TS has been identified and measured in human urine and blood. In normal males urinary excretion ranges from 1·9 to 17 μg/24 h and in women from 1 to 4μg. Much larger amounts have been found in some patients with rare tumours of the endocrine glands. In peripheral plasma of normal men, values range from 49 to 175 ng/100 ml, and one-tenth of this value has been claimed to be present in women.
TS is secreted by the normal human testis; the concentration in spermatic vein plasma is 1 to 4 μg/100 ml, and does not rise after HCG administration. In peripheral plasma of patients with testicular feminization or adrenal tumours, and in women with masculinizing disorders TS was higher than in normals. In these cases the TS in the spermatic, adrenal and ovarian veins, respectively, was higher than in the peripheral circulation, suggesting that TS was secreted by these abnormal testes, adrenal tumours and ovaries. However, determination of TS in urine or plasma seems, for the present, to be of little help in clinical diagnosis.
Most evidence indicates that the human testis forms TS via the free steroid pathway. The low rate of conversion indicates that the testicular enzyme systems are oriented towards the preservation of T in free form, available for secretion, and it is generally supposed that TS does not serve as a reservoir for easy conversion into free T.
During pregnancy TS increases ten-fold (in maternal plasma). At delivery it is higher in the foetus than in the mother, suggesting foetal secretion of TS. T is readily sulphurylated by several foetal tissues, the adrenals especially having a much higher capacity in the foetus than in the adult. The foetal testis does not sulphurylate T, which suggests that T or some metabolite(s) remains in free form and is involved in the genital development of the human male foetus. The placenta does not hydrolyse or aromatize TS. Most TS is retained in the foeto-placental circulation, some being transferred unchanged across the placenta to the maternal compartment. Part of the TS formed in the foetus is further metabolized as the conjugate.
TS has low androgenic potency and also haemolytic properties. It binds to albumin and transcortin but not to S.B.P. and has a longer M.C.R. than T. It is not hydrolysed by several enzymes that split other steroid sulphates. Species and sex differences in TS biosynthesis and metabolism have been reported. Further information is needed on a number of points, such as whether production alters in connection with endocrine function tests, and whether there is any diurnal variation or change linked with the menstrual cycle or with increasing age. Most of the available evidence indicates that TS occurs as the 17-sulphate. But it is conceivable that the enolic 3-sulphate exists at least in the circulation. It is not yet known whether TS is present in bile. Finally, it seems that the physiological role of TS needs further investigation.
