Neonatal animals excretion

Absorption extent from the gastrointestinal tract (GIT) is very low (of the order of <1-2% of administered dose), although higher bioavailability may be achieved in neonatal animals and where there is dismption of the intestinal mucosa, caused by, for example, parvovirus infection. Within the GIT, aminoglycosides are stable and excreted unchanged in feces. 

The main rout of excretion of the drug and its metabolites is the kidney with a half-life of 9-18 h in human. In contrast to human, animal models have a lower elimination half-life ranging from 0.6-9 h [78]. The elimination half-life of valproic acid and some metabolites was found to be much longer in the neonates (40-50 h) than adult subjects (9-18 h) [78,81]. One study reported no difference between the elimination half-life between elderly and young subjects (15.4 and 13.0 h, respectively) while other found an increase in for older patients (14.9 versus 7.2 h for young patients) [78,90], Insignificant amounts of valproic acid are found in breast milk, approximately 3% of maternal drug levels [84]. 

Data are limited on elimination of metallic and inorganic mercury in animals. Initial excretion of mercury is predominantly in the fecal matter following inhalation of metallic mercury vapor, but as mercury concentrations increase in the kidneys, urinary excretion increases (Rothstein and Hayes 1964). After inhalation, approximately 10-20% of the total excreted metallic mercury is by exhalation (Rothstein and Hayes 1964). Mercury is excreted in the urine of mice exposed orally to mercuric sulfide ( 8-200 mg Hg/kg) (Yeoh et al. 1986, 1989). The amount of mercury in the urine of the treated group was 4.5-15-fold greater than the control levels. Urinary rates of mercury excretion were 1.6-2.2 ng/hour. Neonatal rats (1, 8, and 15 days old) eliminated mercury slower than older rats (22 and 29 days old) given mercuric chloride subcutaneously (Daston et al. 1986). 

The rate of mercury excretion was also slower in younger animals (7 or 15 days) than in older animals (24 and 56 days) (Thomas et al. 1982). This age-dependent difference in the rate of mercury excretion may reflect differences in the sites of mercury deposition (i. e., hair, red blood cells, skin). In neonatal rats, the excretion of methylmercury is longer than in adult rats because of the inability of the neonatal liver to secrete the toxicant into the bile. Therefore, the immaturity of the transport system in neonatal rats affects the elimination of mercury. 

---