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.

Effect of zinc supplementation on S. mansoni-infected hamsters.

Golden hamsters were used to determine whether intraperitoneal Zn supplementation can improve the outcome of infection with Schistosoma mansoni. The animals were divided into two groups; one received an initial intraperitoneal dose of Zn chloride (0.75 mg 100 g body wt.-1) followed by booster doses (0.25 mg 100 g body wt.-1) twice weekly for four weeks, the other group received no Zn supplement. After one week, when the initial and one booster doses were given, half of the animals in each group were exposed to S. mansoni cercariae for two hours using body immersion technique. After five weeks (one week after the final Zn supplement) the animals were killed, their worm burdens determined and their livers, kidneys, spleens, hearts and sera examined. There was a significant reduction in total worm counts in the Zn supplemented group (P less than 0.05). Also, Zn supplementation of infected animals protected them against the hepatomegaly which is very often associated with schistosomiasis. Spleen weight and Zn uptake were highest in the infected Zn supplemented group, indicating that this organ requires larger amounts of Zn to perform its various Zn-dependent immunological functions. The data suggest that Zn may enhance the ability of the body organs to resist some of the harmful effects of schistosomal infection.

The relationship between serum carnitine levels and the nutritional status of patients with schistosomiasis.

Serum carnitine levels were investigated in a group of normal adults and two groups of patients with active schistosomiasis who also showed signs of malnutrition and vitamin deficiency. The first group consisted of 16 patients with Schistosoma mansoni and/or Schistosoma haematobium infection. They received an adequate diet supplemented with vitamin and iron therapy and received no treatment for their parasitic infection till their hemoglobin levels were restored to normal. The second group consisted of 12 patients with schistosomiasis as well as intestinal polyposis. They received the same diet as the first group but because of their poor condition were immediately treated for parasitic infection. Results showed that both groups of patients had subnormal levels of serum carnitine with the polyps patients (Group II) having a significantly lower level than patients with simple schistosomiasis (Group I). After nutritional repletion a significant increase was observed in the carnitine levels of most patients in group I indicating a relationship between the nutritional status of the patients and their serum carnitine levels. The patients with polyps also showed considerably increased carnitine levels after treatment and dietary repletion. The usefulness of serum carnitine measurement as an index of protein malnutrition in man is discussed.