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Biomedical subjects

R Doi

Publications and source records attributed to R Doi.

At least 145 records · Page 8Linked to original sources

Mercury in feathers of wild birds from the mercury-polluted area along the shore of the Shiranui Sea, Japan.

Total mercury content in the feathers of 95 stuffed, wild birds collected all over the shore of the Shiranui Sea (where Minamata disease occurred in many towns and villages in the 1960's) was measured. They were collected over 25 years, from 1955 to 1980. They showed relatively high mercury levels till the late 1970's, although drainage of waste water containing methylmercury from the Chisso Corporation's Minamata Factory was stopped in 1968. In addition, a strong correlation between feeding habits and mercury content was observed; thus the five groups in order of diminishing mercury content were: fish-eating sea birds (mean +/- SD = 7.1 +/- 3.7 ppm, n = 14), omnivorous water fowl (5.5 +/- 5.6 ppm, n = 17), predatory birds (3.6 +/- 2.9 ppm, n = 16), omnivorous terrestrial birds (1.5 +/- 1.2 ppm, n = 31), and herbivorous water fowl (0.9 +/- 0.4 ppm, n = 17). Mercury content of the feathers of omnivorous terrestrial birds in the Shiranui Sea was exceedingly high compared with those in China and Korea. The findings in the present study suggest that stuffed, wild birds may be a good index of past environmental pollution.

Animals↗

Comparison of cytotoxicity of mercury-selenium and mercury compounds on cultured cells.

In vitro effects of mercury-selenium (Hg-Se) compounds, as compared with their original mercury compounds, against growth and viability of HeLa cells were studied. A water-soluble, ethanol-insoluble black complex (GX) formed from HgCl2, Na2SeO3 and GSH was less toxic than HgCl2, but the cytotoxicity of bis(methylmercuric) selenide (BMS) seemed to be similar to that of methylmercury. This may be due to the instability of BMS; i.e., there is a possibility that BMS decomposed to methylmercury and selenium under our culture conditions.

Cell Survival↗

Effects of carbon monoxide exposure on the distribution of methylmercury in mice.

Effects of long-term exposure to sublethal concentration (300-350 ppm) of carbon monoxide (CO) on the distribution of methylmercury (MeHg) in the blood and organs of mice were examined using 6th week-old ICR mice of both sexes. Firstly, female mice were exposed to CO immediately after single ip injection of CH3HgCl (1 mg/kg). At the earliest stage, brain mercury level was higher in CO mice than in control mice, while blood mercury level was lower in CO mice than in control mice. There were indications that compensatory hemoconcentration and resultant increase of mercury levels in the blood, brain and liver occurred in CO mice by the 8th day of CO exposure. Mercury in the blood, brain, liver and kidney decreased more rapidly in CO mice than in control mice for a short period after hemoconcentration had occurred. Secondly, male mice were pre-exposed to CO for 7 days, received single ip injection of CH3HgCl (1 mg/kg) and were re-exposed to CO for an additional 21 days. Hemoconcentration, increased mercury levels in the blood, brain and liver were observed in CO mice. Thirdly, male mice were pre-exposed to CO for 7 days, administered po with CH3HgCl (2 mg/kg) and re-exposed to CO for 24 hr. Mercury levels in the blood, brain and liver but not the kidneys were higher in CO mice than in control mice. The relationships between hemoconcentration and MeHg distribution in vertebrates were discussed.

Animals↗

Hereditary analysis of the strain difference of methylmercury distribution in mice.

Hereditary analyses of strain differences in the distribution of methylmercury (MeHg) were carried out with various strains of mice. First, dose-response relationships were examined with 6-week-old male mice of four strains at seven dose levels from 0.25 to 6.0 mg CH3HgCl/kg. Significant strain differences in dose-response were found for both blood and brain. Second, the frequency distribution of blood mercury concentration was examined with two inbred strains, C3H and C57BL, their hybrid (F1), F2 generation, and back-cross mice. The F1 generation showed an intermediate value between their parents, and characteristic hereditary segregations were found in the frequency of blood mercury concentration in F2 and back-cross mice. Third, the relationship between blood mercury concentration and the molecular structure of mouse hemoglobins (Hb) was examined with 14 strains of inbred mice and a single wild mouse strain. Five strains with Hb-beta d and one strain with Hb-beta p showed blood mercury concentrations twice as high as the other Hb-beta strains. Through these experiments, Hb structure, especially the number and position of cysteinyl residue in the molecule, was found to play a primary role in binding with MeHg and in determining blood mercury concentration.

Animals↗

A study on the biochemical and biological behavior of methylmercury.

The biochemical and biological behavior of methylmercury (MeHg) was investigated by measurement of MeHg release rate from erythrocytes (RBC) of selected animal strains and species, by measurement of the intracellular distribution of MeHg in RBC, and by measurement of the binding affinity of hemoglobin (Hb) for MeHg. Methylmercury chloride was used throughout the experiments. Significant strain and species differences were found in the release rate of MeHg from RBC of mice, rats, and man and in the distribution of MeHg in RBC. Significant correlations were found between the above two indexes and the brain/blood ratio of mercury concentration 24 hr after MeHg injection, ip. The affinity of Hb for MeHg was examined by ultrafiltration techniques and Scatchard plots. There were Hbs with only one type of binding site and others with two types of binding sites. Both sites were considered to be cysteinyl residues. Primary sites involved cysteinyl residues oriented externally at the outside of the alpha 1 beta 1 contact junction and cysteinyl residues in the junction, while secondary sites involved only cysteinyl residues in the junction.

Alleles↗

Studies on Japanese encephalitis virus infection of reptiles. I. Experimental infection of snakes and lizards.

Experimental infection of four species of snakes, Rhabdophis tigrinus tigrinus, Elaphe quadrivirgata, Elaphe climacophora and Agkistrodon halys, and five species of lizards, Takydromus tachydromoides, Eumeces latiscutatus, Eumeces barbouri, Eumeces marginatus oshimensis and Gekko japonicus, with Japanese encephalitis virus (JEV) was carried out. Evidence of JEV multiplication in snakes was not obtained at least under the conditions used in the present study. All lizards except G. japonicus were infected with JEV by ip injection of virus suspension. The minimum infectious dose for a lizard was around 10(3) MLD50/0.05 ml, and this dose was considered to be proportional to the virus dose which is injected into a host by a vector mosquito at a single bite. Temperature dependence of JE virus growth in the lizards was demonstrated. JEV multiplied slower at 20 degrees C than at 26 degrees C, though the peak titers of viremia were equivalent in both groups of lizards kept at 20 degrees C and 26 degrees C. E. latiscutatus developed viremia with ip injection of a partially attenuated strain, Nakayama NIH which could not infect adult mice by peripheral inoculation. T. tachydromoides and E. latiscutatus were also infected by oral feeding of JEV infected mosquitoes. E. latiscutatus was infected by oral feeding of only one infected mosquito.

Animals↗

Studies on Japanese encephalitis virus infection of reptiles. II. Role of lizards on hibernation of Japanese encephalitis virus.

A series of experiments on the role of lizards as overwintering hosts of Japanese encephalitis virus (JEV) was carried out. Two species of lizards, T. tachydromoides and E. latiscutatus, 2 species of mosquitoes, Cx. p. fatigans and Cx. p. pallens, and 2 strains of JEV, JaGAr#01 and JaGAr 19461, were used in this study. Firstly transmission of JEV from infected mosquitoes to uninfected lizards and from infected lizards to normal mice by the bite of mosquitoes was demonstrated successfully. Cx. pipiens group mosquitoes were found to feed readily on lizards as compared to Cx. tritaeniorhynchus, the primary vector of JEV in Japan. Secondly simulated hibernation of JEV in lizards was carried out under indoor and outdoor conditions. In the outdoor hibernation, lizards were injected with JEV on October 14, 1968, entered in hibernation on October 19 and were recovered from hibernation on April 10, 1969. Viremias were demonstrated in the lizards for a few weeks in late April. Thirdly JEV isolation and HI antibody detection were attempted from blood samples of field-caught reptiles, 7 species of snakes and 3 species of lizards and among amphibians, 2 species of frogs. HI antibody against JEV was found at a rate of 14.3% from E. latiscutatus and 4.0% from T. tachydromoides, though JEV was not isolated from all the blood samples of these cold-blooded animals. The roles of lizards as overwintering hosts of JEV were discussed.

Animals↗

In vitro effects of mercury-selenium compounds on enzymes.

In vitro effects of mercury-selenium compounds, as compared with mercurials, against glucose-6-phosphate dehydrogenase (G6PD), catalase and trypsin were studied. Inhibitory potencies of two mercury-selenium (Hg-Se) compounds, bis(methylmercuric) selenide (BMS), and a reaction product of HgCl2, Na2SeO3 and glutathione (GSH), were markedly weaker than those of their original mercurials, methylmercury and mercuric mercury, respectively.

Animals↗

Organ distribution and biological half-time of methylmercury in four strains of mice.

The organ distribution and biological half-time of methylmercury were examined in male mice of 3 inbred strains, BALB/c, C3H/HeN and C57BL/6N, and a random-bred strain, CD-1 (ICR), at 6 weeks after birth. Methylmercury chloride was administered intraperitoneally at the dose of 1 mg per kilogram of body weight. At various time intervals after methylmercury administration 9 to 12 mice of each strain were killed and the total mercury concentrations in the blood, brain, liver and kidneys were determined with cold-vapor atomic absorption spectrophotometry. A significant strain difference was found in the mercury concentrations in the organs, especially in the blood. BALB/c and C3H had twice as high blood mercury levels than C57BL and ICR. The brain/blood, liver/blood and kidney/blood ratios of mercury concentration appeared to be hereditarily stable characteristics. The biological half-time of mercury in the organs was longest in C57BL (except in the case of the kidneys) and shortest in ICR. Some biological features such as relative organ weight and body weight were considered to affect the chemobiokinetics of methylmercury in mice.

Animals↗