Boobialla (Myoporum tetrandrum)leaf contains from 0.25 to 0.5% wet weight of furanoid sesquiterpene essential oils of which the main component is dehydrongaione. The plant was toxic when dosed to calves at equivalent dose rates of oils of from 50 to 134 mg/kg, causing mainly extensive haemorrhagic centrillobular necrosis; and to sheep at equivalent dose rates of oil of from 55 to 66 mg/kg, causing either centrilobular or periportal liver lesions with or without acute pulmonary oedema. An essential oil mixture of similar composition derived from Myoporum deserti produced similar syndromes. In addition, treatment of calves with phenobarbitone or Melaleuca linariifolia essential oils prior to dosing with the Myoporum oils caused periportal hepatic necrosis rather than the centrilobular lesion which occurred usually in this species. The liver lesions found in the experimental calves and sheep respectively, were thus similar to those reported in suspected field cases of Boobialla poisoning in cattle and goats in Western Australia. The liver injury that may be expected in intoxication of livestock by myoporaceous plants containing this type of essential oils can thus be either periportal, midzonal or centrilobular necrosis, depending, probably, on the nutritional regime of the animal immediately prior to consumption of the toxic plant.

Toxic Lantana camara taxa growing in Queensland all contain the triterpene acids lantadene A, reduced lantadene A and lantadene B. These when dosed as pure compounds orally to sheep were similarly toxic at 65 to 75, 42 to 80 and 200 to 300 mg/kg body weight respectively, causing jaundice, photosensitisation, kidney and liver lesions typical of natural and experimental lantana poisoning. Because of its comparative toxicity and abundance lantadene A is the most significant toxic principle in the plant. Reduced lantadene A because of its low concentration in the leaves (5% of lantadene A) and lantadene B because of its significantly lower toxicity are thus unlikely to be of much importance in the poisoning of ruminants following consumption of the plant. In addition, the structural features of both lantadene A and B molecules given to sheep by the oral route do not conform to the chemical structures previously reported to be required for liver damaging action of the verbenaceous triterpenes administered to rabbits by the intraperitoneal route.

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Some of the more interesting and significant recent Australian studies of plant toxins are those dealing with furanosesquiterpenoid essential oils, irritant diterpene esters, thiaminase I, trihydroxyindolizidine, carboxyatractyloside and oxalates. Furanosesquiterpenes, found mainly in Myoporum spp., require activation by microsomal mixed-function oxygenases in order to produce injury in the tissues in which they accumulate. One such compound isolated from M. deserti, deisopropylngaione, causes necrotizing lesions in the liver, kidney and lung. The native pteridophyte Marsilea drummondii contains thiaminase I at such a high level of activity that it can cause clinical thiamine deficiency in adult sheep which graze it at times of the year when it is growing profusely. Potent diterpene esters (which have been found t o be potent cocarcinogens in mice) are to be found in thymelaeaceous plants such as Pimelea spp. One such compound, simplexin, also causes marked contraction of vascular smooth muscle, giving rise to the cardiopulmonary and hepatic circulatory disorder in cattle, known as St. George Disease. Carboxyatractyloside has recently been found to be the toxin in Xanthium spp. The compound is a hypoglycaemic agent, an inhibitor of mitochondria1 oxidative phosphorylation and causes acute liver necrosis. Swainsona spp. contain the a-mannosidase inhibitor trihydroxyindolizidine. Consumption of the plants by animals results in the typical lysosomal storage disease a-mannosidosis. Oxalate or acid oxalate ions in plants normally cause toxicity per se in grazing animals, but when present in low levels in various native and introduced grasses eaten by horses, they can produce negative calcium balance and secondary nutritional hyperparathyroidism within several months. 0 Heyden The constituents of Australian Pimelea simplex I. The isolation and structure of the toxin of Pimelea simplex and P. trichostochya Form B responsible for St. George Disease of cattle. Aust. J. Chem.,