Rodent urinary

Bocskei Z., Groom C., Flower D. Wright C.E., et al. (1992). Pheromone binding to two rodent urinary proteins revealed by X-ray crystallography. Nature 360, 186-188. 

Behavioral aspects of rodent urinary chemosignals. American Zoologist 16,118A. 

Drickamer LC (2001a) Intrauterine position effects on rodent urinary chemosignals. In Marchlewska-Koj A, Lepri JJ, Miiller-Schwarze D (eds) Chemical signals in vertebrates, vol 9. Kluwer, New York, NY, pp 211-216... 

Cohen, S. M., Ohnishi, T., Qark, N. M., He, J., and Arnold, I.. L. (2007). Investigations of rodent urinary bladder carcinogens Collection, processing, and evaluation of urine and bladders. Toxicol Pathol 35,... 

Adams, R, and L. Sawyer. 1990. Structure of rodent urinary proteins. Biochemical Society Transactions 18 936-937. 

Jemiolo B., Gubemick D.J., Yoder M.C. and Novotny M. (1994). Chemical characterization of urinary volatile compounds of Peromyscus califomicus, a monogamous biparental rodent. J Chem Ecol 20, 2489-2500. 

One explanation for the adverse effects of excessive phosphorus intakes on bone health of rodents is that of secondary hyperthyroidism (4,j>,6). Under these circumstances, PTH activities and cAMP urinary excretions would be expected to increase and blood serum phosphorus would be expected to increase. This in turn would be expected to result in formation of calcium-phosphorus complexes, decrease in serum ionized calcium, parathyroid stimulation and bone resorption. 

At the endocrinological level, the VNO mediates the surge of luteinizing hormone and testosterone in males after exposure to females. This surge does not occur if a male with deafiferentiated VNO is exposed to an anesthetized female or her urine (Wysocki etal., 1983). But VNO-deafferentiated males will show a surge in luteinizing hormone in response to awake females (Coquelin etal., 1984). In female mice, stimulation of the VNO by male urinary cues activates the limbic system (discussed in Ch. 8). The roles of the VNO in the behavior of some rodents are listed in Table 5.3. 

Although demethylation, which occurs in the liver, is normally considered to be a catabolic process, it may result in conversion of an inactive form of a drug to the active form. Thus 6-(methylthio)purine (XXXIX) is demethylated by the rat to 6-mercaptopurine [205]. This demethylation occurs in the liver micro-somes and is an oxidative process which converts the methyl group to formaldehyde [204, 207]. The 1-methyl derivative of 4-aminopyrazolo[3,4-d] pyrimidine (XLI) is demethylated slowly, but 6-mercapto-9-methylpurine (XLII) not at all [208]. The A -demethylation of puromycin (XLlIl) [209, 210], its aminonucleoside (XLIV) [211], and a number of related compounds, including V-methyladenine and V,V-dimethyladenine, occurs in the liver microsomes of rodents [212]. In the guinea-pig the rate-limiting step in the metabolism of the aminonucleoside appears to be the demethylation of the monomethyl compound, which is the major urinary metabolite [213]. The relationship of lipid solubility to microsomal metabolism [214], and the induction of these demethylases in rats by pre-treatment with various drugs have been studied [215]. 

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