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H Tanii

Publications and source records attributed to H Tanii.

61 records · Page 4Linked to original sources
PubMed1982

Structure-toxicity relationship of acrylates and methacrylates.

The structure-toxicity relationships of acrylates and methacrylates were analysed in mice. In all test compounds, the acute oral toxicity (LD), the partition coefficient (P), and the second order rate constant (K) with reduced glutathione were measured experimentally. The toxicities of both acrylates and methacrylates were found to be dependent significantly upon log P or log K, especially upon the former. The correlation coefficient between log (1/LD50) and log P, was -0.9909 for acrylates and -0.795 for methacrylates, both being statistically significant. The correlation coefficient between log P and log K was -0.935 for acrylates and -0.744 for methacrylates.

Acrylates↗
PubMed1981

Studies on in vitro metabolism of acrylamide and related compounds.

The in vitro biotransformations of acrylamide and ten related compounds in the hepatic enzyme system of the mouse were studied in order to learn more about their toxic actions in vivo. Of nine analogues, which could be analyzed quantitatively by gas chromatography, seven compounds--N-tert-butylacrylamide, diacetone acrylamide, N,N-dimethylacrylamide, N-isobutoxymethylacrylamide,--were metabolized in microsomal enzymes with NADPH generating system. One or two metabolites from each of the seven compounds, except for N-isobutoxymethylacrylamide were detected by gas chromatography. The metabolite of N-isopropylacrylamide was identified as acrylamide by gas chromatography-mass spectrometry. The metabolite of N,N-dimethylacrylamide showed a RT value identical with and a mass spectrum similar to N-methylacrylamide. No metabolites from the other four compounds have yet been identified. Acrylamide and crotonamide did not seem to be metabolized in the same system. Phenobarbital pretreatment of mice enhanced the metabolic reactions of the seven compounds, but did not elevate those of acrylamide and crotonamide. The Km value of N-isopropylacrylamide was 0.35 mM, which was the smallest of all the test analogues. All of the eleven analogues studied were found to be metabolized by hepatic glutathione S-transferases as well. This reaction was also elevated by the phenobarbital treatment of mice. The relationships between the in vitro metabolisms and the in vivo toxicities of acrylamide analogues are discussed.

Acrylamides↗
PubMed1981

Neurotoxicity of acrylamide and related compounds and their effects on male gonads in mice.

Neurotoxicity of acrylamide and related compounds and their effects on the testis after repeated oral doses were studied in mice. Of fourteen analogues tested, five produced neuropathy. In decreasing order of potency as assessed by the rotated performance test, these were as follows: acrylamide greater than N-isopropylacrylamide greater than N-methylacrylamide = methacrylamide greater than N-hydroxymethylacrylamide. The development of neurotoxicity was either greatly reduced or delayed by phenobarbital treatment. Acrylamide, N-hydroxymethylacrylamide, N-isopropylacrylamide, N-methylacrylamide and N,N'-methylene-bis-acrylamide produced testicular atrophy. Atrophy was either prevented by phenobarbital treatment, as in the cases of acrylamide and N-isopropylacrylamide, or reduced, as in the case of N-hydroxymethylacrylamide. Histological changes in the testis produced by the active compounds were degenerations of the epithelial cells of the seminiferous tubules, with the interstitial cells being normal.

Acrylamides↗
PubMedDate not supplied

Structure-toxicity relationship of monoketones: in vitro effects on beta-adrenergic receptor binding and Na(+)-K(+)-ATPase activity in mouse synaptosomes.

The structure-toxicity relationship of monoketones, a class of organic solvents widely used in industry, was investigated with respect to their in vitro effects on synaptosomal membrane proteins. The toxic parameters used were Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase), a well-known marker enzyme often used as a membrane toxicity model, and 3H-dihydroalprenolol (3H-DHA)-labeled beta-adrenergic receptor binding that has been shown to be vulnerable to solvent-induced changes in membrane fluidity. In vitro treatments with 12 kinds of monoketones (carbon chain length from 3-10) dose-dependently inhibited both 3H-DHA binding to mouse synaptosomes and Na(+)-K(+)-ATPase activity. The potency of inhibition (IC50) for both the two parameters was linearly related to n-octanol/water partition coefficient and synaptosome/buffer partition coefficient of the test compounds. Additions of monoketones did not significantly alter the number of 3H-DHA binding sites but markedly decreased their affinity. In each monoketone, the IC50 values for 3H-DHA binding and Na(+)-K(+)-ATPase activity were generally within the same range. The anisotropy of fluorescence probe 1,6-diphenyl-1,3,5-hexatriene-labeled synaptosomal membranes was dose-dependently decreased by the monoketones, implying increased membrane fluidity. These results indicate that increasing lipophilicity of monoketones results in increased solvent penetration of synaptic membrane preparations, leading to conformational changes in membrane structure and increased ability to inhibit both neuroreceptor binding and enzyme activity. The present data confirm the importance of the lipid micro-environment of membranes in maintaining the normal functions of membrane-bound proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Physical-chemical-activity relationship of organic solvents: effects on Na(+)-K(+)-ATPase activity and membrane fluidity in mouse synaptosomes.

Physical-chemical-activity relationship of aromatic hydrocarbons (n = 10) and alkyl acetates (n = 16) with respect to their in vitro effects on synaptosomal membranes was studied. Na(+)-K(+)-adenosine triphosphatase (Na(+)-K(+)-ATPase) activity and membrane fluidity, which was determined using the fluorescence probe 1,6-diphenyl-1,3,5-hexatriene, were used as potential indicators of neuronal cell toxicity. The potency of inhibition for the enzyme (IC50), the potency of increasing membrane fluidity (IC12.5), and n-octanol/water partition coefficient (P) were all determined experimentally for 26 solvents. Correlation analyses were made on aromatic hydrocarbons and on alkyl acetates. There were linear relationships between log P and pIC50 (log1/IC50) values, and between log P and pIC12.5 (log1/IC12.5) values, indicating that the hydrophobicity of the solvents determines their toxic ability to affect membrane environment; the more hydrophobic the solvents are, the more toxic they are. A direct linear relationship between Na(+)-K(+)-ATPase activity pIC50 and membrane fluidity pIC12.5 values was also shown. This predictive correlation suggests a similar mechanism of membrane surface interaction govering both processes that are common to the test solvents. The present results confirm the importance of the lipid environment of neuronal membranes in maintaining the normal function of membrane-bound protein.

Acetates↗
PubMedDate not supplied

Variation of urinary pH and bicarbonate concentrations of students in metropolitan and rural areas of Japan.

Changes in urinary pH and bicarbonate levels were studied in urine collected before and after final examinations taken by 91 medical students (65 males, 26 females) in Tokyo and from 87 students (73 males, 14 females) in Kanazawa, a rural municipality. Bicarbonate levels and pH in the urine of students in both cities increased significantly after attending 2 h of final examinations. The highest pH value and highest bicarbonate level were 7.66 and 80.3 mM, respectively, found in the urine of a student in Kanazawa. Urinary pH and bicarbonate levels averaged 6.48 and 11.1 mM, respectively, for students in Tokyo and 6.26 and 8.91 mM, respectively, for students in Kanazawa. Given that the concentrations of carbon dioxide in the air of the classrooms in both cities increased drastically during the final examinations (i.e., from 700 ppm to 1 200 ppm in Tokyo and from 700 ppm to 1 500 ppm in Kanazawa), it appears that the increases in urinary pH and bicarbonate levels were correlated with the increase of carbon dioxide (known to be convertible to bicarbonate in blood) in the rooms. This was also supported by the increase in urinary pH and bicarbonate levels found in urine collected from 20 students who stayed in a cinema for 3 h, at which location carbon dioxide levels in air reached 1 200 ppm.

Adult↗