Untrained healthy male volunteers were subjected to the study of the effects of physical exercise (bicycle ergometer, 150 W for 30 min) upon the activities of aspartate aminotransferase (AST [GOT]) isoenzymes, soluble and mitochondrial (AST-s and AST-m) with and without reactivation by the co-enzyme pyridoxal 5'-phosphate (PALP) in plasma. Blood samples were drawn at the beginning and end of the exercise periods and then 20 min, and 1, 6, 24 and 48 hours later. There was a marked increase in AST-m activity with reactivation by PALP immediately after the exercise, whereas AST-s activity activated with PALP did not vary substanti-ally. Inversely, a significant increase in AST-s activity with PALP added was observed at 48 hours after the exercise, but not in AST-m with PALP added. The changes in the effects of PALP on the activities of AST isoenzymes after physical exercise are discussed.

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Physical examinations of peripheral circulation and vibratory sensation were undertaken on 120 postal workers in S. and N. Prefectures and 61 in G. Prefecture. The items measured were skin temperature of the finger, the nail press test and vibratory sense threshold. The differences in the values of peri-pheral circulation and vibratory sensation obtained by the cooling load test between the groups using motorcycles and those using only bicycles or working indoors were often found to be statistically significant. On the whole, the disorders in peri-pheral circulation and vibratory sensation were severe in the group with waxy white changes in the fingers.
It is reported that the maximum vibration acceleration level on the handle bars of motorcycles on paved roads exceeds the exposure guidelines of the ISO. Thus, it may be suggested that mailmen's vibration hazards induced by motorcycle riding are widespread in our country.

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Following World War II, mechanized tools utilizing compressed air, electric motors and gasoline engines were introduced in various industries in Japan in order to achieve higher productivity and reduction of labor. Accordingly, many vibration hazards began to present themselves. In 1947, the Japanese Ministry of Labor recognized vibration hazards as an occupational disease. However, until the vibration hazards induced by using chain saws in national forestries became a serious social problem in 1965, no preventive measures were taken.
In 1975, the Ministry of Labor decided to apply "the guidelines for counter-measures against vibration hazards" to six industries. Moreover, 1977, it allowed workers using 18 sorts of mechanized tools involving vibration exposure to seek protection under labor insurance regulations.
In order to promote the countermeasures against vibration hazards, the Japan Association of Industrial Health organized "The Committee on Vibration Haz-ards" in 1977, and its activities continued for three years. This report is con-cerned with the studies of which the authors took partial charge among various committee projects. It has become clear that the extent and scope of present local vibration hazards in Japan, which were surveyed through case and epide-miological reports, as well as vibration and noise measurement, are extremely large.

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Hematological and biochemical changes were studied in pregnant and nonpregnant rats that had been given drinking water containing 5 ppm of lead for 23 days. Pregnant and nonpregnant rats administered distilled water served as controls. The red blood cell count, packed cell volume and hemoglobin con-centration were significantly decreased in the pregnant rats, but there were no significant differences in these values between the control and lead-treated groups. Erythrocyte delta-aminolevulinic acid dehydratase (ALAD) activity was significantly reduced in the lead-treated pregnant rats. There was no significant difference in liver AL AD activity between the control and the lead-treated groups, whether pregnant or not. The concentration of blood lead (Pb) ranged from one to three, μg/100 ml in the nonpregnant rats and from three to eight μg/100 ml in the pre-gnant rats. A statistically significant negative correlation between erythrocyte AL AD activity and the blood Pb level was observed only in the pregnant rats. These results indicate that the response level of lead on erythrocyte AL AD activity may be much lower than that on changes in the concentration of blood Pb during pregnancy and empasized that special attention should be paid to avoiding exposure of expectant mothers to lead even at a low level.

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Differences in the amount of δ-aminolevulinic acid dehydratase (AL A-D) as determined by radioimmunoassay, hematology, and body weight increase were observed between infant and adult rats after lead treatment. Administration of the lead through drinking-water containing 25 mM lead acetate resulted in an in-crease in blood lead contents in both infant and adult rats to almost the same degree. The influence of lead on the body weight, however, was significant only in infant rats, with a reduction in body weight to 70% of the controls. The in-crease in AL A-D content of peripheral erythrocytes of infant rats (about 4 times that of the controls) was more marked than that of adult rats (about twice that of the controls). A possible explanation of this difference is that, in the case of adult rats, the increase in the amount of AL A-D is due to increased synthesis of the enzyme in bone marrow cells, while the increase of the enzyme in infant rats results from anemia with increased numbers of young erythrocytes in the peri-pheral blood in addition to the increased synthesis of ALA-D. The findings sug-gest that rapid growth during the infant stage prevents the hematological com-pensation for the effect of lead, resulting in anemia and marked increase in the amount of ALA-D. It was found in the present study that the European Stand-ardized Method is not suitable for AL A-D assay in exposure of rats to lead.

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The microsomal fraction (pellet: 105, 000 x g for 60 min) from the livers of rats poisoned with CCl₄ showed uncoupled normal mitochondrial oxidative phos-phorylation in vitro. The supernatant fraction (105, 000 × g for 60 min) antagonized the uncoupling action of the microsomal fraction and stimulated the respiratory control of mitochondria caused by central depression of state 4 respiration.

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Cd (10 mg/Kg of body weight) uncoupled the oxidative phosphorylation of liver and kidney mitochondria in vivo. MgC1₂ administered intraperitoneally immediately after injection of Cd into rat had protective effect againrt uncoupling dysfunction of liver mitochondria, but did not against uncoupling dysfunction of kidney mitochondria in vivo. A similar phenomenon was observed in vitro.

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Molybdenum and copper when administered to animals are known to accumulate predominantly in liver, causing identifiable toxic effects on enzyme systems. Since, molybdenum and copper are known as antagonists, effects of their combined treatment have been described in the present investigation taking enzy-mes of key importance viz. alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, 5-nucleotidase, esterases and cholinesterase in the liver of rat, Rattus rattus albino. Comparison of controls with the combined effects revealed an in-crease in the activity of enzymes studied, however, some remarkable differences in their topography were observed. Antagonistic behaviour of molybdenum and copper at the enzymological level has been explained on the basis that copper becomes unavailable through interaction with molybdate to form either cupric molybdate or copper thiomolybdate which is ultimately excreted. The results have further been interpreted in terms of combined effects of molybdenum and copper on cel-lular organelle, levels of enzyme protein and microenvironment of the hepatic parenchyma.

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Mutagenicity of the urine extracts of the rats to which either o-tolidine or Evans Blue, an o-tolidine-based azo dye, had been orally given was assayed in the Salmonella/mammalian-microsome test. The urine extracts obtained from the rats treated with o-tolidine showed stronger mutagenicity than o-tolidine itself. While Evans Blue did not show mutagenicity at all, the urine extracts derived from the substance were found mutagenic. Both 3, 3'-dimethyl-N-acetylbenzidine and 3, 3'-dimethyl-N, N'-diacetylbenzidine were identified as urinary metabolites of o-tolidine. They were found not only in the urine of the rats treated with o-tolidine but also in the urine of the rats to which Evans Blue had been orally administered. The experimental results suggest that the accidental intake of biphenyl-based dyestuffs through the mouth should be cautiously avoided. Some aspects of the metabolism of o-tolidine and Evans Blue are discussed along with the problem associated with the mutagenic activities of the o-tolidine metabolites.

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Di-isopropylnaphthalenes (KMC) and 1-phenyl-1-xylyl-ethanes (SAS) have been widely used, especially in non-carbon paper (pressure sensitive copying paper), since 1971 in place of PCBs. The toxicity of the solvents has been studied as one of the national special studies in Japan. First, in 1972, distribution and disappearance in the living body was investigated in rats. Although a little ac-cumulation of the substances was observed in the fat after a single oral dose, it was later found that continuous oral administration for a month caused no ac-cumulation in the other organs. Accumulation in the liver, blood, kidneys and brain was not observed. In experiments in vitro, furthermore, the substances were found to be decomposed by liver homogenate. The rates of decomposition of all components of KMC were similar, but the rates for SAS were not. The rate for 1-phenyl-1-orthoxyly1-ethane was larger than that for 1-phenyl-1-metaxyly1 ethane.

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An assay method for the determination of dopamine, norepinephrine, serotonin and all metabolites of these biogenic amines in the rat striatum or hypo-thalamus was developed using a high-performance liquid chromatograph connected to an electrochemical detector. Among amines and metabolites, catechol com-pounds were purified by alumina adsorption and non-catechol compounds were ex-tracted by ethyl acetate. Two-and-a-half pmole or lower detection limits and a linear relationship between the amounts and peak areas ranging from 2.5 to 10, 000 pmoles were obtained for all substances. The results of the administration of haloperidol and U-14, 624 to rats supported the validity of the present assay method.

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The sequential two-phase extraction technique (5 mL CS₂ extraction followed by 10 mL water extraction) was applied to the determination of methanol and/or toluene on carbon felt in a passive diffusion dosimeter. The loading amount of methanol increased linearly as the exposure intensities increased in cases of exposure at around the current permissible concentration for four hours. It was also observed that the loading amount of methanol was lower than its the-oretical value. The spontaneous desorption rate of methanol from carbon felt was high enough to explain its low recovery. In the mixed vapor exposure to toluene at 150 ppm and methanol at 350 ppm, the adsorption rate of methanol decreased to 80% of that observed in the exposure to methanol only, and spont-aneous desorption was accelerated. These two suppressive effects of toluene could result in the low amount of methanol in the mixed exposure to toluene and meth-anol. Spontaneous desorption of toluene from carbon felt was not detected after eight hours of exposure to fresh air or methanol. Adsorption of toluene was not affected by co-existing methanol either. The applicability of carbon felt dosimetry to methanol monitoring was validated insofar as a single exposure to methanol is concerned, even when the concentration is fluctuating, while generalized applic-ability should be restricted especially in cases of exposure to combinations of methanol and non-polar substances.

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