Rodents laboratory

Efficacy of 0.005% Bromethalin Against Warfin-Resistant Rodents Laboratory 3-Day Choice Test With Warfarin-Resistant Wild Norway Roats and House Mice... 

Many of the animal neurotoxicity studies are complicated by a lack of reported information on aluminum content in the base diet. This is an important issue because, as discussed in the introduction to Section 2.2.2, commercial rodent laboratory feed has a high aluminum content which can significantly contribute to total exposure. Dosages in studies with insufficient information on aluminum content in the base diet therefore must be assumed to underestimate the actual experimental dosages. The magnitude of the underestimate may be considerable, particularly for maternal dietary intake during lactation (an exposure period used in many neurobehavioral studies of aluminum in mice), which can be markedly... 

Mandavilli U, Schmidt J, Rattner DW et al. (1991) Continuous complete collection of uncontaminated urine from consdous rodents. Laboratory Animal Science 41 258-261 Mann WA, Landi MS, Homer E et al. (1987) A simple procedure for direct blood pressure measurements in conscious dogs. Lab Animal Sci 37(1) 105—108 Newman DJ, Price CP (1999) Renal function and nitrogen metabolites. In Burtis CA, Ashwood ER (eds) Tietz Textbook of Clinical Chemistry, 3rd edn. W.B. Saunders Company, Philadelphia, pp 1204-1270 Pitts RF (1968) Physiology of the Kidney and Body Fluids, 2nd edn. YearBook Medical Publishers Inc, Chicago Ragan HA, Weller RE (1999) Markers of renal function and injury. In Loeb WF, Quimby FW (eds) The Clinical Chemistry of Laboratory Animals, 2nd edn. Taylor and Francis, Philadelphia, pp 519-548... 

Purina Rodent Laboratory Chow After 8/79 Purina Certified Laboratory Chow... 

Most species possess only one type of I., but three rodents (laboratory rat, mouse, spiny mouse) and two fish (tuna, toadfish) have two distinct hormones. Accordingly, the rat possesses two I. genes, whereas only one is present in humans. Rat and human I. genes have been sequenced [G. I. Bell et al. Nature... 

Laboratory experiments using rodents, or the use of gas analysis, tend to be confused by the dominant variable of fuel—air ratio as well as important effects of burning configuration, heat input, equipment design, and toxicity criteria used, ie, death vs incapacitation, time to death, lethal concentration, etc (154,155). Some comparisons of polyurethane foam combustion toxicity with and without phosphoms flame retardants show no consistent positive or negative effect. Moreover, data from small-scale tests have doubtful relevance to real fine ha2ards. 

Based on tests with laboratory animals, aniline may cause cancer. The National Cancer Institute (NCI) and the Chemical Industry Institute of Toxicology (CUT) conducted lifetime rodent feeding studies, and both studies found tumors of the spleen at high dosage (100 —300 mg/kg pet day of aniline chloride). CUT found no tumors at the 10—30 mg/kg per day feeding rates. The latter value is equivalent to a human 8-h inhalation level of 17—50 ppm aniline vapor. In a short term (10-d) inhalation toxicity test by Du Pont, a no-effect level of 17 ppm aniline vapor was found for rats. At high levels (47—87 ppm), there were blood-related effects which were largely reversible within a 13-d recovery period (70). 

Cholinergic mechanisms have long been studied with respect to memory and learning. An interesting study demonstrated that the age-related decline in memory observed in laboratory rodents can be reversed by administration of choline [62-49-7] (13). 

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. 

Roberts DK, Silvey NJ, Bailey EM Jr. 1988. Brain acetylcholinesterase activity recovery following acute methyl parathion intoxication in two feral rodent species comparison to laboratory rodents. Bull Environ Contam Toxicol 41 26-35. 

The consistency of the effects noted above and in Chap. 5 which modulate reproduction and involve the operation of the AOS, are unlikely to be wholly artifacts of captivity. Nevertheless, it needs to be shown which of the influences on male and female fertility have relevance to natural populations (Fig. 7.12). As mentioned, very few experiments on free-living social mammals have been reported, since the logistical problems of stimulus manipulation and control are formidable. A semi-feral population is an acceptable substitute, and provides some means of testing assumptions on the relevance of findings on caged laboratory-bred rodents. 

In order to extrapolate laboratory animal results to humans, an interspecies dose conversion must be performed. Animals such as rodents have different physical dimensions, rates of intake (ingestion or inhalation), and lifespans from humans, and therefore are expected to respond differently to a specified dose level of any chemical. Estimation of equivalent human doses is usually performed by scaling laboratory doses according to observable species differences. Unfortunately, detailed quantitative data on the comparative pharmacokinetics of animals and humans are nonexistent, so that scaling methods remain approximate. In carcinogenic risk extrapolation, it is commonly assumed that the rate of response for mammals is proportional to internal surface area... 

Armstrong, D.W., Gasper, M.P., Lee, S.H., Ercal, N., Zukowski, J. (1993c). Factors controlling the level and determination of D-amino acids in the urine and plasma of laboratory rodents. Amino Acids 5, 299-315. 

The first two antidepressants, iproniazid and imipramine, were developed in the same decade. They were shown to reverse the behavioural and neurochemical effects of reserpine in laboratory rodents, by inhibiting the inactivation of these monoamine transmitters (Leonard, 1985). Iproniazid inhibits MAO (monoamine oxidase), an enzyme located in the presynaptic neuronal terminal which breaks down NA, 5-HT and dopamine into physiologically inactive metabolites. Imipramine inhibits the reuptake of NA and 5-HT from the synaptic cleft by their transporters. Therefore, both of these drugs increase the availability of NA and 5-HT for binding to postsynaptic receptors and, therefore, result in enhanced synaptic transmission. Conversely, lithium, the oldest but still most frequently used mood stabiliser (see below), decreases synaptic NA (and possibly 5-HT) activity, by stimulating their reuptake and reducing the availability of precursor chemicals required in the biosynthesis of second messengers. 

Figure 2.3 Researchers are currently studying laboratory rodents, like the mice in the upper photograph, to try to identify specific genes that may lead to obesity. The two mice shown are the same, except that the mouse on the left has had one gene removed. As you can see, the mouse on the left is thin, while the mouse on the right is obese. This leads researchers to believe that the gene removed may help cause obesity. By better understanding the causes of obesity, researchers will be better able to develop treatments for this condition in humans.

Toxicity and exposure studies indicate PFOA is immunosuppressive and can cause developmental problems and other adverse effects in laboratory animals, such as rodents [Lau et al (2004), Lau et al (2006)]. In 2005 the US Environmental Protection Agency (EPA) released a draft risk assessment of its potential human health effects [U S. EPA (2005)]. A subsequent review by the EPA science advisory board concluded that there is sufficient evidence to classify PFOA as likely human carcinogenic. 

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. 

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