Copper is essential to the proper functioning of organs and metabolic processes and is vital to the health of all living things (humans, plants, animals, and microorganisms).
The human body has complex homeostatic mechanisms which attempt to ensure a constant supply of available elements like copper. However, like all essential elements and nutrients, too much or too little nutritional ingestion of copper can result in a corresponding condition of copper excess or deficiency in the body, each of which has its own unique set of adverse health effects.
For example, copper deficiency alters the role of other cellular constituents involved in antioxidant activities. In both humans and animals, the major target organs for copper deficiency are the blood and hematopoietic system, the cardiovascular system, connective tissue and bone, the nervous system, and the immune system.
Conditions linked to copper deficiency include osteoporosis, osteoarthritis, rheumatoid arthritis, cardiovascular disease, colon cancer, and chronic conditions involving bone, connective tissue, heart, and blood vessels, lowered resistance to infection, general fatigue, impaired neurological function.
Copper deficiency and toxicity can be either of genetic or non-genetic origin. For example, Menkes disease (MNK) is of genetic origin that affects copper levels in the body, leading to copper deficiency. It is an x-linked recessive disorder, and is therefore considerably more common in males. The disorder was originally described by John Hans Menkes et al. in 1962.
Ongoing research into Menkes disease is leading to a greater understanding of copper homeostasis, the biochemical mechanisms involved in the disease, and possible ways to treat it. Investigations into the transport of copper across the blood/brain barrier, which are based on studies of genetically altered mice, are designed to help researchers understand the root cause of copper deficiency in Menkes disease.
The research to date has been valuable – genes can be ‘turned off’ gradually to explore varying degrees of deficiency. Researchers have also demonstrated in test tubes that damaged DNA in the cells of a Menkes patient can be repaired.
It is known that during pregnancy, the concentration of copper in the maternal serum rises and copper is transported from the maternal to the fetal circulation via the placenta. In mammalian fetal life, copper is transported via the bloodstream from the placenta to the liver, where it is stored in the Cu-metallothionein complex. The copper content in the fetal liver is higher than in adult liver and reaches a maximum concentration on day 16 of pregnancy. Earlier authors showed that CuCl2 administration to the female during pregnancy leads to an increase in the copper concentration in the liver of the fetus.
In current study in which Cucl2 alone and combination of Cucl2 and dimethyldithiocarbamate (DMDTC) administered in the prenatal stage suggest that prenatal treatment with CuCl2 is more effective than prenatal treatment with a combination of CuCl2 and DMDTC with regard to normalizing the copper level in the liver.
The current study is interesting and hope that more and more research on prenatal stage is encouraged to prevent diseases entering the new ones and the procedures needed to repair damaged genes in the human body may be found.
Note: Copper deficiency can be confirmed by very low serum metal and ceruloplasmin concentrations in the blood.
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