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Toxicity tissue

While ammonia, derived mainly from the a-amino nitrogen of amino acids, is highly toxic, tissues convert ammonia to the amide nitrogen of nontoxic glutamine. Subsequent deamination of glutamine in the liver releases ammonia, which is then converted to nontoxic urea. If liver function is compromised, as in cirrhosis or hepatitis, elevated blood ammonia levels generate clinical signs and symptoms. Rare metabolic disorders involve each of the five urea cycle enzymes. [Pg.242]

Gorzinski SJ, Nolan RJ, McCollister SB, et al. 1985. Subchronic oral toxicity, tissue distribution and clearance of hexachloroethane in the rat. Drug Chem Toxicol 8 155-169. [Pg.153]

Hallett DJ, Khera KS, Stoltz DR, et al. 1978. Photomirex synthesis and assessment of acute toxicity, tissue distribution and mutagenecity. J Agric Food Chem 26(2) 388-391. [Pg.259]

Agents for chemical disinfection ideally should cause rapid, complete, and persistent inactivation of all germs, but at the same time exhibit low toxicity (systemic toxicity, tissue irritancy, antigenicity) and be non-deleterious to inanimate materials. These requirements call for chemical properties that may exclude each other therefore, compromises guided by the intended use have to be made. [Pg.290]

Ratio of toxic tissue in absence of competitive toxin - 1,0... [Pg.311]

In the non-toxic tissues the ratio (1.11 0.07) in the presence of purified CTX remained essentially the same. This may be attributable to non-specific binding of the immune complexes to the normal fish tissue. [Pg.314]

Table II summarizes the concentration in ng/ml of the other toxic polyethers examined which inhibited approximately 50% of the interactions between sheep anti-CTX and toxic fish tissue. The % inhibition was calculated based on the interactions between sheep anti-CTX and toxic tissue ratio as 100%. Table II summarizes the concentration in ng/ml of the other toxic polyethers examined which inhibited approximately 50% of the interactions between sheep anti-CTX and toxic fish tissue. The % inhibition was calculated based on the interactions between sheep anti-CTX and toxic tissue ratio as 100%.
Gorzinski SJ et al Subchronic oral toxicity, tissue distribution and clearance of hexa-... [Pg.375]

It is possible to predict what happens to Vd when fu or fur changes as a result of physiological or disease processes in the body that change plasma and/or tissue protein concentrations. For example, Vd can increase with increased unbound toxicant in plasma or with a decrease in unbound toxicant tissue concentrations. The preceding equation explains why because of both plasma and tissue binding, some Vd values rarely correspond to a real volume such as plasma volume, extracellular space, or total body water. Finally interspecies differences in Vd values can be due to differences in body composition of body fat and protein, organ size, and blood flow as alluded to earlier in this section. The reader should also be aware that in addition to Vd, there are volumes of distribution that can be obtained from pharmacokinetic analysis of a given data set. These include the volume of distribution at steady state (Vd]SS), volume of the central compartment (Vc), and the volume of distribution that is operative over the elimination phase (Vd ea). The reader is advised to consult other relevant texts for a more detailed description of these parameters and when it is appropriate to use these parameters. [Pg.105]

CCI3 radical can yield trichloromethanol, a precursor to carbonyl chloride (phosgene). Since reactive metabolites are responsible for the bulk of the toxicity, tissues rich in CYP2E1, such as the liver and kidney, are the most sensitive toxicity targets for the compound. The unmetabolized fraction also produces some toxicity, and is associated with central nervous system (CNS) depression and irritation of the gastrointestinal tract. [Pg.427]

Cell Proliferation as a Compensatory Response to Toxic Tissue Injury... [Pg.497]

Paul M, Mason R, Edwards R. 1989. Effect of potential antidotes on the acute toxicity, tissue disposition and elimination of selenium in rats. Res Commun Chem Pathol Pharmacol 66(3) 441-450. [Pg.378]

Figure 16.2. Mechanisms of cellular toxicity. Tissues are comprised of cells, and each cell is defined by its cell membrane. The cell membrane is composed of a lipid bilayer, which contains proteins that function as ion channels and receptors. Compounds that disrupt the membrane environment can directly or indirectly alter the normal function of these proteins. In each cell, there are numerous subcellular organelles, all of which are potential targets for toxicity. Cytochrome P450 enzymes in the endoplasmic reticulum may metabolize drugs that enter the cell. Metabolism has one of two effects on the drug s potential toxicity (l)it may reduce toxicity by eliminatingparent compound, or (2) it may increase toxicity by generating a reactive (electrophilic) metabolite. Drugs may inhibit critical functions in mitochondria or damage DNA in the nucleus, which can lead to cell death by apoptosis or necrosis. Figure 16.2. Mechanisms of cellular toxicity. Tissues are comprised of cells, and each cell is defined by its cell membrane. The cell membrane is composed of a lipid bilayer, which contains proteins that function as ion channels and receptors. Compounds that disrupt the membrane environment can directly or indirectly alter the normal function of these proteins. In each cell, there are numerous subcellular organelles, all of which are potential targets for toxicity. Cytochrome P450 enzymes in the endoplasmic reticulum may metabolize drugs that enter the cell. Metabolism has one of two effects on the drug s potential toxicity (l)it may reduce toxicity by eliminatingparent compound, or (2) it may increase toxicity by generating a reactive (electrophilic) metabolite. Drugs may inhibit critical functions in mitochondria or damage DNA in the nucleus, which can lead to cell death by apoptosis or necrosis.
Subconjunctival, Prompt or sustained. Anterior segment Local toxicity, tissue injury. [Pg.1096]

The industrial canning process can decrease the levels of PSP toxins present in some shellfish species, but it was only shown to be practical when the initial toxin levels were relatively low and usually it is necessary to eliminate some toxic tissues. The cockle, Acanthocardia tuberculatum, is harvested on the Mediterranean Coast of Spain and marketed exclusively as a canned product. In 1996, the Commission of European Conununities (CEC) published a decision (91/492/EEC) that established conditions for harvesting and processing of certain bivalves from areas where PSP levels exceeded the 80 J,g STXeq/100 g safety limit [6]. This decision applies specifically to... [Pg.914]

A new chemical method for decontamination of PSP toxins was developed by Lagos et al. [15] that involves alkaline immersion of contaminated products followed by heating and washing steps. This method together with elimination of more toxic tissues was reported to yield 99% decontamination of Chilean mussels. However, data do not allow calculation of the relative contribution to decontamination of each processing step (alkaline treatment versus evisceration). [Pg.915]

Wanebo HJ, Chung MA, Levy AI, Turk PS, Vezeridis MP, Bel-liveau JF (1996) Preoperative therapy for advanced pelvic malignancy by isolatedpelvic perfusion with the balloon-occlusion technique. Ann Surg Oncol 3(3) 295-303 Wieberdinck K, Benckhuijsen C, Braat RP et al (1982) Dosimetry in isolation perfusion of the limbs by assessment of perfused tissue volume and grading of toxic tissue reactions. Eur J Cancer Clin Oncol 18 905-910... [Pg.46]

Tris-acryl gel microspheres were the first spherical embolic agents to be commercially available [32]. Tris-acryl is an entirely synthetic, hydrophilic, and nonresorbable material. It has been demonstrated that this material produces non-toxic tissue reaction, thus allowing absorption and cellular adhesion [32]. Colored and non-colored tris-acryl gelatin microspheres (Embogold and Embosphere Microspheres Biosphere Medical, Rockland, MA) are currently commercially available. [Pg.226]

The doubling of mg% cholesterol in plasma (Table 1) shows that the 3 fractions were active. The values for uric acid suggest that the activity was not due to toxic tissue destruction. The apparent greater potency of anterior fraction H was not seen with the lower dose at which no extract was active. [Pg.442]

The comparatively low tolerance of ruminants to 5-triazines, which has been experimentally established by several authors, has led to loss of cattle that ingested concentrated products on the farm. The mechanism of this peculiar sensitivity has not been elucidated. A successful therapy is based on administering repeated large doses of activated charcoal this method eliminates the herbicide from the enterohepatic circulation before intestinal reabsorption produces toxic tissue levels and eventual death. [Pg.55]


See other pages where Toxicity tissue is mentioned: [Pg.209]    [Pg.720]    [Pg.455]    [Pg.720]    [Pg.162]    [Pg.806]    [Pg.2334]    [Pg.116]    [Pg.150]    [Pg.70]    [Pg.467]    [Pg.502]    [Pg.639]    [Pg.209]    [Pg.111]    [Pg.67]   
See also in sourсe #XX -- [ Pg.230 ]




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