beta-Glucuronidase activity in liver and spleen homogenates of mice experimentally infected with Schistosoma mansoni.

A study on the beta-glucuronidase activity in liver and spleen homogenates of mice infected with an Egyptian strain of Schistosoma mansoni and of non infected control animals was carried out for a follow up period of four months. A decreased enzyme activity was observed in the spleen up to the 40th day after infection. From the 60th day on, the enzyme level in both liver and spleen was found above that in the control. The possible causes for such changes in enzyme activity are discussed.

Biochemical studies on beta-glucuronidase in the urinary bladder of normal and Schistosoma mansoni infected mice treated with hycanthone.

beta-Glucuronidase activity is elevated in the urine of patients with bilharziasis hematobium. In the present study the enzyme level was estimated in whole urinary bladder tissue homogenates of mice experimentally infected with Schistosoma mansoni. In the infected mice the enzyme activity is significantly higher than in the controls. The effect of the schistosomicidal drug hycanthone was also evaluated. Treatment with the drug did not affect the level of the enzyme activity in the infected mice; it induced an increase in the enzyme activity of the controls.

Functional capacity of the tryptophan-niacin pathway in the premenarchial phase and in the menopausal age.

Studies on the interrelationship between female hormones associated with reproduction and the vitamin B6-dependent enzymes along the kynurenin pathway of trytophan metabolism were carried out in girls with an age less, and more than 10 years (just before the onset of the first menstrual cycle), and in postmenapausal women with and without relative (excess) production of estradioll from the adrenal cortex. It is found that most of the determined metabolites are retained by the girls with age less than 10 years after tryptophan loading without and with vitamin B6 supplementation. Estradiol from either the ovaries (in girls just before menarch), or the adrenal cortex-in postmenopausal women with relative (excess) production of this hormone-interferes with the further degradation of 3-hydroxyanthranilic acid. However, this interference could be completely restored by vitamin B6 supplementation. The extra presence of a partial impairment in the kynureninase enzyme is also suggested in these postmenopausal women. In the latter case, this enzymatic activity could be partially resored by vitamin B6 supplementation. On the contrary, the enzymes: kynureninases and adrenocortical estradio. Pyridoxine supplementation partially corrected the inhibition especially that of 3-hydroxykynurenine transaminase enzyme.

The influence of sex, age, synthetic oestrogens, progestogens and oral contraceptives on the excretion of urinary tryptophan metabolites.

PIP: The excretion of urinary tryptophan metabolites was studied in normal and postmenopausal women and in women taking norethindrone and ethinyl estradiol, singly and in combination. The results showed that the altered tryptophan metabolism found in the preovulatory phase of the cycle and in postmenopausal women was the result of an interaction between Vitamin-B6 and endogenous sex hormones. During the preovulatory phase, endogenous estradiol disrupted the normal activity of the Vitamin-B6-dependent quinolinic acid decarboxylase, which resulted in the accumulation of bladder carcinogens in urine. During the postovulatory phase, endogenous progesterone and the production of metabolites antagonized this effect. Administration of naturally occurring progesterone and of ethinyl estradiol, alone and in combination with norethindrone, was able to counter the interaction between Vitamin-B6 and endogenous estradiol. It is suggested that the cyclic excretion pattern of endogenous bladder carcinogens in young, nonpregnant women may contribute, in part, to the low incidence of bladder cancer in women.^ieng