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Lack Of Zinc In The Body Causes

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Zinc Supplement: Benefits, Side Effects, Foods & Dosage

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Laura M. Plum Laura M. Plum Scilit Preprints.org Google Scholar Lothar Rink Lothar Rink Scilit Preprints.org Google Scholar and Hajo Haase Hajo Haase Scilit Preprints.org Google Scholar *

Zinc Benefits, Dosage, Foods, Supplements, Side Effects

Received: 27 January 2010 / Revised: 8 March 2010 / Accepted: 10 March 2010 / Published: 26 March 2010

Compared to several other metal ions with similar chemical properties, zinc is relatively harmless. Only exposure to high doses produces toxic effects, making acute zinc intoxication rare. In addition to acute intoxication, long-term, high-dose zinc supplementation interferes with copper absorption. Therefore, many of its toxic effects are caused by copper deficiency. Although systemic homeostasis and effective regulatory mechanisms at the cellular level generally prevent the uptake of cytotoxic doses of exogenous zinc, endogenous zinc plays an important role in cytotoxic events within a single cell. Here, zinc influences apoptosis by affecting several molecular regulators of programmed cell death, including caspases and proteins in the Bcl and Bax families. One organ where zinc is particularly involved in cell death is the brain, and ischemia or trauma involves the accumulation of cytotoxic free zinc. More than a toxic metal ion, zinc is an important trace element. Overexposure to intoxication is rare, zinc deficiency is common and affects growth, neurodevelopment, and immunity, and in severe cases, the consequences are fatal. Zinc deficiency caused by zinc deficiency and low bioavailability of food is a much more common threat to human health than intoxication.

In the periodic table of elements, zinc is found in group IIb, along with the two toxic metals cadmium and mercury. Nevertheless, zinc is considered to be relatively non-toxic to humans [1]. This is reflected in the LD comparison

Of sulfate salts in rats. According to the US National Library of Medicine’s Toxnet database, oral LD

Zinc Deficiencies In Dogs, Explained

For zinc is close to 3 g/kg body weight, more than 10 times higher than cadmium and 50 times higher than mercury [2]. An important factor appears to be zinc homeostasis, which allows efficient processing of excess orally administered zinc, as LD after intraperitoneal injection in mice

For zinc was about four times higher than for cadmium and mercury [3]. Unlike the other two metals, for which no role in human physiology is known, zinc is an essential trace element not only for humans, but for all organisms. It is part of more than 300 enzymes and many more other proteins, which emphasizes its important role for human health. Optimal nucleic acid and protein metabolism, as well as cell growth, division, and function, require adequate zinc [4].

In this review, we provide a brief summary of zinc homeostasis, followed by a description of the effects of acute zinc intoxication and long-term exposure to high doses of zinc. In addition to systemic intoxication, there is evidence for physiological involvement of endogenous zinc in toxicity at the cellular level, such as the regulation of apoptosis and neuronal death in many different cell types. Finally, we also briefly discuss the harmful effects of zinc deficiency, as healthy individuals are at high risk of suffering adverse effects associated with zinc deficiency unless they are exposed to zinc in the workplace or accidentally. those associated with intoxication.

The human body contains 2-3 g of zinc and about 90% is in muscles and bones [5]. Other organs containing estimated concentrations of zinc include the prostate, liver, gastrointestinal tract, kidney, skin, lung, brain, heart, and pancreas [6-8]. Oral administration of zinc results in absorption through the small intestine and distribution occurs later in the serum, where it is mainly bound to several proteins such as albumin, α-microglobulin and transferrin [ 9 ].

What Are The Functions Of Zinc?

At the cellular level, 30-40% of zinc is in the nucleus, 50% in the cytosol, and the rest is bound to membranes [4]. Cellular zinc underlies efficient homeostatic control that prevents excessive zinc accumulation (see also Figure 1a). Cellular zinc homeostasis is mediated by two protein families; the zinc importer (Zip; Zrt-, Irt-like proteins) family of 14 proteins that transport zinc into the cytosol, and the zinc transporter (ZnT) family of 10 proteins that transport zinc from the cytosol [10].

The same transporter families also regulate the intracellular distribution of zinc to the endoplasmic reticulum, mitochondria, and Golgi. In addition, many types of mammalian cells contain membrane-bound vesicular structures called zincosomes. These vesicles sequester high amounts of zinc and release them when stimulated, for example by growth factors [ 11 , 12 ].

Finally, metallothioneins (MTs) play an important role in zinc homeostasis by complexing up to 20% of intracellular zinc (Figure 1b) [13, 14]. MTs are proteins characterized by low molecular weight of 6–7 kDa, high cysteine ​​content, and metal ion complexing ability. One MT molecule can bind up to seven zinc ions. Due to the different affinity of metal ion binding sites, it can act as a cellular zinc buffer of several sizes [15]. Dynamic regulation of cellular zinc by MT results from the synthesis of the apo-form thionein (T) in response to increased intracellular zinc by triggering the metal response element-binding transcription factor (MTF)-1 [ 16 ]. In addition, oxidation of cysteine ​​residues can alter the number of metal-binding thiols, coupling redox and zinc metabolism. An in-depth discussion of this complex subject can be found in a recent review [17].

There are three main ways zinc enters the human body; by inhalation, through the skin or by ingestion [18]. Each type of exposure affects specific parts of the body (Figure 2) and allows for different amounts of zinc to be taken up.

Zinc Deficiency: Symptoms, Diagnosis, And Treatment

Inhalation of zinc-containing fumes often results from industrial processes such as electroplating, primarily affecting production workers. In addition, military smoke bombs contain zinc oxide or zinc chloride, making soldiers a group in which several cases of zinc-containing smoke inhalation have been described. For example, Homma and colleagues reported the case of two soldiers who developed adult respiratory distress syndrome (ARDS) after exposure to a zinc chloride smoke bomb [19]. Two people died 25 and 32 days after the accident. Another soldier was exposed to concentrated zinc chloride for several minutes during military training [20]. It also occurs after 48 hours of ARDS. He was discharged after eight days of tracheal intubation and mechanical ventilation, and returned to work four months after the event with no respiratory impairment [20]. There are several additional reports involving smoke bombs with similar effects on the respiratory tract [21, 22].

However, there was no clear evidence that zinc was the primary cause of the respiratory symptoms in any of the cases. Not only is there no information on concentrations, but there are several other ingredients in inhaled smoke besides zinc chloride. In addition, zinc chloride is generally corrosive, so the effect may be due to specific properties of the compound rather than a direct effect of zinc intoxication.

The most widely known effect of inhaling zinc-containing fumes is metal fume fever (MFF), which is mainly caused by inhaling zinc oxide. This acute syndrome is an industrial disease caused by inhalation of fresh metal fumes with particle size < 1 μm in occupational situations such as zinc smelting or welding [23]. Symptoms of this reversible syndrome usually begin several hours after a severe attack and include fever, muscle aches, nausea, fatigue and chest pain, cough,

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