Mammal poisoning

Atrophy of the thymus is a consistent finding in mammals poisoned by 2,3,7,8-TCDD, and suppression of thymus-dependent cellular immunity, particularly in young animals, may contribute to their death. Although the mechanisms of 2,3,7,8-TCDD toxicity are unclear, research areas include the role of thyroid hormones (Rozman et al. 1984) interference with plasma membrane functions (Matsumura 1983) alterations in ligand receptors (Vickers et al. 1985) the causes of hypophagia (reduced desire for food) and subsequent attempts to alter or reverse the pattern of weight loss (Courtney et al. 1978 Seefeld et al. 1984 Seefeld and Peterson 1984) and excretion kinetics of biotransformed metabolites (Koshakji et al. 1984). 

Organophosphate insecticides such as parathion may lead to a variety of symptoms in mammals poisoned by them. List five such symptoms and explain these in terms of the mechanism of action. 

The oxime HI-6 with atropine is reasonably effective against soman regardless of the choice of experimental animals while currently used oximes (pralidoxime and obidoxime) seem to be practically uneffective to protect mammals poisoned with supralethal dose of soman (Table 4). Presented data confirm that soman appears to be one of the most resistant nerve agent to the antidotal treatment because of the rapid aging of soman-phosphonylated AChE and the existence of a soman depot in the poisoned organisms (31, 54, 55). The soman-AChE complexes age very quickly and this fact prevents the oxime-induced reac-... 

One important group of insecticides, the avermectins, works differently by being agonists and not antagonists as the other, acting on the chloride channels. The avermectins are produced by Streptomyces avermitilies. The binding site is different, and cross-resistance to fipronil, the cyclodienes, and lindane does not seem to occur. The toxic symptoms in insects and mammals are different. Mammals poisoned with avermectins exhibit hyperexcitability, incoordination, and tremor followed by ataxia and paralysis. In insects and nematodes, the hyperexcitation phase is absent. Their symptoms are... 

Once the capacity of quantitative FD for alkali and alkaline earth cations was established the investigations were expanded to a wide variety of metals. One focal point in this analytical expansion of the method represents the toxic, heavy metal thallium. This metal exerts a pronounced toxic effect on mammals. Poisonings by thallium ions normally proceed very slowly they are accompanied by loss of hair, severe polyneuritic symptoms and tachycardia, and can culminate in paralysis of the central nervous system. Atomic absorption is a common spectroscopic method for the determination of thallium concentrations down to a few ppm . The direct determination of thallium from human urine reveals a limit of detection of approximately 30 ppb, whereas direct estimation from plasma and brain tissue is not successful without pretreatment. 

Atrophy of the thymus is a consistent finding in mammals poisoned by 2,3,7,8-TCDD,... 

Many other bisben2ylisoquinoliae alkaloids, such as tetrandriae (80), from Cjcleapeltata Hook., are also known. Compound (80), for example, although it causes hypotension and hepatotoxicity ia mammals, ia other tests, possessed enough anticancer activity to be considered for preclioical evaluation (55). The arrow poison tubocurare prepared from Chondrendendron spp. also contains the bisben2yhsoquiQoline alkaloid tubocurariae (9). 

Mode of Action. All of the insecticidal carbamates are cholinergic, and poisoned insects and mammals exhibit violent convulsions and other neuromuscular disturbances. The insecticides are strong carbamylating inhibitors of acetylcholinesterase and may also have a direct action on the acetylcholine receptors because of their pronounced stmctural resemblance to acetylcholine. The overall mechanism for carbamate interaction with acetylcholinesterase is analogous to the normal three-step hydrolysis of acetylcholine however, is much slower than with the acetylated enzyme. 

Tb allium, which does not occur naturaHy in normal tissue, is not essential to mammals but does accumulate in the human body. Levels as low as 0.5 mg/100 g of tissue suggest thallium intoxication. Based on industrial experience, 0.10 mg /m of thallium in air is considered safe for a 40-h work week (37). The lethal dose for humans is not definitely known, but 1 g of absorbed thallium is considered sufficient to kHl an adult and 10 mg/kg body weight has been fatal to children. In severe cases of poisoning, death does not occur earlier than 8—10 d but most frequently in 10—12 d. Tb allium excretion is slow and prolonged. For example, tb allium is present in the feces 35 d after exposure and persists in the urine for up to three months. 

In comparison to the situation in birds, there is far less evidence of dieldrin having had harmful effects in the field in mammals. It has been suggested that this is a reflection of the fact that mammals tend to be more reclusive and therefore more difficult to observe, catch, or count (Shore and Rattner 2001). That said, at the time when cyclodienes were widely used in Western Europe and North America, there were a fair number of reports of mammals being poisoned by them on agricultural land. Such animals included predators such as the fox (Vulpes vulpes) and badger (Meles meles), which had evidently acquired lethal doses from their prey. 

As discussed earlier, a problem with these field incidents is that the low levels of rodenticides found in many of the poisoned birds are of similar magnitude to those in birds surviving exposure. A low residue level may signify everything or nothing. Additional evidence is needed to establish that the concentrations of rodenticide present in the livers of birds or mammals found in the field are sufficient to have caused death, for example, the presence of hemorrhaging in the carcasses. 

When used to control rodents and predatory mammals in conserved areas, they have caused both primary and secondary poisoning of nontarget species, sometimes associated with population declines. 

DDT met all but one of Muller s ideal characteristics for an insecticide. It was a cheap, contact poison without objectionable odors. It was stable in air and light. Because it was so powerful, extremely small doses could be used. And finally, it dissolved so poorly in water that warm-blooded organisms absorbed only traces of it. The fact that DDT dissolves well in oils did not seem dangerous only later did scientists realize that, because DDT accumulates in animal fat and mammals milk, it becomes increasingly more concentrated in predator species as it moves up the food chain. DDT s only failing, as far as Muller s original conception was concerned, was that it did not kill immediately. 

Mammals may die from pesticide poisoning not immediately, but many months later, when they more actively use their fat deposits, for example, when waking up after hibernating they are then poisoned by deposits of toxic substances in their fat [3,6]. 

Just like mammals, birds have a delayed reaction to lipotropHc pesticides such as OCPs and their metabolites. These toxic substances dissolve and accumulate in the fatty tissues of well-fed birds, and are comparably harmless in this form. However, once the bird starts using the stored fat (at the end of a long flight or when laying eggs), the substances are carried through the bloodstream to the brain, liver, or yolk of the egg, and poison all the systems [1]. In particular, well-fed raptors have lower DDE concentrations in their liver (0.5 mg/kg) than less well-fed (3.5 mg/kg) and emaciated birds (7.3 mg/kg) [6]. 

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). 

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