Animal intoxications

What are the characteristic features of skeletal fluorosis in animals intoxicated by fluoride ... 

Fifty human intoxications from the literature, 13 from our database, and hundreds of animal intoxications were analyzed. The following OP-caused intoxications are mentioned ... 

In laboratory animals intoxicated over a long period with inorganic selenium, a wide distribution of Se in organs and tissues was found [71] with the highest concentrations in liver, kidney, spleen. 

Yoshizawa T (2003) Human and animal intoxication episodes caused by trichothecene mycotoxins. Mycotoxins 53 113... 

Poisonous plants and their seeds could be used to adulterate feedstuffs (Keremidis et al., 2013). Seeds of poisonous plants have been incorporated into animal rations and have resulted in animal intoxication (Burrows and Tyrl, 2001). For example, grain screenings that contain high levels of toxic plant seeds could be distributed as potential feed ingredients. Toxic seeds can be directly introduced into animal rations. 

Intoxication by aflatoxkis is referred to as aflatoxicosis. Edema and necrosis of hepatic and renal tissues seem characteristic of aflatoxicosis, and hemorrhagic enteritis accompanied by nervous symptoms often appear ki experimental animals. The mode of action of aflatoxkis kivolve an kiteraction with DNA and inhibition of the polymerases responsible for DNA and RNA synthesis (96). 

Lipopolysaccharide (LPS) endotoxins are characteristic Gram-negative outer-cell components which are produced by many cyanobacteria. Although LPS have been characterized and found to be toxic to laboratory animals after isolation from cyanobacteria, their toxicity to rodents is less potent than the endotoxins of enteric pathogens such as Salmonella Typical symptoms of animals suffering from LPS intoxication include vomiting, diarrhoea, weakness and death after hours rather than minutes. 

The ability to identify and quantify cyanobacterial toxins in animal and human clinical material following (suspected) intoxications or illnesses associated with contact with toxic cyanobacteria is an increasing requirement. The recoveries of anatoxin-a from animal stomach material and of microcystins from sheep rumen contents are relatively straightforward. However, the recovery of microcystin from liver and tissue samples cannot be expected to be complete without the application of proteolytic digestion and extraction procedures. This is likely because microcystins bind covalently to a cysteine residue in protein phosphatase. Unless an effective procedure is applied for the extraction of covalently bound microcystins (and nodiilarins), then a negative result in analysis cannot be taken to indicate the absence of toxins in clinical specimens. Furthermore, any positive result may be an underestimate of the true amount of microcystin in the material and would only represent free toxin, not bound to the protein phosphatases. Optimized procedures for the extraction of bound microcystins and nodiilarins from organ and tissue samples are needed. 

Among aminoacetylenes with different numbers of morpholinopropynyl groups, a substance has been found that displays antihypotoxic, thermoprotecting properties, increasing the stability of animals to intoxication by phosphor organic compounds and the salts of toxic metals. Because the efficiency of this substance exceeds that of azomopine 103 and it is nontoxic, it could be of interest to clinical medicine after additional studies. 

Developmental Effects. Adverse effects of methyl parathion on hirman fetal development have not been reported. Based on studies in animals, such effects appear to be possible if pregnant women were exposed during the first trimester to high concentrations of methyl parathion that resulted in significant depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less likely as a result of low-level exposure. 

No studies were located regarding gastrointestinal, hematological, musculoskeletal, or dermal effects in humans or animals after inhalation exposure to methyl parathion. Dean et al. (1984) reported that seven children exposed to methyl parathion by many routes exhibited pinpoint pupils, abdominal pain, and diarrhea. The respiratory, cardiovascular, hepatic, and renal effects reported by Fazekas (1971) that were found in humans acutely exposed to methyl parathion intoxication resulted from exposure by all three routes however, the results did not distinguish between the routes. 

Signs of acute endosulfan intoxication similar to those reported in humans have been observed in animals. Also, cerebral congestion and edema is often observed at necropsy in animals that die following acute ingestion of endosulfan (Boyd and Dobos 1969 Boyd et al. 1970 Terziev et al. 1974). The severe... 

Braun HE, Lobb BT. 1976. Residues in milk and organs in a dairy herd following acute endosulfan intoxication. Canadian Journal of Animal Science 56 373-376. 

Experimental animals exposed to sublethal doses of cyclodienes show a similar picture, with changes in EEG patterns, disorientation, loss of muscular coordination and vomiting, as well as convulsions, the latter becoming more severe with increasing doses (Hayes and Laws 1991). It is clear from these wide-ranging studies that a number of neurotoxic effects can be caused by cyclodienes at levels well below those that are lethal. In the human studies described here, subclinical symptoms were frequently reported when dieldrin blood levels were in the range 50-100 pg/L, an order of magnitude below those associated with lethal intoxication. 

Mouse Bioassay. The mouse is the traditional animal of choice for detecting biological activity due to STX and TTX. Mice receive an intraperitoneal injection of sample and are observed for symptoms of intoxication, i.e., dypsnea, convulsions, and death. This method is effective for detecting biological activity of STX and TTX in numerous samples. For the standard STX assay, one mouse unit is defined as that quantity of STX injected i.p. in 1 ml solution that will... 

There are only two animals that are used in the search for criteria rat (intoxication by inhalation, skin and orally) and rabbit (by skin). The only means of penetration that can be used are inhalation, skin and orally. When a substance is not subjected to regulations, the absence of one or several animal/means of penetration combinations prevents the proposal of any level of danger for the substance labelling and also any suitable prevention measures. 

Effects in Laboratory Animals. As highlighted in other chapters, the central toxicities during and after repeated stimulant bingeing may be related to neuronal or terminal destruction and/or depletion of neurotransmitter in the brain. In monkeys and cats, the report by Duarte-Escalante and Ellinwood (1970) of neuronal chromatolysis associated with decreased catecholamine histofluorescence following chronic METH intoxication has been followed by extensive neurochemical demonstrations of damage to the monoamine pathways by chronic stimulants (Seiden and Ricaurte 1987). 

Ellinwood, E.H., Jr., and Kilbey. M.M. Chronic stimulant intoxication models of psychosis. In Hanin, I., and Usdin, E., eds. Animal Models in Psychiatry and Neurology. New York Pergamon Press, 1977. pp. 61-74. 

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