Surface sediments were collected from eight sampling points, representing upper, mid-and downstream regions, of the Tama River, to obtain background information on the polychlorinated dibenzo-p-dioxin/dibenzofuran (PCDD/DF) levels, profiles and transport in this river. The sediment profiles of PCDD/DF were strongly dependent on the sampling points, with total PCDD/DF levels ranging from 27.0 to 231.6pg/g dry weight (mean value, 90.7pg/g) and the I-TEQ values ranging from 0.05 to 2.8pg/g (mean value, 1.2pg/g). Two maxima in the PCDD/DF concentrations were observed for the sediment samples taken from stations 3 (midstream) and 7 (upstream) in this river, although none for the samples from downstream (industrial area). Sediment samples taken from the midstream near waste water discharges and a municipal solid waste (MSW) incinerator plant showed high TEQ values of 0.5 to 1.2 and 13.0pg/g, respectively, indicating a potential PCDD/DF source in this river. In contrast, the PCDD/DF concentrations in the sediment samples taken from five tributaries flowing into the midstream region were very low, indicating no PCDD/DF impact into the studied areas. These data suggest a multiplicity of sources ranging from agricultural activities to urban activities such as emission gas from MSW incinerators and effluents from wastewater treatment plants.
Trichloroethylene (TCE) is a highly toxic compound which belongs to the class of volatile halogenated hydrocarbons, which are well-known pollutants of drinking water and the atmosphere. The effects of moderately toxic concentration of TCE on the levels of cytochrome P450 (CYP) isoforms and on their phenobarbital (PB) induction in rats were studied. Monooxygenase activities associated with individual CYP isoforms, i.e., CYP1A, 2B, 2E1 and 3A, were measured in microsomal fractions prepared from both lungs and livers of male and female Wistar rats (7-weeks old). Differences in constitutive levels of CYP isoforms were observed between liver and lung of mock-treated rat ; microsomal CYP2B activity was solely detected in lung while the activities of CYP1A, 2EI and 3A, but not 2B were detected in liver. Among these, the pulmonary CYP2B and hepatic CYP2E1 activities were reduced by TCE-treatment. PB-treatment resulted in the detection of increased levels of hepatic CYP1A and 2E1 and of pulmonary CYP2B activities, and also the appearance of hepatic CYP2B activity. Coadministration of TCE was suppressive against the activities of CYP isoforms except for hepatic CYP2E1 in PB-treated rats. The lowered CYP2B activity in the presence of TCE was accompanied by the reduction in the amount of CYP2B apoprotein.
To investigate the possible involvement of metallothionein (MT) in acetaminophen (AC)-induced liver damage, MT-I and MT-II gene knock-out transgenic mice (MT-null mice) and wild-type control mice were i.p. treated with AC at a single dose of 250mg/kg and compared. At 24h after AC treatment severe liver damage characterized by necrosis of hepatocytes and increased serum GPT activity was found in MT-null mice while a limited degree of change such as a slight increase in serum GPT activity without necrosis was observed in wild-type mouse liver. MT-null hepatocytes also showed elevated PCNA (proliferating cell nuclear antigen)-positive activity around the necrosis area. AC administration resulted in an increase in lipid peroxidation in MT-null mice, but not in the wild-type mice. The liver in the wild-type mice showed an increased MT amount after AC treatment. These results indicate that MT acts as an endogenous defensive factor against AC-induced hepatotoxicity via oxidative stress.
Brain parenchyma is protected against excess metals by the barrier system in the brain. To evaluate the expression of metallothionein (MT), a protective protein against heavy metals, in the brain parenchyma, zinc sulfate (0.2 or 2μmol) or cadmium chloride (2 or 20nmol) was injected into the left striatum of rats. Seventy-two h later, the MT level in the ipsilateral striatum injected with 0.2μmol of zinc sulfate was not significantly higher than that after injection with vehicle. When the striatum was injected with 2μmol of zinc sulfate, on the other hand, the MT level in the ipsilateral striatum, showing apparent degeneration, was significantly higher than that after injection with vehicle : the former was approximately 1.5 times the latter. In the case of injection with cadmium chloride at doses of 2 and 20nmol, the MT levels in the ipsilateral striatum was approximately twice that after injection with vehicle. The MT level in the contralateral striatum and other brain regions were not affected by injection with either metal salt at any dose. When zinc sulfate of 100μmol/kg body weight, corresponding to the lower dose tested(0.1μmol/g brain), was subcutaneously injected, the hepatic MT level was approximately four times higher than the normal hepatic level. These results suggest that the changes of MT level in the brain were small compared to those observed in the liver.
To elucidate the involvement of reactive oxygen in in vivo demethylation of methylmercury(MeHg), the effects of paraquat (PQ) and other reactive oxygen modulators on inorganic-Hg (I-Hg) production in MeHg-administered rats were examined. Rats were intravenously (i.v.) injected with MeHgCl (2mg/kg). After MeHg administration, I-Hg levels time-dependently increased in the liver up to 9h, whereas the renal levels did not change during the first 3h, and then increased up to 24h in a time-dependent manner. PQ stimulated I-Hg production in the liver but not in the kidney, whereas it increased 2-thiobarbituric acid-reactive substance (TBA-RS) levels in both tissues. PQ-induced stimulation of I-Hg production was not further accelerated by an OH· enhancer, such as FeSO4 or Fe(III)EDTA. Hepatic I-Hg production in MeHg-administered rats (without PQ) was suppressed by NaCN (a potent inhibitor of mitochondrial cytochorome oxidase) but not by desferal or Fe(III) EDTA (an OH· modulalator). These results suggest that hepatic mitochondria may play an important role in in vivo demethylation of MeHg, and that reactive oxygen species other than OH· may participate in it.
Since early 1980s Drosophila melanogaster larvae heterozygous for recessive visible markers and those with defective DNA repair capability have been intensively used as simple in vivo testers of mutagenicity of environmental agents. In pallalel with this activity, the somatic tests have recently been deployed as tools for the detection of modifiers of the mutagenicity and understanding of basic mechanisms of the effects. Here, I characterize the somatic systems in relation to the biotransforming ability of promutagens and the outcomes from the mutagenicity tests and review some aspects of the deployment.
A Ferric-EDTA(Fe-EDTA)-degrading bacterium, strain A-1 was characterized by its physiological properties. The rate of degradation of Fe-EDTA was measured by the titration method and ion chromatography. The former method has the advantage of allowing a greater number of sample measurements of samples at one time. The rate of degradation of Fe-EDTA was higher in a stationary culture than in a shaked one. The optimum pH for the degradation rate was approximately 8.2. Strain A-1 grew in the presence of various kinds of metal-EDTA chelates, but a Na salt, Mg and Ca chelates of EDTA inhibited the growth. Their MICs (minimual inhibitory concentration) were 0.0045, 0.03 and 0.006%, respectively. These characteristics of strain A-1 have similarities to those of strain B-3, but were different from those of Agrobacterium sp. which were reported by Lauff previously (Appl. Environ. Microbiol., 56, 3346 (1990)). All of the detail taxonomic characters indicate that the isolate strain A-1 belongs to a Pseudomonas sp.
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