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Tissue-turnover time

By the end of the summer all zooplankton were enriched in 15N, and Daphnia had 815N values similar to those of POM (Figures 4 and 5). Because zooplankton are labeled on a time scale that depends on their tissue-turnover time, the final 15N values represent equilibration with the 15N content of... [Pg.108]

POM at some earlier time in the summer. Exact measures of the fraction of POM in the zooplankton diet or, conversely, measures of tissue-turnover time in the zooplankton are possible only if the 15N pool in POM has come to equilibrium. Even though this equilibrium in the POM was not reached, it is clear that the growth and maintenance of these zooplankton depended... [Pg.109]

The difference between zooplankton and POM 813C values at the end of the experiment could be explained by lags in tissue-turnover time of... [Pg.111]

Fish rapidly eliminate residues of MS-222 after exposure to the anesthetic (27). Blood, kidney, liver, and muscle show different rates of elimination, which probably reflect the form of the drug present and fluid turnover times in the tissues. The concentration of the anesthetic in these tissues decreased to the detection limit of their method within 5 h. [Pg.126]

Plant productivity is determined by factors such as plant species composition, moisture, soil fertility, growing season length, and solar radiation—many of which are affected by human activities. All else equal, increases in primary productivity and production of plant tissues will lead to increases in soil C stock, while decreases will lead to decreases in soil C stock. The rate of change in soil C stock is determined by the difference between C inputs and outputs, as well as the turnover times of the soil C, which are often not known. Here we review briefly how some environmental factors are expected to alter productivity and explore how the effects on stock depend on the number of soil carbon pools and their turnover times. [Pg.246]

The only other method of studying the cell cycle is with the use of colchicine and its congener Colcemid. This technique is based on the observation that colchicine in sufficient concentration stops all the dividing cells in metaphase. By exposing a cell population for a given known period of time and determining the percentage of cells in metaphase one can determine the turnover time of the tissue. This technique requires... [Pg.335]

Role of HDL in peripheral cholesterol removal. Free cholesterol in plasma membranes of peripheral tissues is transferred to apo A-I containing pre-/ -HDL (nascent HDL), via an ATP-binding cassette transporter 1 (ABCl). Cholesterol is esterified by LCAT and stored in the core of the HDL particle. In the presence of suitable acceptor lipoproteins (VLDL or LDL), cholesteryl esters are transferred from HDL via apo D and CETP to the lower density lipoproteins, thereby shortening the half-life of plasma cholesterol since VLDL and LDL have a much faster turnover time than HDL. PL = Phospholipid. [Pg.439]

LDL-receptor deficiency. In the normal condition (a), VLDL produced by the liver loses triacylglycerol as free fatty acids (FFA) via lipoprotein lipase to peripheral tissues and then proceeds down the metabolic cascade to IDL and LDL. A major portion of these two lipoprotein species is taken up by the liver or peripheral tissues via the LDL (apo B, E) receptor. In individuals with down-regulated or genetically defective LDL receptors (b), the residence time in the plasma of IDL is increa.sed, a greater proportion being converted to LDL. LDL production and turnover time are increased, and total plasma cholesterol levels become grossly abnormal. [Pg.442]

Using the serial data for the cerebral cortex, plasma, and erythrocytes, we constructed accumulation and decay curves for several key fatty acids in these tissues, which provided gross estimates of their turnover times after fish-oil feeding to n-3 fatty acid-deficient monkeys (Table 2). For cerebral cortex, a steady state was reached after 12 wk of fish-oil feeding for DHA, but 22 5n-6 took longer to decline to the low levels found in the cortex of control animals. The half-lives of DHA in cerebral phospholipids ranged from 17 to 21 d 21 d for phosphatidylethanolamine, 21 d for phosphatidylserine, 18 d for phosphatidylinositol, and 17 d for phosphatidylcholine. The corresponding values for 22 5n-6 in these same phospholipids were 32,49,14, and 28 d, respectively. The half-lives of linoleic acid, EPA, and DHA in plasma phospholipids were estimated to be 8,18, and 29 d, respectively. In the phospholipids of erythrocytes, linoleic acid, arachidonic acids, EPA, and DHA had half-lives of 28, 32, 14, and 21 d, respectively. [Pg.182]

The most important differences between the selenite and selenomethionine models lie in the turnover times. The estimated turnover times in the plasma, liver/pancreas, and tissues are shorter for selenomethionine than for selenite, but the estimated turnover time for the whole body is more than twice as long for selenomethionine as for selenite. This is probably because selenite is not recirculated, whereas selenomethionine is extensively recycled, passing through the individual organs and tissues many times before being excreted. [Pg.179]

SOC from woody tissues has a longer turnover time than nonwoody tissues... [Pg.188]

Aspirin covalently modifies COX-1 and COX-2, irreversibly inhibiting COX activity. This is an important distinction from all the NSAIDs because the duration of aspirin s effects is related to the turnover rate of COX in different target tissues. The duration of effect of nonaspirin NSAIDs, which competitively inhibit the active sites of the COX enzymes, relates more directly to the time course of drug disposition. The importance of enzyme turnover in relief from aspirin action is most notable in platelets, which, being anucleate, have a markedly limited capacity for protein synthesis. Thus, the consequences of inhibition of platelet COX (COX-1) last for the lifetime of the platelet. Inhibition of platelet COX-1-dependent TXA formation, therefore, is cumulative with repeated doses of aspirin (at least as low as 30 mg/day) and takes roughly 8-12 days (the platelet turnover time) to recover once therapy has been stopped. [Pg.429]

To increase retention time. When intended for a part of the body with high tissue turnover rate, such as intestinal mucosa, a drug linked to a mucoadhesive polymer can increase adhesion to the site and increase bioavailability of a drug that has low residence time. [Pg.572]

The measurement of thiamine levels in human tissue other than blood is limited to biopsy or autopsy samples. This limitation translates into high sample variability due to factors such as age and nutritional, disease and medication status. Another limitation associated with measurement of thiamine in human tissue is the biological instability of thiamine derivatives. Because the turnover time of TTP is approximately one hour, significant hydrolysis can occur during extended delays between death and sample retrieval, preparation, and storage (Bettendorff et al. 1996a). [Pg.266]

The potential for harm from radioactive materials within the body depends upon half-life, turnover time in the body, type and energy or radiation emitted, organ or tissue in which deposited, radiation sensitivity of the organ or tissue, and chemical form of the radioactive material. [Pg.227]

Through the study of Roth el al. with carboxyl C -labeled niacin, it has been estimated that the turnover time of niacin in tissues is from 4 to 8 days 19ff). More recent data, however, indicate that in liver the half-life of the pyridine nucleotides may be considerably shorter 197). The observation that the injection of nicotinamide into mice can produce large increases in the levels of liver DPN has provided a useful means of studying the in vivo metabolism of the P3uidine coenzymes. The results obtained with this method of approach are presented in this section. [Pg.649]

One further difference between the tissues should be noted briefly—that of turnover—which holds implications for the nature of the isotopic signal recorded and its interpretation. Bone is constantly resorbed and reformed during life, i.e., it turns over , whereas enamel and dentine do not, although secondary dentine can be later accreted. Enamel and dentine form during a discrete period in the individual s life. This means that carbon isotope dietary signals in bone, for both collagen and apatite, reflect diet integrated over years, whereas those in enamel and dentine increments reflect diet at time of formation. [Pg.93]


See other pages where Tissue-turnover time is mentioned: [Pg.222]    [Pg.203]    [Pg.195]    [Pg.71]    [Pg.110]    [Pg.252]    [Pg.72]    [Pg.96]    [Pg.2156]    [Pg.4095]    [Pg.2665]    [Pg.440]    [Pg.331]    [Pg.315]    [Pg.179]    [Pg.198]    [Pg.458]    [Pg.917]    [Pg.427]    [Pg.376]    [Pg.383]    [Pg.649]    [Pg.297]    [Pg.212]    [Pg.278]    [Pg.510]    [Pg.154]    [Pg.171]    [Pg.488]    [Pg.480]    [Pg.145]   


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