changes were observed in the epithelium of the forestomachs. There was also necrosis of the lymphoid tissue. Skeletal muscles showed hyaline degeneration and fiber necrosis. The necrotic fragments contained floccular or granular debris with infiltration by macrophages and satellite cells.<br>Folhas verdes de Melia azedarach foram administradas em dose única a 11 bovinos nas doses de 5 a 30g/kg de peso vivo. Os sinais clínicos caracterizaram-se por depressão, atonia ruminal, fezes duras com sangue, incoordenação, tremores musculares, decúbito esternal, hipotermia e dores abdominais. Os níveis séricos de AST e CPK estavam aumentados. O aparecimento dos sinais clínicos foi observado entre 8-24 horas após a ingestão das folhas e o curso clínico durou entre 2 e 72 horas. Três animais que receberam 30g/kg morreram. Os achados macroscópicos caracterizaram-se por congestão dos intestinos e do cérebro, fígado amarelado e presença de fezes duras com sangue no reto. Os hepatócitos estavam tumefeitos e com vacuolização citoplasmática. Observaram-se hepatócitos necróticos distribuídos no parênquima ou próximos à veia centrolobular. Lesões degenerativas e necróticas foram observadas no epitélio dos pré-estômagos. Havia também necrose do tecido linfóide. Nos músculos esqueléticos observaram-se degeneração hialina e necrose das fibras. Os fragmentos necróticos apresentavam necrose flocular ou granular com infiltração de macrófagos e células satélites