SUMMARY Androgen synthesis after administration of cadmium chloride to rats has been studied histologically, histochemically and biochemically. Incubation in vitro of testicular tissue removed 10 days after cadmium administration revealed markedly decreased testosterone synthesis. After 100 and 150 days, testosterone synthesis in vitro had increased progressively and significantly, but there was a marked decrease in the testosterone: androstenedione ratio. Surviving Leydig cells, giving typical histochemical reactions for 3β-, 16β- and 17β-hydroxysteroid dehydrogenase, were observed under the tunica albuginea immediately after cadmium poisoning. Fifty days after the cadmium treatment, mesenchymal cells, giving a histochemical 3α- and 16α-hydroxysteroid dehydrogenase reaction, but no other hydroxysteroid dehydrogenase reaction of normal Leydig cells, grew into the testes from the tunica albuginea. Weight, citric acid and fructose contents of seminal vesicles of cadmium-treated rats fell nearly to castration levels, but showed some degree of recovery thereafter. Studies in vitro on adrenal tissue from cadmium-poisoned rats suggested that the rate of testosterone biosynthesis from pregnenolone was increased.

Accumulation of 99m Tc-Sn-pyrophosphate in pleural effusions has been evaluated in 56 patients grouped as follows: 8 with bacterial effusion (Group A), 27 with malignant effusion treated by local and/or parenteral antitumor chemotherapy (Group B), 21 with malignant effusion treated only by supportive therapy (Group C). Results, expressed as effusion to plasma PPi ratio, ranged from 0.1 to 0.28 in group A, from 0.04 to 0.64 in group B and from 0.60 to 1.73 in group C, with significant differences among the three groups. In no case was uptake found in cells of the sediment. Chemical analysis (including total and ionized calcium, total protein, acid and alkaline phosphatase) of plasma and exudate in neoplastic patients showed a slight, but significant, difference between groups B and C as regards plasma-effusion gradient for total calcium and acid phosphatase. Negative correlation also exists between effusion to plasma PPi ratio and plasma-exudate gradient for ionized calcium in neoplastic patients. The data support the hypothesis that acid phosphatase content and calcium gradient are among the factors involved in the mechanism of PPi accumulation in pleural effusions.

A method is described for the quantitative determination of 131I-triiodothyronine and 131I-tetraiodothyronine in human plasma after oral administration of 131I-iodide. Steps in the method are: acidified n-butanol extraction of the thyroid hormones from the plasma deprived of inorganic iodine by means of an ion exchange resin; addition of stable iodo-aminoacid carriers to the butanol extract and its evaporation to dryness under reduced pressure; bidimensional thin layer chromatography of the rediluted extract on cellulose in combined organic alkaline and organic acid systems; staining of the carriers with eerie sulphate-sodium arsenite reagent and diluted methylene blue; radioactivity measurements of the cellulose scraped from the stained spots in a well type scintillation counter. The reliability of the method was established by recovery experiments and by duplicate chromatography of plasma to which mixtures of 131I-T3 and 131I-T4 and 131I-iodide were added. Its specificity was confirmed by autoradiography. Good agreement was found with the results yielded by simultaneous paper chromatography of the same extracts. The method requires smaller amounts of plasma and allows quicker determinations than paper chromatographic procedures. Relative determinations of 131I-T3 and 131I-T4 are reported in some euthyroid and hyperthyroid patients given therapeutic and diagnostic doses of 131I-iodide.

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