The action of various metals on calcium metabolism is described in this review. Some metals have a toxic effect on calcium metabolism and its related bone metabolism in mammalian systems. Especially, lead induces hepatic calcium accumulation that is not caused by other heavy metals. This mechanism is based on the action that lead stimulates the mobilization of calcium into blood from bone ; thus lead-induced hypercalcemia stimulates secretion of calcitonin, and hormone causes accumulation of calcium into liver cells. Tin induces calcium accumulation in renal cortex, due to the action that tin increases calcium-binding protein in the cytosol and inhibits Ca-ATPase in the plasma membrane. Such phenomenon is not observed in other metals. Moreover, tin inhibits intestinal calcium transport and increases bile calcium excretion, resulting in hypocalcemia. Zinc produces hypocalcemia, based on the stimulation of gastric calcium secretion mediated through the action of acetylcholine, and the hypocalcemia induces bone resorption related to parathyroid hormone. Cadmium inhibits the stimulation of intestinal calcium transport due to 1, 25-dihydroxy vitamin D₃. Also, cadmium directly causes both prevention of bone calcification and stimulation of bone resorption. On the other hand, aluminium is accumulated into bone and reveals a porotic effect. Lithium or manganese causes hypercalcemia. Copper inhibits bone resorption. However, the mechanism of action of these metals is not clarified. Thus action of metals is important as the toxic effect of metals, since disorder of calcium metabolism affects on some physiological functions.

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In order to investigate the relation between growth and aflatoxins production of Aspergillus parasiticus on solid foods or plant materials, powdered plant materials were used as media for cultivating this aflatoxinogenic strain. Cultivation was carried out under 100% humidity, resulting in active fungal growth and aflatoxins production. Experiments were carried out on 13 types of plant materials, and it was found that the fungus grew actively on powdered plant materials containing large amounts of glucides or lipids. The production of aflatoxins was especially active in the latter media containing lipids. However, in Castor seeds, in spite of rapid fungal growth (as in the other samples rich in lipids), aflatoxins production was remarkably low. Some chemical constituents in Castor seeds may inhibit aflatoxins production.

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The distribution of copper in selected tissues and the metabolic interaction of copper with other essential metals were determined after oral administration of cupric carbonate, basic, and the results were compared with those of cupric sulfate. Male Wistar rats were orally administered for 2, 5, and 11 d with 0.5 mmol/kg of cupric compounds. Distribution of copper and change in essential metal levels were quantified by atomic absorption analysis. In the case of cupric carbonate, the copper was much more distributed in tissues, especially in the liver, than in that of cupric sulfate. Copper level increased progressively in mitochondria-lysosomal fraction of the liver in proportion to the period of administration. In the 105000g supernatant fraction, copper was distributed in metallothionein fraction rather than in superoxide dismutase fraction which had been considered as copper storage protein. The administration of cupric compounds resulted in an increase of zinc level in the liver, kidney, and spleen, preferentially in metallothionein fraction of the liver, but it seemed to affect little on iron metabolism.

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Colorimetric determination of vanadium in foods with N-cinnamoyl-N-(2, 3-xylyl) hydroxylamine (CXA) was studied. Vanadium was extracted effectively with CXA in C₆H₆ from 1-4N HCl acidic solution of digested sample. This reagent proved to be more sensitive and more selective than both of N-benzoylphenylhydroxylamine and N-benzoyl-o-tolylhydroxylamine which have been recommended as a chelating reagent for colorimetric determination of vanadium. By using CXA, vanadium in various foods could be determined with the recovery of 91.2-103.2% and the coefficient of variation of 2.0-5.5%.

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Fluorometric determination for hydrogen peroxide based on the formation of thiochrome was studied. Thiochrome is oxidation product of thiamine and gives intense fluorescence. Though bromine cyanide or pottasium ferricyanide has been generally used as oxidizing agent of thiamine, it was proved that hydrogen peroxide was useful as oxidizing agent. Then, hydrogen peroxide can be determined from the quantity of produced thiochrome. The analytical procedure was as follows ; to a sample solution containing a proper quantity of hydrogen peroxide, 1 ml of thiamine (30μg/ml), peroxidase (10 units/ml), and sodium hydroxide solution (20%) were added. The mixture was stood for 30 minutes at room temperature and saturated with sodium sulfate. Ten ml of isobutanol was further added and shaken to extract thiochrome produced here. Fluorescence intensity of the separated isobutanol after treatment with sodium sulfate was measured (λEx ; 375 nm, λEm ; 430 nm). The calibration curve was linear up to H₂O₂ 0.2μg/tube. On the basis of the proposed method, remaining hydrogen peroxide in Japanese noodle (udon) could be determined with the recovery of 90.6% and coefficient of variation of 1.1%.

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Four unconjugated metabolites of 2-isopropylnaphthalene (2-IPN) were identified by thin-layer chromatography and gas-liquid chromatography (GLC) from the bile of rats receiving 2-IPN orally ; they were 2-(2-naphthyl) propionic acid, 2-(2-naphthyl)-2-propanol, 2-(2-naphthyl)-2-hydroxypropionic acid, and 2-(2-naphthyl)-1, 2-propanediol, together with the unchanged compound. The presence of glucuronides of these four metabolites was also suggested by GLC of the extract obtained after hydrolysis by β-glucuronidase. In addition, quantitative determination of the metabolites indicated that the total urinary and biliary excretions of these metabolites in 24 h after administration were about 23% and about 18% of the dose, respectively, and that the urinary and biliary metabolite excretion patterns were the same.

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