Essential in rats

Vanadium. Vanadium is essential in rats and chicks (85,156). Estimated human intake is less than 4 mg/d. In animals, deficiency results in impaired growth, reproduction, and Hpid metaboHsm (157), and altered thyroid peroxidase activities (112). The levels of coen2yme A and coen2yme Q q in rats are reduced and monoamine oxidase activity is increased when rats are given excess vanadium (157). Vanadium may play a role in the regulation of (NaK)—ATPase, phosphoryl transferases, adenylate cyclase, and protein kinases (112). 

Cadmium Weak evidence for ultratrace essentiality in rats.7 Moderately toxic to all organisms a cumulative poison in mammals, causing renal failure possibly linked with hypertension in man. Has caused serous disease f ita] itai") in Japan from pollution. May also pose pollution problem associated with industrial use of zinc, e.g., galvanization. 

Tin Weak evidence for ultratrace essentiality in rats Organotin compounds used as bacteriostatsand fungistats its use in anti-foulant boat paints now discouraged because of danger to estuarine and marine life. ... 

Having approached the matter from the point of view of nutrition and growth, we would like to conclude this contribution by mentioning that lead has recently been shown to be essential in rats and that it may turn out to be indispensible for man as well. Therefore, we may face the problem of ensuring adequate lead intake during infancy one day. (Reichlmay-Lais and Kirchgessner, 1981). 

Tellurium is not an essential element, and teUurium compounds are in general more toxic than their selenium counterparts. MetaUic teUurium is known to have a teratogenic effect in rats, though no studies have been done on the toxicity of teUurium donor compounds (35). 

Amino acids essential for young rats (98) and fishes (99) have been reviewed. Rats preferably eat a diet with sufficient amounts of essential amino acids rather than one that is deficient (100). Each essential amino acid, consumed in self-selection, has been reviewed (101). A protein diet with an excess of essential amino acids has been described as a poor protein diet from investigations that showed remarkable growth inhibition and occurrence of fatty fiver disease in rats (102). This is called amino acid imbalance (103). 

The available evidence suggests that excretion of methyl parathion metabolites in humans and animals following acute oral exposure is essentially the same and occurs rapidly. Excretion occurs primarily via the urine. Methyl parathion can also be excreted in breast milk, although it has been detected only in a limited number of samples from women of central Asia, for which exposure data were not available (Lederman 1996) (see also Section 3.4.2.2). A study in rats also reported excretion of methyl parathion in the milk (Golubchikov 1991 Goncharuk et al. 1990). 

Intravenous administration of endosulfan (7 3 ratio of a- and P-isomers) in rabbits produced slower elimination of the a-isomer (Gupta and Ehrnebo 1979). Excretion of the two isomers occurred primarily via the urine (29%) with much less excreted via the feces (2%). Given the earlier evidence in rats and mice describing the principal route of elimination of endosulfan and its metabolite to be via the feces, the differences in the excretion pattern in this study may be attributable to differences in exposure routes, to species differences, or to both. Nevertheless, studies in laboratory animals suggest that both renal and hepatic excretory routes are important in eliminating endosulfan from the body. Elimination of small doses is essentially complete within a few days. 

Furthermore, we found that the two types of tumor promoters induced common biological effects, such as irritation of mouse ear, and stimulation of prostaglandin E2 production and of arachidonic acid metabolism in rat macrophages. These common effects seem to be the most essential biological activities in tumor promotion (6). 

Figure 5 Ex vivo autoradiography of [123I]AM281 in rat brain gave distribution patterns that were essentially identical to in vitro autoradiographs obtained using tritiated high affinity agonists.

Huang, L., Smit, J. W., Meijer, D. K., Vore, M., Mrp2 is essential for estradiol-17beta( beta-D-glucuronide)-induced cholestasis in rats, Hepatology 2000, 32, 66-72. 

It was shown that microsomal epoxide hydrolase-catalyzed trans-addition of water to BaP 9,10-epoxide occurs stereospecifically at the C-9 position (15). Since BaP is metabolized essentially to an optically pure 9R,10R-dihydrodiol (13 and L5 Table I), the 9,10-epoxide formed in BaP metabolism must have 9S,10R absolute stereochemistry (Figure 1). Similarly, the 7,8-epoxide formed in BaP metabolism is hydrated specifically at the C-8 position to form the 7R,8R-dihydrodiol (14.21). Hence the enzymatically formed 7,8-epoxide intermediate has 7R,8S absolute stereochemistry (Figure 1). Although the 7R,8R-dihydrodiol is formed almost exclusively from BaP metabolism in rat liver microsomes (Table I) and in bovine bronchial explants (25). the 7S,8S-dihydrodiol is also formed from BaP metabolism in mouse skin epidermis in vivo (5). 

LTP has been shown in many parts of the brain but it has been most extensively studied in the hippocampus, a phy-logenetically old part of the cerebral cortex that in humans is embedded in the temporal horn and in rats and rabbits lies beneath the parietal and temporal neocortex (Fig. 15-3A). The hippocampus is essential for (declarative) memory formation in rats the role of hippocampus in acquisition of spatial information has been studied in... 

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