Calcium homeostasis in untreated pulmonary tuberculosis II--dynamic study.

Oral calcium tolerance test was done for 17 normal subjects and 26 pulmonary tuberculous patients. Ingestion of 1 gm calcium did not alter serum calcium levels significantly, while urinary calcium significantly increased in normal controls (p less than 0.001) and significantly decreased in tuberculous patients. The decrease in urinary calcium in untreated TB patients may be attributed to the associated decrease in serum concentration of 25-hydroxyvitamin D. Serum PTH and nephrogenous cAMP showed insignificant changes both in controls and TB patients. Meanwhile, these changes are antiparallel to serum calcium, denoting a normal response (function) of parathyroid gland to serum calcium alterations.

Calcium homeostasis in untreated pulmonary tuberculosis. I--Basic study.

This study has been done to evaluate serum calcium, phosphorus (P), magnesium, parathyroid hormone (PTH), calcitonin (CT), and cyclic adenosine monophosphate (cAMP) in recently diagnosed pulmonary tuberculous patient, (n = 61) and the results were compared with the healthy control group (n = 22). Twenty four hours urine was collected for estimation of these electrolytes as well as cAMP. Nephrogenous cAMP (NcAMP) was calculated. Serum Ca and PTH were significantly reduced in TB groups, but CT was elevated. Serum Mg, P and cAMP as well as urinary Ca and Mg in TB groups were similar to that of the control group. Urinary P, cAMP NcAMP were increased in patient groups compared with the control. The reduced serum Ca could be due to impaired intestinal absorption of Ca, or deficient intake as a result of anorexia, decreased plasma albumin, decreased active metabolites of vitamin D or elevated CT. The rise in serum CT in TB might be due to increased CT secreted from the bronchial K-cells. Increased NcAMP might be due to the associated increase in serum antidiuretic hormone (ADH). The elevated urinary P in TB could be attributed to tissue breakdown, decreased serum PTH or increased CT.

Role of zinc in regulating the testicular function. Part 3. Histopathological changes induced by dietary zinc deficiency in testes of male albino rats.

Zinc deficiency affects the testicular tissues adversely. The testes of zinc-deficient rats showed variable degrees of degeneration compared to both control and zinc-supplemented ones. Initially, there was an early pronounced spermatic arrest followed by a series of degeneration of the cellular layers constituting the seminiferous tubules in the zinc-deficient rats. Degenerative changes were additionally demonstrated in the interstitial tissue cells of the zinc-deficient rats. These histopathological observations in testes of zinc-deficient rats run in parallel provide an additional support to our previous publications in which we recorded a significant reduction in both serum and testicular levels of testosterone in the same group of animals, since spermatogenesis in rodents appeared to depend primarily on testosterone level.

Role of zinc in regulating the testicular function. Part 1. Effect of dietary zinc deficiency on serum levels of gonadotropins, prolactin and testosterone in male albino rats.

Hypogonadism is a major manifestation of zinc deficiency in both humans and animals. In this study, we try to elucidate the main role of zinc in regulating the testicular function. Ninety male weanling albino rats were divided into three groups: control, zinc-deficient (ZD), and zinc-supplemented (ZS) groups. Six rats from each group were sacrificed every two weeks over a total period of ten weeks. Serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL) and testosterone (T) were estimated by radioimmunoassay technique. Serum zinc concentrations were also determined. Data revealed that serum zinc concentrations were significantly low in ZD group compared to both control and ZS groups. Normal FSH and LH but low PRL and T levels were demonstrated in sera of ZD group compared to both control and ZS groups. We came to the following conclusions: zinc deficiency has no effect on the pituitary gonadotropin output. Zinc deficiency affects the testicular function either directly through its effect on the testicular steroidogenesis and/or indirectly through its effect on the pituitary synthesis and/or secretion of PRL.

Role of zinc in regulating the testicular function. Part 2. Effect of dietary zinc deficiency on gonadotropins, prolactin and testosterone levels as well as 3 beta-hydroxysteroid dehydrogenase activity in testes of male albino rats.

Induced zinc deficiency in male albino rats caused a great reduction in the testicular levels of testosterone as compared to control and zinc-supplemented (ZS) rats. Estimation of the testicular levels of follicle-stimulating hormone, luteinizing hormone and prolactin (PRL) in the zinc-deficient (ZD) rats showed higher levels in comparison with both control and zinc-supplemented rats. However, the increase in PRL levels was statistically insignificant. A great reduction in the activity of 3 beta-hydroxysteroid dehydrogenase, an important enzyme involved in testosterone biosynthesis, was demonstrated histochemically in the testes of ZD rats as compared to both control and ZS ones. These results reflect a direct action of zinc deficiency on the testicular steroidogenesis and strongly support the idea that the hypogonadal state associated with zinc deficiency results mainly from some alteration in the testicular steroidogenesis or in other words Leydig cell failure.

Electrolyte concentration in semen.

Sodium and Potassium ion concentrations were determined in the semen by the atomic absorption photometry technique in three groups of infertile patients and values were compared with those of a normal control group. Comparison showed that differences are not statistically significant. Also no correlation was established between the concentration of the two electrolytes in any of the studied groups, or between electrolyte concentration and sperm motility or density.