Source: Landcare Research (1964). Control of poisons. Royal ...

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1080 Reassessment Application October 2006 Appendix C tatredecyglycidic acod (10 -4 mM) in the absence of exogenous substrates consistently reduced hypoxic cell injury to mTAL. Similarly the direct inhibition of substrate oxidation by the citric acid cycle with monofluoroacetate (5 mM) also reduced the extent of damage to this nephron segment. Bringmann, G. and Kuhn, R. (1976). Vergleichende Befunde der Schadwirkung wassergefahrender Stoffe gegen Backterien (Psuedomonas putida) und Blaualgen (Microcystis aeruginosa). GWF-wasser/abwasser 117, 410-413. Keywords: bacteria/algae/toxicity/sodium fluoroacetate Brock, E. M. (1965). Toxicological feeding trials to evaluate the hazard of secondary poisoning to gopher snakes, Pituophis catenifer. Copeia 2, 244-245. Keywords: poisoning/reptiles/secondary poisoning/non-target species Abstract: No observable reaction was shown by snakes which accpeted mice that had consumed lethal quantities of either thallium sulphate or of warfarin, diphacin, or prolin. Snakes fed rodents poisoned with sodium fluoroacetate, endrin, arsenic trioxide or zinc phosphide baits often regurgitated the mice but exhibited no other response. In fourteen snake feeding trials, the Microtus used had accepted baits soaked in a high concentration of sodium fluoroacetate. Twelve of these mice were regurgitated. Snakes fed mice which had eaten baits treated with strychine alkaloid became irritable and reacted with tremors. Five of these snakes died of secondary poisoning. Brockmann, J. L., McDowell, A. V., and Leeds, W. G. (1955). Fatal poisoning with sodium fluoroacetate : report of a case. Journal of the American Medical Association 159, 1529-1532. Keywords: diagnosis/treatment/pathology/sodium fluoroacetate/humans Abstract: Certain drugs can be used with benefit in a case of sodium fluoroacetate poisoning. These are (1) procainamide (Pronestyl) hydrochloride for cardiac arrythmias, (2) intravenously used alcohol for central nervous system irritability, and (3) vasodepressor drugs such as mephentermine (Wyamine) sulfate to maintain blood pressure. In the future these drugs, which we feel prolonged the life of our patient, should be tried in cases of sodium fluoroacetate poisoning, as they may save the lives of patients who have ingested smaller amounts of the poison. Brothers, N. P. (1982). Feral cat control on Tasman Island. Australian Ranger Bulletin 2, 9. Brown, C. J. (1993). Test of compound 1080 from a poison collar on a captive vulture. Vulture News 29, 19-26. Keywords: 1080/poison/birds/toxicity/USA/predators/lethal dose/poisons Abstract: The poison collar was developed in the USA in the late 1970s. It was designed to be an effective and highly selective means of killing Coyotes Canis latrans that preyed on domestic stock, without harming non-target individuals and species (Connolly et al. 1978; Saverie & Sterner 1979). The collar has been exported to other parts of the world, where it is used against mainly medium-sized mammalian predators. The poison collar consists of two rubber pouches containing poison under low pressure, and two straps with velco attachments. The collar is fitted around the neck of a sheep or goat and the pouches are positioned around the throat, which is the site of attack by most mammalian predators. The exact position of the pouches depends on the expected predator. A number of young domestic animals (usually at least 20) are fitted with collars and released with a larger flock of adult animals into the camp where losses are being experienced. The predator usually atacks one of the smaller animals. On biting into one of the poison pouches, a lethal dose of poison squirts into the predator's mouth and is ingested. In the USA a wide spectrum of poisons were tested for use in the collar (e.g. Connelly et al. 1978); Saverie & Sterner 1979; Sterner 1979). Compound 1080 (sodium monofluoroacete) was found to be the most suitable toxin and was registered for this purpose (Scrivner 1983; Howard & Schmidt 1984). The use of the poison collar and compound 1080 were vigorously opposed and intensively monitored by a number of environmental pressure groups in the USA (e.g. Anon. 1982; Doherty 1982; Sibbison 1984). The issue was eventually settled in court. The verdict was in favour of the use of the collar and compound 1080 because, after extensive testing by impartial organisations, no secondary poisoning was found and no nontarget animals were killed (Connolly 1983; Eastland & Beasom 1986). Recent investigations of secondary poisoning concluded that consuming carcasses of Coyotes killed by 1080 poison from a collar poses little, 22
1080 Reassessment Application October 2006 Appendix C if any, hazard to Striped Skunks Mephitis mephitis and Golden Eagles Aquila chrysaetos (Burns et al. 1991). Results: The vulture's first meal was at about 18h00 on day one. About 0.5 kg of food was taken. Within 30 min the bird regurgitated its entire crop contents. The bird fed again at midday on day two, taking about 0.3 kg, which it kept down. It fed again at about 17h00 on day two, from the carcass (about 0.5 kg) and from the meat ergurgitated on day one (about 0.2 kg). Within about 20 min it regurgitated about 0.3 kg but kept the remainder down until nightfall. On arrival at the cage at 07h30 on day three it was apparent that the vulture had regurgitated about 0.2 kg of food during the night, and that it had been pulling at the carcass, but not feeding much, as its crop was empty. In addition to feeding from the incisions, and gaining access through them to meat between the skin and skeleton, the bird had tugged and torn the contaminated skin. At no stage did the vulture show any symptoms of 1080 poisoning other than regurgitation. Common symptoms are depression, unsteady gait and loss of balance, closed eyes, hunched posture and raised or fluffed feathers (McIlroy 1984). After returning the bird to the large aviary, it fed on clean meat on the afternoon of day three and showed no signs of having been poisoned. Brown, F. G. (1972). Heart-leaf, poisonous to livestock. Unknown. Abstract: The distribution in Queensland, clinical symptoms and control of heart-leaf poison bush (Gastrolobium grandiflorum), which is toxic to livestock at all stages of growth, are described. The toxin is a fluoroacetate. 2,4,5-T diluted with dieselene and applied to the main stem at ground level gave effective control Brown, T. D., Jones-Mortimer, M. C., and Kornberg, H. L. (1977). The enzymic interconversion of acetate and acetyl coenzyme A in Escherichia-coli. J Gen Microbiol 102, 327-336. Abstract: Mutants of Escherichia coli K12 have been isolated that grow on media containing pyruvate or proline as sole carbon sources despite the presence of 10 or 50 µm-sodium fluoroaetate. Such mutants lack either acetate kinase [ATP: acetate phosphotransferase; EC2.7.2.I] or phosphotransacetylase [acetyl- CoA:orthophosphate acetyltransferase; EC2.3.I.8] activity. Unlike wild-type E coli, phosphotransacetylase mutants do not excrete acetate when growing aerobically or anearobically on glucose; their anaerobic growth on this sugar is slow. The genes that specify acetate kinase (ack) and phosphotransacetylase (pta) activities are cotransducible with each other and with purF and are thus located at about min 50 on the E coli linkage map. Although Pta- and Ack- mutants are greatly impared in their growth on acetate, they incorporate [2- 14 C]acetate added to cultures growing on glycerol, but not on glucose. An inducible acetyl- CoA synthetase [acetate: CoA ligase (AMP-forming); EC6.2.I.I] effects this uptake. Browne, J. L., Sanford, P. A., and Smyth, D. H. (1977). Transport and metabolic processes in the small intestine. Proceedings of the Royal Society of London, B 195, 307-321. Keywords: citrate/fluoride/fluoroacetate/citric acid/inhibition/gut Abstract: The transfer of alpha -methylglucoside and citrate was studied in experiments with everted sacs of rat and hamster small intestine. The transfer of alpha -methylglucoside was stimulated in the hamster tissue by metabolizable hexoses and by citrate, succinate and pyruvate. In the rat jejunum metabolizable hexoses only were effective. Fluoride (10 mmol/litre) inhibited endogenous transfer in the hamster and glucose-dependent transfer in both rat and hamster. Fluoroacetate (10 mmol/litre) inhibited endogenous transfer in tissue of both animals, but inhibited glucose-dependent transfer only in the hamster. This indicated that in the hamster the citric acid cycle is the major source of energy both for endogenous substrate and for added glucose. In the rat, added glucose supplies energy mainly through the glycolytic pathway, although endogenous energy is derived from the citric acid cycle. In the rat, glucose abolished completely the inhibition of alpha -methylglucoside transfer produced by L-proline, although the inhibitory effects of galactose could be only partially overcome. In the hamster, L-proline caused an inhibition which was not completely abolished by the additional energy. The results indicate that in the rat sugars and amino acids compete for energy rather than interact at the carrier level. In the hamster it is possible that sugars and amino acids interact at carrier level in addition to competing for energy. Citrate is more rapidly transferred and metabolized by hamster than by rat intestine. Citrate and unidentified radioactive metabolites accumulated in the serosal fluid, thus establishing the existence of a specific mechanism for citrate transfer 23
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Source: Landcare Research (1964). Control of poisons. Royal ...

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