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Liver tissue of rats

Deutschmann, S. Laib, R.J. (1989) Concentration-dependent depletion of non-protein sulfhy-dryl (NPSH) content in lung, heart and liver tissue of rats and mice after acute inhalation exposure to butadiene. Toxicol. Lett., 45, 175-183... [Pg.206]

Paradisi L, Panagini C, Negro F, et al. 1984. Behavior of cyclic nucleotides and Ca2+ levels in liver tissue of rats poisoned by white phosphorus and trichlorobromomethane. Cell Biochem Funct 2 111-114. [Pg.226]

Fedorov SN, Balansky RM, Novikov LB, et al. 1991. Properties of mitochondrial DNA from liver tissue of rats treated with 1,2-dimethylhydrazine. Vapor Med Khim 37 82-84. [Pg.162]

The mode of action of kasugamycin is similar to that of blasticidin S. It inhibits protein synthesis in fungi and bacteria. It inhibits binding of the aminoacyl-tRNA complex to the ribosome (Tanaka et al., 1966), but does not disturb the synthesis of nucleic acids. The inhibitory effect is considerably lower in the liver tissue of rats. The selectivity of toxicity may be due to the particular sensitivity to kasugamycin of the ribosomes of each type of organism. This may also explain the relatively rapid development of resistance to kasugamycin. [Pg.477]

TABLE 4, Radioactivity Counts/min) Associated with Hsp89oi and Hsp89p mRNA Expression in Brain and Liver Tissues of Rats ... [Pg.540]

Cytosol was prepared from the kidney and liver tissue of rats by homogenizing the tissue in buffered sucrose media containing 2-mercaptoethanol and centrifuging the homogenate at 5,000 and subsequently at 40,000 ) S. to yield a particulate free supernatant. At this point, a heat treatment step, in which the cytosol was heated in boiling water bath to 60 C, held at 60°C for 60 sec and cooled in an ice bath, was applied, after which the cytosol was recentrifuged at 40,000 (20 min) to remove de-... [Pg.358]

It shoud be noted that decaborane, the most active inhibitor of serine transhydroxymethylase in in vivo experiments, decreases the SAM and SAH content in liver tissue of rats no more than MTX does, namely by 50-55% as compared with the control (see Fig.3). [Pg.124]

Fig. 3. SAM and SAH content in liver tissue of rats treated with decaborane (BiqHia). Fig. 3. SAM and SAH content in liver tissue of rats treated with decaborane (BiqHia).
In a recent comprehensive study, Feelish and coworkers (Bryan et al, 2004) determined the concentrations of RSNOs, N-nitrosamines (RNNOs) N02 , N03, heme nitrosyl (NO-heme) in plasma, RBCs, as well as brain, heart, liver, kidney, lung, and aortic tissues of rats. Furthermore, the levels of these analytes were monitored under conditions of eNOS inhibition, hypoxia and redox state. The emerging picture was that RSNOs were detected in all of the tissues examined in comparable levels to NO-... [Pg.94]

Evidence of oral absorption in rats is demonstrated in the studies by Albro and Moore (1974), Oishi (1990), and Poon et al. (1995). Forty-eight hours after a gavage dose of di-w-octylphthalate, metabolites were detected in the urine. The major metabolite (60% of the metabolites in urine) was derived from the monoester (Albro and Moore 1974). The mono- -octylphthalate metabolite was found in the blood and testes of rats from 1-24 hours after oral dosing with peak levels reported at 3 hours (for blood) and 6 hours (for testes) (Oishi 1990). Di-ra-octylphthalate was found in the liver and adipose tissue of rats after they were fed this compound for 13 weeks in dietary concentrations up to 5,000 ppm, indicating its absorption (Poon et al. 1995). Although there are insufficient quantitative data for estimating the oral absorption rate, di-/ -octylphthalate appears to be absorbed readily however, it may have to be converted to mono- -octylphthalate for intestinal absorption to occur (Lake et al. 1977). [Pg.52]

Following a single oral dose of 2,000 mg/kg of di-/ -ocLylphthalatc in rats, mono- -octylphthalate was detected in blood with peak levels observed at 3 hours and in the testes with peak levels observed at 6 hours (Oishi 1990). The biological half-life and mean residence time of mono-w-octylphthalate in blood were 3.3 and 5.4 hours, respectively. After 13 weeks of oral exposure of rats to di-w-octylphthalate in the diet at concentrations up to 5,000 ppm (350 and 403 mg/kg/day in males and females, respectively), the livers contained di -/ -oc1y lphthalate residues that were either below or just slightly above the detection limit (<3 ppm) (Poon et al. 1995). The adipose tissue of rats fed 5,000 ppm showed di-/ -octylphthalate residue levels of 15 ppm (males) and 25 ppm (females). This study is limited in that it did not analyze tissues for the presence of metabolites. [Pg.53]

We also note that some 2,2-disubstituted oxiranes have toxicological significance, as exemplified by 2,2-dimethyloxirane (2-methyl-l, 2-epoxypropane, 10.43, R = Me). This compound is the toxic metabolite of 2-methyl-prop-1-ene (isobutene), a gaseous alkene widely used as a monomer in the industrial production of adhesives, plastics, and other polymers. Interestingly, detoxification of this epoxide catalyzed by liver epoxide hydrolase was high in the human, intermediate in the rat, and low in the mouse [125], These activities were inversely correlated with the epoxide levels measured in vitro in liver tissue of these species. [Pg.636]

High concentrations of radioactivity were observed in body fat and livers of rats, mice, and squirrel monkeys given oral doses of 60 mg/kg " C-labeled chloroform (Brown et al. 1974a). The maximum levels of radioactivity in the blood appeared within 1 hour and were 3 pg equivalents chloroform/mL for mice and 10 pg equivalents chloroform/mL for monkeys, which represented -0.35 and 1%, respectively, of the total radioactivity. In monkeys, bile concentrations peaked within 6 hours. The distribution of radioactively labeled chloroform was studied in three strains of mice (Taylor et al. 1974). No strain-related differences were observed however, higher levels of radioactivity were found in the renal cortex of males and in the liver of females. The renal binding of radioactive metabolites may have been altered by variations in the testosterone levels as a result of hormonal pretreatment in females or castration in males. Sex-linked differences in chloroform distribution were not observed in rats or monkeys (Brown et al. 1974a). Chloroform accumulates in the adipose tissue of rats after oral exposure of intermediate duration (Pfaffenberger et al. 1980). [Pg.117]

No studies were located regarding quantitative absorption of PBBs in animals after inhalation exposure to PBBs. However, increased bromine concentrations were found in the liver and adipose tissue of rats exposed continuously to a commercial mixture of octabromobiphenyl for 15 weeks, suggesting that absorption had occurred (Waritz et al. 1977). [Pg.199]

Following the topical application of silver nitrate for the treatment of burns in two humans, silver was distributed to the muscles (0.03-2.3 ppm), liver (0.44 ppm), spleen (0.23 ppm), kidney (0.14 ppm), heart (0.032-0.04 ppm), and bones (0.025 ppm) (Bader 1966). No studies were located that quantitated the distribution of silver in animals following dermal exposure to silver or its compounds. However, Sano et al. (1982) detected silver in the same tissues of rats following topical application of silver sulphadiazine cream. [Pg.46]

In rodents, silver has been shown to cross the placenta and to enter the fetuses following an intraperitoneal injection of silver lactate to the mothers (Rungby and Danscher 1983a). Silver was detected in the liver and brain tissues of rat fetuses (Danscher 1981 Rungby and Danscher 1983a). when Administered Alone and when Coadministered with Additional Silver as Silver Nitrate... [Pg.46]

Retinoic acid is a metabolite of retinol in the liver, intestine, and bile of rat, and of retinyl acetate in the kidney and blood,378 and studies have been reported concerning the metabolism of retinoic acid and of vitamin A in various tissues of rats that are deficient in vitamin A.379... [Pg.211]

Liver tissue from rat was homogenized in 16 volumes of ice-cold normal saline by sonication. The whole homogenates were used in assay. [Pg.266]

MVA is now known to be metabolized by routes other than those which give rise to terpenoids and steroids. The breakdown occurs predominantly in the kidneys to give C2 units that can be utilized in fatty-acid synthesis. The sterol and the shunt pathways have been evaluated in nine different tissues of rat previous conclusions that the kidneys are the predominant site of both types of metabolism have been confirmed. MVA is known to accumulate, at a low level, in the blood, and these results suggest that impairment of renal clearance of serum MVA by either route may account for the hypercholesterolaemia associated with some kidney disorders. A study of the effects of possible antimetabolites of MVA (for example the 2,3-anhydro-compound) on the formation of cholesterol in cell-free systems from liver has been reported. ... [Pg.179]

Siman CM, Ericsson UJ. Effect of butylated hydroxytoluene on alpha-tocopherol content in liver and adipose tissue of rats. Toxicol Lett 1996 87(1-1) 103-8. [Pg.155]


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