The present study examines the absorption and excretion of chlorella cadmium-binding protein (Ch-CdBP) in rats incomparison to the same functions for inorganic cadmium. Ten daily administrations of inorganic cadmium, significantly curbed increases in body weight but the same number of oral administrations of Ch-CdBP.
Cadmium accumlations in the liver, kidneys and spleen were smaller in rats given Ch-CdBP than in those which had received the cadmium. Cadmium concentration in blood maximized 60min after one oral dose, but it did not change significantly after Ch-CdBP administration.
Cadmium excretion in urine was more rapid and the amount much greater when Ch-CdBP had been administered than when cadmium had been administered.

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In an effort to clarify the mechanism underlying stress-induced hyperuricemia, rises in uric acid in the plasma of rats which had been subjected to immobilization stress were investigated. Two types of stress were investigated-fixation in a supine position for 3mins and immobilization in a Ballman cage for 6mins.
Immobilization in a supine position caused immediate increases of up to 400% in uric acid levels. This hyperuricemic response could be enhanced slightly by pre-treatment with propranolol, or depressed to approximately 50% that of the control level with phentolamine, or to 60% by adrenal demedullation. In demedullated rats, although hexamethonium markedly inhibited the rise of uric acid, it did not eliminate it entirely. Neither phentolamine nor atropine had any significant effects. Such results indicate that two different mechanisms are involved in the hyperuricemic response-the adrenal epinephrine-dependent reaction mediated via α-receptors, and the epinephrine-independent reaction in which autonomic nerves other than the adrenal medulla might be involved.
The uric acid levels in the liver markedly increased in response to stress, however those in other tissues did not change. As with changes in plasma, increases in liver uric acid went only as far as 60% of the levels of the control group after adrenal demedullation. These results support the view that the stress-induced increases of plasma uric acid levels are due to raised production of uric acid occurring only in the liver.
Stress did not cause changes in liver adenine nucleotides-ATP, ADP and AMP. Although tissue lactate levels had increased following stress, they did not parallel changes in tissue uric acid, which may exclude the possibility that increased dproduction of liver uric acid is caused by decreases in adenine nucleotides or by non-specific effects, such as tissue hypoxia.
Immobilization in a Ballman cage did not raise the levels of uric acid in plasma. However, after treating rats with phentolamine, the amount of plasma uric acid doubled after stress. Propranolol had no such effects. In demedullated rats, stress failed to cause increases in uric acid even after phentolamine-treatment. It can be concluded therefore that the hyperuricemic response is caused by adrenal epinephrine and that in sharp contrast to the stress caused by immobilization in a prone position, the action of epinephrine is mediated via β-receptors.

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To determine the effects of chronic exposure to nitrogen dioxide (NO₂) on arterial blood pHa, PaCO₂ and PaO₂, rats were exposed continuously to concentrations of 0.04, 0.12 and 0.4ppm for 6, 9 and 18 months. Heart rate (HR), respiratory rate (RR), blood hemoglobin (Hb), arterial blood pHa, PaCO₂ and PaO₂ were examined. The respiratory rates of rats exposed to 0.4ppm were at levels 104-106%, of those controls but this difference was not significant. Rats exposed to 0.12ppm for 6 months had significantly lower HR's, but in rats exposed to 0.4ppm NO₂ for 18 months, the HR's were significantly higher than those of controls. Hemoglobin levels were identical. Arterial blood PaO₂'s in rats exposed to 0.4ppm NO₂ for 9 or for 18 months were significantly lower than those of the controls, but the PaO₂'s in rats exposed to 0.12ppm NO₂ for 9 or for 18 months and those of the control group were identical. From the results, it is clear that in rats hypoxemic conditions can be caused by long-term low level exposure to NO₂. The relationship between NO₂ concentration and exposure period can be calculated from the hypoxemic condition as well.

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Whole-body retention of ⁵⁴MnCl₂ after a single oral administration in rats of various ages was investigated. In adult rats, 0.3% of the dose was retained at 14 days, whereas new-born and suckling rats had higher retention rates than adults; these rates decreased sharply after weaning.
⁵⁴MnCl₂ was administered through the tail veins of pregnant rats between the 13th and 20th days of gestation in order to study the relationship between age and ⁵⁴Mn intake. The rat conceptus and individual portions (the placenta, fetal membrane, amniotic fluid and fetus) were sampled periodically from each group. Placental ⁵⁴Mn concentrations were slightly less when administration was in the later stages of pregnancy, but concentrations in the fetal membrane and amniotic fluid were relatively low and did not seem to vary on the basis of stage of gestation. For example, the values for 15-day pregnant rats increased from 0.2% of the initial dose 2 days after administration to 0.4% of dose on the sixth day.
⁵⁴MnCl₂ was administered intravenously to 8-, 14- and 20-day pregnant rats. In order to study the ⁵⁴Mn transferred through the placenta and mother's milk, the“foster mother method”was adopted using the following three groups: 1) Sucklings born of and nursed by contaminated mothers received ⁵⁴Mn through both the placenta and milk. 2) Sucklings born of contaminated mothers but nursed by controle foster mothers received only transplacental ⁵⁴Mn. 3) Sucklings which were born of control mothers but nursed by contaminated foster mothers received ⁵⁴Mn only from milk. Transplacental ⁵⁴Mn in 8-, 14- and 20-day pregnants was 0.3, 0.9 and 1.3% of initial dose, respectively. The result showed the effect of the gestation age at the dosing on the transplacental ⁵⁴Mn. It was observed that 0.4-1.4% of initial dose of ⁵⁴Mn were transferred to sucklings via milk. The amount of milk transfer ⁵⁴Mn in sucklings was dependent on the gestation age at the time of dosing.

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Dogs were exposed for one hour to trichloroethylene at concentrations of 700, 1, 500 and 2, 000ppm. Metabolite (trichloroethanol (F-TCE), trichloroacetic acid (TCA) and total trichloroethanol (T-TCE)) changes in serum and urine were measured from the beginning of exposure until one hour after termination. Particulary, in 700ppm exposure group, other dogs were exposed for two hours to trichloroethylene and these metabolites were mesured in urine and in serum. These two groups were compaired with each other.
The results were as follows.
1. Trichloroethylene metabolites in serum and in urine correlated significantly with trichloroethylene concentration, and with absorption by the lungs, respectively.
2. Renal excretion rates of metabolites were T-TCE, TCA and F-TCE in order of highest to lowest.
3. The percentage of trichloro-compounds in the urine to total trichloroethylene absorption by the lungs was about 0.7% at one hour following the termination of exposure.
4. Ninety and 120 minutes of the beginning of exposure, trichloroethylene metabolites in serum and urine of the group being exposed were lower than those group where exposure had been terminated.

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Epidemiological surveys of asymptomatic gallstones were conducted in the towns of N (Aichi Prefecture) in 1980-1981 and S (Gifu Prefecture) in 1981. Of the 2, 321 people and the 1, 308 people (aged 30-65) in N and S town respectively, 1, 861 (827 males and 1, 034 females) were examined in the former and 1, 074 (486 males and 588 females) in the latter. This is a response rate of 80.2% for N and 82.1% for S. Examinations included anthropometric measurements, urinalysis, electrocardiography, serum lipids concentration, funduscopy and ultrasonography. Ultrasonography validity tests, performed on 213 people with clinically confirmed gallstones, gave sensitivity and specificity rates of 97.9% and 98.8%, respectively.
Fifty-one out of the 2, 936 respondents had gallstones; all but two cases of which were asymptomatic gallstones. The overall prevalence of asymptomatic gallstones, was 0.5% for males and 2.7% for females, and the latter had a higher rate in each town. Gallstone rates were higher in N than in S, particularly in the ages over 40's, but were much lower than those found in Japanese urban areas. In order to evaluate the epidemiological characters of asymptomatic gallstones, a case-control study was attempted. Cases with asymptomatic gallstones were compared to people randomly selected, but matched by age, sex and residence, from the 2, 831 control subjects without any episodes of gallstone. Two respondents who had previous episodes had currently showed no clinical symptoms, were included above. Self-administered questionnaires provided information on previous illness, family history, current health status, and personal habits such as smoking, drinking and diet. Biochemical and physiological data, e. g. serum lipid concentration and electrocardiographic findings were compared.
Matched analysis demonstrated higher mean serum triglyceride concentrations and earlier menopause in those with gallstones.

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The amount of zinc in human and cow's milk was evaluated in in vitro experiments using gel chromatography on Sephadex G-75 to simulate the action of gastrointestinal enzymes. The HCl-peptic digestion of both types of milk demonstrated that most of the zinc eluted at the same position as Zn(NO₃)₂. The sequential digestion of both types of milk by pepsin and trypsin demonstrated that most of the zinc eluted at a position corresponding to a molecular weight slightly less than 12, 000. The results suggest that zinc may be liberated in the stomach and that when the pepsin-digested milk passes into the duodenum, which has an alkaline pH and where trypsin is secreted, zinc may bind to substance (s) formed during intestinal digestion. There was no difference between the elution profiles of the two kinds of milk. This indicates that differences in zinc availability in human and cow's milk is not responsible for the molecular weight of zinc-binding substances.

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Lead was initially transmitted through mother's milk until weaning, then was mixed directly into the diet of the experimental animals after weaning. The effects on rats of post-natal indirect exposure to low levels of lead were evaluated based on locomotor activity, body weight, and time-dependent changes in lead concentration. Throughout the experiment, there were no deaths due to lead exposure, but growth was slightly retarded.
Locomotor activity levels were measured daily from the date of weaning until the 56th day. Time-dependent changes of lead-treated rats were significantly lower than those of controls matched by age (p<0.01).
The mean lead concentrations in the blood of treated rats reached a maximum of 336.7μg/100g at 14 days, in the brain of 111.4μg/100g at 21 days, in the liver of 698.6μg/100g at 7 days, and in the kidneys at 793.2μg/100g at 14 days. All of the above concentrations decreased steadily until the 56th day. Although lead poisoning is thought to induce several serious behavioral problems, a causal relationship between lead ingestion and behavioral dysfunction has not been demonstrated here.

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Use of the rapid lowering of age of maximum increment in height (MI age) in Japan after the World War II has permitted investigation of how changes in nutritional levels relate to the acceleration of growth. MI age calculations were based on the Annual Statistical Report of the School Health Survey published by the Ministry of Education. Data on nutritional level were derived from the National Nourishment Situation produced by the Ministry of Health and Welfare.
The results were as follows:
1) Similar tendencies towards lowered MI ages are seen for intake of nutrients (fats and oils, carbohydrates, calcium, and vitamin B₂), intake of eggs by food groups, energy supply-ratios from cereals and from starchy foods.
2) Time lags are read on time lag analysis as 17-22 years at the maximum correlation coefficient observed between each birth-year cohort and the greatest portion of nutritional changes. The nutritional level for the group 17-22 years of age over MI age closely corresponded with the MI age.
3) It is therefore difficult to affirm that change in nutritional level is an indicator of MI age, but social changes in Japan including economic development have presumably brought about changes in the diet and simultaneously caused the acceleration.

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