A thirty days' balance study of cadmium and the cadmium ingestion experiment was carried out in two adults living in Tokyo, Japan. The mean daily amount of cadmium ingestion from foods and beverages were 48.18±7.89 (conc. 0.0203±0.00304 μg/g) and 46.92±7.17 μg/day (conc. 0.0181±0.00222 μg/g) for the two subjects. The mean daily excreted amount of cadmium in feces were 35.92±10.02 and 35.95±6.68 μg/day. The mean daily excreted amount of cadmium in urine were 4.23±0.77 and 3.68±0.87 μg/day for the two. The rates of not recovered cadmium ingested to feces were 23 to 26% in the both experiments. The other sources of intake, cigarette smoking and respiration, and the other routes of excretion, moustache, hair, nail, sweat and desquamated epidermis, were also discussed and tentative balance sheets of cadmium were presented.
The activity of 5-aminolevulinate hydro-lyase (ALAD) in blood decreases in lead-exposed subjects. The activity of the hemolysed blood is restored by heat treatment (60°C, for 5 min) almost completely. A parameter of "activity ratio", dividing the enzyme activity before heat treatment by that after heat treatment, is proposed for evaluation of lead exposure, and this ratio was calculated in 167 human subjects, including those exposed to lead in work, lead concentration in their blood ranging 3.5 to 82μg/100 g blood. Correlation of the ratio against blood lead concentration was higher than that of the ALAD activity itself. As there are, in addition, subjects with lower-than-normal ALAD activity values regardless of lead exposure, the ratio is available as an index to evaluate the extent of lead exposure.
I describe a fluorometric micromethod for determining delta-aminolevulinic acid dehydratase (ALA-D) activity in whole blood. In this method, the porpho-bilinogen formed under the incubation condition using 0.05ml of whole blood is easily converted to uroporphyrin by heating for 15 min at 100°C in an acidic medium in the presence of air. The uroporphyrin formed is a stable and highly fluorescent substance and its fluorescence intensity is measured using a spectrofluorophoto-meter. The ALA-D activity is expressed as nanomoles of uroporphyrin formed per hour per milliliter of erythrocytes. This method offers some advantages that it is much sensitive and is employed without Ehrlich's reagent. The erythrocyte ALA-D activity measured by the fluorometric method has a good correlation with that measured by the colorimetric method with Ehrlich's reagent (r=0.9484).
The β2-microglobulin levels of serum and urine in some diseases: (I) kidney malfunction, (II) nephrosis and nephritis, and (III) other diseases were measured. Serum level in the group (I) was found to be abnormally high. The patients who were treated with artifical dialysis had the extremely high levels. The serum and urinary levels seem to increase slightly in the group (II). In the group (III) the serum level in the cirrhosis of liver was found to be high. As shown for the references, serum levels in the malignant diseases were similarly observed to be moderately high.
Rats were rendered iron deficient by maintaining them on iron deficient diet. Manganese chloride (15 mg/kg) was administered intraperitoneally daily for 15 days to these rats. Morphological studies in the brain tissue showed neuronal degener-ation scattered in the cerebral cortex. Manganese produced marked enzymic alter-ations in the brain of iron deficient rats as compared to similar treatment to rats fed on normal diet. Marked morphological and enzymic alterations in the brain of manganese treated iron deficient rats appear to be due to greater accumulation of the metal in brain tissue of these animals as compared to controls. It may, therefore, be suggested that workers in manganese industry should be checked frequently for iron deficiency as a prophylactic measure.
The effect of various concentrations of hydrogen sulfide gas on the activities of rat lung enzymes was tested in vitro using a simple gas bubbling method. Adenosine triphosphatase, acid phosphatase, alkaline phosphatase, glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase activities were inhibited. Various levels of the gas increased arginase activity while fructose 1, 6 diphosphate aldolase activity remained unaffected.
Male rats were given 5 mg/kg of lead intraperitoneally and after an interval of 3 days were given 50 mg/kg of lead intraperitoneally. The distributioh of lead in the body after receiving challenge dose of lead was compared with that of rats non-pretreated with lead. Lead contents of each organ, especially that of liver, of the pretreated rats were found to be reduced. The rate of lead content in nuclei fraction, where lead taken into liver mainly concentrated, to lead content in liver was significantly low in rats pretreated with lead compared with non-pretreated rats after challenging. The rate of lead content in other fractions of liver to lead in liver of pretrerted rats rose from that of non-pretreated rats. From these results, it was recognized that the pretreatment remarkably changes the lead distribution in body and in liver.
It has been reported that phenobarbital produced a reduction in mortality in acute cadmium poisoning of mice and also remarkably accelerated cadmium ac-cumulation in the liver. In the present study, the cadmium distribution and metallothionein induction in the liver after injecting cadmium in mice treated with phenobarbital was examined. Phenobarbital concentrated cadmium in the super-natant fraction of the liver, but diminished it in the nuclei fraction. No difference in cadmium content was found in mitochondria and in microsome fractions between mice treated with and without phenobarbital. The amount of cadmium contained in metallothionein fractions in the liver increased slightly after cadmium injection in mice treated with phenobarbital, and only a trace amount of cadmium bound to metallothionein fraction in the liver was found when cadmium was added in vitro to a supernatant solution of the liver of mice treated with phenobarbital. When these results are compared with the results in rats pretreated with a small dose of cadmium, it is evident that metallothionein induction alone does not explain completely the acceleration of cadmium accumulation in the liver. The result of the present experiment suggests a mechanism other than induction of metallothi-onein to explain the effect of phenobarbital on cadmium distribution.