**6. Zinc in Parkinson**

Zinc is essential as a cofactor for a variety of enzymes and transcription factors and plays a role in various biological processes ranging from gene expression to the immune response. There are two distinct gene families of zinc transporters, 10 ZnT (Slc30a) and 14 Zip (Slc39a) transporter genes (Ohno et al., 1985; Liuzzi & Cousins, 2004). The zinc concentration is ∼15 times greater in mature RBC than in plasma (Eide, 2006). More than 90% of RBC zinc functions as a component essential for the activity of zinc metalloenzymes, particularly carbonic anhydrase and Cu2+/Zn2+-superoxide dismutase (Ryu et al. 2008). Abnormal levels of Zn2+plays a role in many diseases, including Alzheimer's and type-2 diabetes. Zn is an essential element for plants and other organisms and is involved in many cellular processes, including activation of enzymes, protein synthesis, and membrane stability (Welch et al., 1982). Zinc is involved in numerous aspects of cellular metabolism (Jiménez-Jiménez et al. 1992; Forsleff et al. 1998; Brewer et al. 2010). Zinc deficiency is characterized by growth retardation. The global extent of zinc deficiency is debated, but diets that are high in whole grains and low in meat could lead to deficiency (Qureshi et al. 2006; MacDiarmid et al. 2013). Low zinc supply has the same effect on human cells as on yeast, zinc deficiency might contribute to human diseases that are associated with a build-up of "junked" proteins, such as Parkinson's and Alzheimer's. A similar protective system to Tsa1 also exists in animals, and the research group plans to move ahead by studying that system in human cell culture (MacDiarmid et al. 2013). The authors demonstrated that cells that are low in zinc also produce proteins that counter the resulting stress, including one called Tsa1. Tsa1 could reduce the level of harmful oxidants in cells that are short of zinc (MacDiarmid et al. 2013).

sensitive, selective analytical technique was developed around 1980, ICP-MS (inductively

Possible Relation Between Trace Element Status and Clinical Outcomes in Parkinson Syndrome

http://dx.doi.org/10.5772/57612

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Trace elements were originally viewed as nutrients and they excerpt pharmacological actions. Some of these possibly essential elements also are receiving attention because of their toxico‐ logical or pharmacological properties that can affect health and wellbeing. However possible relation between trace element status and clinical outcomes are insufficient. Extrapyramidal symptoms reflecting nigrostrial dopaminergic hypofunction are common in patients with neuronal ceroid lipofuscinosis and Parkinson's disease. Inadequacy or imbalance of trace elements supply consequently affects a number of physiological functions. Zinc as an elements that may play a protective anti-atherosclerotic role, decreases. Zn is considered an efficient antioxidant (Prasad, 2008). Zn controls metallothionein expression and is involved in, cellular redox regulation (Maret, 2000). Oxidative stress can be corrected by dietary Zn as demon‐ strated of hepatic antioxidant enzymes (Tupe et. al. 2010). Zn metabolism may be influenced by low intake, lack of protective factors, e.g. Se. Another possibility may be Cd competition with Zn. Cd has higher binding capacity than Zn, e.g. in metallothionein and may displace Zn from its carrier sites. In a study of Parkinson's disease Mn was implicated (Normandie and Hazell, 2002) and another study demonstrated elevated concentrations of Cd in the erythro‐ cytes (Johansson et.al. 2007). Lack of protective elements e.g. selenium in the metabolism makes it easier for heavy metal ions to enter and interfere the metabolism. As trace elements are active in many parts of the cell metabolism the discussion will be focused on possible effects of

**8. Elemental profiles as an indicator of metal ion and ligand homeostasis**

The cell metabolism is a complex balance of proteins, fatty acids, carbohydrates, metal ions and trace elements regulated by DNA and RNA in nucleus and mitochondria. As the metab‐ olism involve many molecular reactions and species not practical to be monitored a simplified indication of metal ion-ligand status, elemental profile, may be a substitute to monitor effects of important cell reactions. The elemental profile may be looked upon as the integrated results of reactions at the moment the sample was taken. It is important to underline that deviations in the elemental profile may also include effects of compounds with strong association to the examined elements. These deviations may give biochemical and physiological insights to observe early changes in the metabolism. Changes of metabolism of metal ions in e.g. eryth‐ rocytes may help to understand early reactions, if it is normal or an indication of an early

**9. Membrane trafficking and dynamics in presence of heavy metal ions**

In a study of 12 patients (9 men and 3 women) with Parkinson's disease (Johansson et.al. 2013) erythrocytes showed significant increased concentration of Pb and Ag. The concentration

coupled plasma mass spectrometry).

imbalance due to heavy metal ions in Parkinson's disease.

pathophysiological process.

It has been reported that zinc deficiency may be linked to increased inflammation. Liu et al (2013) studied the activity of zinc to control sepsis, the severe systemic response to infection that can lead to death. Using cell models, the team focused on the role of zinc to prevent the inflammation that leads to sepsis; they found that when a pathogen is recognized, the gene that produces the zinc transporter SLC39A8 (ZIP8) is expressed. This transporter then rapidly moves to cell's walls, where it shuttles zinc from the bloodstream into the cell; after cell entry, zinc is then directed to and bonds to a protein that halts further activity (Liu et al., 2013).
