Rodent individual

In the rat and other rodents, individual odors probably reflect genetic differences. Laboratory rats can distinguish individuals. They discriminate between two intact males, two castrated males, two estrous/proestrous females, two diestrous/metestrous females, or two ovariectomized females. Urine odors differ individually despite differences in the levels of gonadal hormones. Individual recognition may be independent of reproductive state or social status, even though hormone-influenced body odors may be used for individual recognition (Brown, 1988). 

Diseases from air- and blood-borne pathogens or feces are spread to humans most often during cleanup because of improper safety equipment. For exan le, hantavirus is transmitted by infected rodents. Individuals become infected with hantavirus by breathing aerosolized urine, droppings, saliva, or nesting materials. A specialized respiratory mask (one that filters viruses) should be used when cleaning suspected nesting areas and rodent feces. 

In risk characterization, step four, the human exposure situation is compared to the toxicity data from animal studies, and often a safety -margin approach is utilized. The safety margin is based on a knowledge of uncertainties and individual variation in sensitivity of animals and humans to the effects of chemical compounds. Usually one assumes that humans are more sensitive than experimental animals to the effects of chemicals. For this reason, a safety margin is often used. This margin contains two factors, differences in biotransformation within a species (human), usually 10, and differences in the sensitivity between species (e.g., rat vs. human), usually also 10. The safety factor which takes into consideration interindividual differences within the human population predominately indicates differences in biotransformation, but sensitivity to effects of chemicals is also taken into consideration (e.g., safety faaor of 4 for biotransformation and 2.5 for sensitivity 4 x 2.5 = 10). For example, if the lowest dose that does not cause any toxicity to rodents, rats, or mice, i.e., the no-ob-servable-adverse-effect level (NOAEL) is 100 mg/kg, this dose is divided by the safety factor of 100. The safe dose level for humans would be then 1 mg/kg. Occasionally, a NOAEL is not found, and one has to use the lowest-observable-adverse-effect level (LOAEL) in safety assessment. In this situation, often an additional un-... 

Coumarin/warfarin, given at a typical dosage of 4 to 5 mg/day, prevents the deleterious formation in the bloodstream of small blood clots and thus reduces the risk of heart attacks and strokes for individuals whose arteries contain sclerotic plaques. Taken in much larger doses, as for example in rodent poisons, Coumarin/warfarin can cause massive hemorrhages and death. 

Leptin has been shown to markedly reduce appetite and weight in the extremely rare individuals who lack leptin. In contrast, in the first clinical study of patients with polygenic obesity and elevated leptin levels, weight loss was variable and relatively small. This disappointing result may be explained by the leptin resistance consistently observed in obese humans and rodents. However, it cannot be excluded that a small... 

WHO (2004) concluded that The mono- and disubstituted compounds that may leach from PVC water pipes for a short time after installation are primarily immunotoxins although they appear to be of low general toxicity, some are developmental toxins in rodents. The data available are insufficient to permit the proposal of guideline values for individual dialkyltins or the mono derivatives, although the concentrations observed in drinking-water are several orders of magnitude lower than the doses reported to cause developmental effects in rats and mice. ... 

There is a shortage of appropriate texts on the ARs. Buckle and Smith (1994) and Mechin (1986) describe the use of ARs in rodent control. Thijssen (1995) gives a concise account of mode of action and resistance mechanisms. For effects on nontarget species, reference should be made to the individual citations given in the foregoing text. 

MiCHAELSEN s, OTTE J, SIMONSEN L-0 and SORENSEN H (1994) Absorption and degradation of individual intact glucosinolates in the digestive tract of rodents , Acta Agric. Scand. Sect. A. Animal Sci., 44 25-37. 

A second approach to the problem of toxic potency measurement has been to expose laboratory animals, usually rodents, to the smoke from the combustion of small samples of a burning material. Measurement of their response to the smoke leads to one of several biological endpoints, such as the LC50 (the concentration of smoke lethal to 50% of the test animals). In this approach, the animals respond to all the toxicants that are present in the smoke. It presumes that rodent mortality can be related to human mortality or, more simplistically, that the relative toxicity of the smokes will be similar in humans and rodents. However, since the relative contributions of the individual toxic chemicals in the smoke are not determined, a quantitative relationship between man and rodent is impossible using this approach. 

Although in most real multimaterial fires, exposure doses of CO produced normally far exceed those of other toxicants, significant combined effects have certainly been demonstrated with rodents in the laboratory. In addition to those described here with CO, HCN and HC1, such effects have also been reported due to C02 and to low oxygen when in combination with the narcotic toxicants (22,25). These all need to be studied further, preferably with nonhuman primates, in order to determine their impact on hazards to humans. Smoke atmospheres are likely to be much more hazardous than one would initially suspect from consideration of the concentrations of the individual toxicants taken separately. Perhaps, the major concern should not be so much the toxicity of HC1 or HCN, but rather, the toxicity of combinations of these gases with CO, C02 and low oxygen as may be present in smoke. 

PCB 156, a mixed inducer of microsomal enzymes, significantly increases the incidences of cleft palates by 2,3,7,8-TCDD in rodents (Bimbaum et al. 1985). Interactions among polychlorinated congeners may range from antagonism to additivity to synergism (Safe 1990), and the toxicity of individual PCBs can be raised by interaction with other PCBs (Table 24.5). 

Individuals of sensitive species died after receiving a single dose between 0.05 and 0.2 mg/kg BW, including species of livestock, marsupials, canids, felids, rodents, and foxes. 

Awareness of immunotoxicology was stimulated by a comprehensive review by Vos in 1977, in which he provided evidence that a broad spectrum of xenobiotics alter immune responses in laboratory animals and subsequently may affect the health of exposed individuals. Several additional reviews, as well as national and international scientific meetings, have reinforced these early observations. In several studies, alteration of immune function was accompanied by increased susceptibility to challenge with infectious agents or transplantable tumor cells, indicating the resulting immune dysfunction in altered host resistance. Clinical studies in humans exposed to xenobiotics have confirmed the parallelism with immune dysfunction observed in rodents. The latter sections in this volume describe studies with xenobiotics that resulted in immune modulation in rodents and man. 

Another problem encountered with rodents, primarily rats, is their susceptibility to respiratory diseases. Controlling temperature, humidity, and the day/night cycle are necessary to maintain the health of these animals. The answer to this problem Is to incorporate of individual controls in each rodent holding area. 

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