Liver of rats

Merkord J, Weber H, Kroning G, Henningshausen G (2001) Repeated administration of a mild acute toxic dose of di-n-butyltin dichioride at intervals of 3 weeks induces severe lesions in pancreas and liver of rats. Human and Experimental Toxicology, 20(8) 386-392. 

Narayan S, Misra UK. 1985. Delta-aminolevulinic acid synthetase and heme oxygenase activity in lung and liver of rats given DDT and endosulfan intratracheally. Bull Environ Contam Toxicol 34 24-28. 

Narayan S, Bajpai A, Tyagi SR, et al. 1985b. Effect of intratracheal administration of DDT and endosulfan on cytochrome P-450 and glutathione-s-transferase in lung and liver of rats. Bull Environ Contam Toxicol 34 55-62. 

DiziK M, CHRISTMAN J K andwAiNFAN E (1991) Alterations in expression and methylation of specific genes in livers of rats fed a cancer promoting methyl-deficient diet . Carcinogenesis, 12, 1307-12. 

Trans fatty acids in liver of rats Silica AgNOj argentation 15... 

Yoshiji, H., Nakae, D., Mizumoto, Y., Horiguchi, K., Tamura, K., Denda, A., Tsujii, T. and Konishi, Y. (1992). Inhibitory effect of dietary iron deficiency on inductions of putative preneoplastic lesions as well as 8-hydroxydeoxyguanosine in DNA and lipid peroxidation in the livers of rats caused by exposure to a choline-deficient L-amino acid defined diet. Carcinogenesis 13, 1227-1233. 

The regulation of superoxide formation by SOD can affect both in vivo and ex vivo lipid peroxidation. Thus, SOD inhibited lipid peroxidation in cats following regional intestinal ischemia and reperfusion [33], Similarly, the treatment of rats with polyethylene glycol superoxide dismutase (PEG-SOD) prevented the development of lipid peroxidation in hepatic ischemia-reperfusion injury [34], Interesting data have been reported by Bartoli et al. [35]. They showed that SOD depletion in the liver of rats feeding with a copper-deficient diet... 

Important studies were performed by Trush and coworkers [42], who showed the advantages of applying lucigenin-amplified CL for the measurement of superoxide production by mitochondria in unstimulated monocytes and macrophages as well as by isolated mitochondria [43,44]. Later on, these authors have shown that mitochondrial superoxide production measured by lucigenin-amplified CL increased in the liver of rats treated with the promoter of hepatocarcinogenesis ethinyl estradiol [45], in liver from obese mice [46], and in children with Down syndrome [47]. 

Laj, S., V.K. Jain, and S.K. Tandon. 1984. Comparative toxicity of trivalent and hexavalent chromium IV biochemical changes in blood and liver of rat. Jour. Environ. Biol. 5 29-35. 

Accumulation of 2,3,7,8-TCDD is reported in the liver of rats during lifetime exposure to diets containing 0.022 pg 2,3,7,8-TCDD/kg (Newton and Snyder 1978), or when administered orally at 0.01 pg/kg body weight once a week for 45 weeks (Cantoni et al. 1981). Liver residues of rats fed 2,3,7,8-TCDD were 0.54 pg/kg, or about 25 times dietary levels livers of rats dosed orally contained 1.05 pg/kg, or about 2.3 times the total dose received on a unit weight basis. Unlike toxicity, elimination rates of accumulated 2,3,7,8-TCDD were within a relatively narrow range. The estimated retention times of 2,3,7,8-TCDD in small laboratory mammals (rats, mice, guinea pigs, and... 

Kendall MW. 1974b. Acute histopathologic alterations induced in livers of rat, mouse, and quail by the fire-ant poison, mirex. Anat Rec 178 338. 

Singh A, Valli VE, Ritter L, et al. 1981. Ultrastructural alterations in the liver of rats fed photomirex (8-monohydromirex). Pathology 13(3) 487-496. 

Scott DO, Lunte CE. 1993. In vivo microdialysis sampling in the bile, blood, and liver of rats to study the disposition of phenol. Pharmaceutical Res 10 335-342. 

Using light microscopy, Broda et al. (1976) did not observe hepatocellular fatty change in livers of rats exposed by gavage to 110 mg/kg 1,2-dibromoethane in olive oil. Rats developed centrilobular dilatation within 8 hours after exposure, hepatocellular degeneration within 17 hours after exposure, and frank centrilobular necrosis 22 hours after 1,2-dibromoethane exposure. 

In male rats, swelling and mild centrilobular vacuolation was observed only in the livers of rats exposed to 271 ppm. Necrosis was minimal and confined to individual hepatocytes immediately adjacent to the central vein livers were dark red and congested. The hepatocyte LI in rats were increased only at 101 and 271 ppm, 3- and 7-fold over controls, respectively. An acute-duration inhalation MRL of 0.1 ppm was based on the NOAEL of 3 ppm for hepatic effects in mice. More information on this MRL and how it was derived is located in the footnote to Table 2-1, Section 2.5 in Appendix A this profile. 

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). 

Landon EJ, Naukam RJ, Sastry BVR. 1986. Effects of calcium channel blocking agents on calcium and centrilobular necrosis in the liver of rats treated with hepatotoxic agents. Biochem Pharmacol 35 697-705. 

Hepatic Effects. No studies were located regarding hepatic effects of 1,2-diphenylhydrazine in Humans. Chronic oral administration of 1,2-diphenylhydrazine produced degenerative alterations the liver of rats (fatty metamorphosis) and mice (coagulative necrosis) (NCI 1978). 

Histopathologic lesions of the liver have been demonstrated in several oral studies in rodents dosed at higher levels of 1,4-dichlorobenzene. Cloudy swelling and centrilobular necrosis were observed in the livers of rats that received 1,4-dichlorobenzene at 500 mg/kg/day for 4 weeks (Hollingsworth et al. 1956). Thirteen-week studies have resulted in degeneration and necrosis of hepatocytes in rats that received doses of 1,200 mg/kg/day and above and in mice, hepatocellular degeneration was observed at... 

Umemura T, Tokumo K, Williams GM. 1992. Cell proliferation induced in the kidneys and livers of rats and mice by short term exposure to the carcinogen p-dichlorobenzene. Archives of Toxicology 66(7) 503-507. 

Starek A, Kaminski M. 1982. [Toxicity of certain petroleum derivatives used as dielectrics in electromachining V. Morphological, cytoenzymic, and biochemical changes in the liver of rats chronically exposed to kerosine hydrocarbons.] Med Pr 33(5-6) 239-253. (Polish)... 

Orotic acid incorporation into nuclear and cytoplasmic RNA is decreased in polycythemic mice [136]. Aflatoxin Bi, a known hepatocarcinogen which induced polysomal disaggregation in the livers of rats, also inhibits the in vivo incorporation of intraperitoneally injected orotic acid into liver RNA [137]. On the other hand, the incorporation of orotic acid into free nucleotides and the RNA of the monkey kidney is rapidly increased twofold after castration and is restored to normal within seven days by the administration of testosterone [134]. It is of interest to note that, in experiments with rats, administration of orotic... 

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