Zinc, copper and selenium in reproduction

Abstract

Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.

Endocrine disruptor & nutritional effects of heavy metals in ovarian hyperstimulation

“…Zinc acts as a co-factor for enzymes promoting DNA transcription and protein synthesis [32], has a role in expression of steroid hormone receptors [33] and has anti-apoptotic [34] and anti-oxidant properties [35]. Studies have demonstrated that a zinc deficiency can lead to subfertility and abnormal reproductive outcomes [36], and to pregnancy complications [37,38]. However, previous studies have failed to confirm a role for zinc in human infertility or the response to fertility treatments.…”

Testicular apoptosis after dietary zinc deficiency: Ultrastructural and TUNEL studies

“…Zinc affects different aspects of mammalian reproduction [Dissanayake et al 2009;Björndahl and Kvist 2010]. Low zinc intake by young males of several species including humans, interferes with normal sexual development [Bedwal et al 1991;Saxena et al 1993;Bedwal and Bahuguna 1994;Kaji 2001;Dissanayake et al 2009] and leads to gonadal dysfunction. Zinc also plays an essential role in the synthesis and secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin, gonadal differentiation, testicular steroidogenesis, and genetic expression of steroid hormone receptors [Bedwal et al 1991;Bedwal and Bahuguna 1994;Ali et al 2007].…”

The placenta as a barrier for toxic and essential elements in paired maternal and cord blood samples of South African delivering women

“…[11][12][13][14] Furthermore, zinc, copper and selenium are essential for reproductive processes. 15 Therefore, the ability of the placenta to transfer nutrients and toxicants alike is of concern in relation to foetal development and health. 16 In most cases, the same processes that aid transport of nutrients through the placenta, may also act as the pathways for toxic elements, especially if these have chemical similarities with the nutrient metabolites, or simply because of passive diffusion.…”