Abstract
The essentiality of zinc as a trace mineral in human health has been recognized for over five decades. Zinc deficiency, caused by diet, genetic defects, or diseases, can cause growth retardation, delayed sexual maturation, depressed immune response, and abnormal cognitive functions in humans. Zinc supplementation in zinc-deficient individuals can overcome or attenuate these abnormalities, suggesting zinc is an essential micro-nutrient in the body. A large number of in vitro and in vivo experimental studies indicate that zinc deficiency also causes apoptosis, cellular dysfunction, deoxyribonucleic acid (DNA) damage, and depressed immune response. Oxidative stress, due to the imbalance of reactive oxygen species (ROS) production and detoxification in the anti-oxidant defense system of the body, along with subsequent chronic inflammation, is believed to be associated with many chronic degenerative diseases such as diabetes, heart diseases, cancers, alcohol-related disease, macular degenerative disease, and neuro-pathogenesis. A large number of experimental studies including cell culture, animal, and human clinical studies have provided supportive evidence showing that zinc acts as an anti-oxidative stress agent by inhibition of oxidation of macro-molecules such as (DNA)/ribonucleic acid (RNA) and proteins as well as inhibition of inflammatory response, eventually resulting in the down-regulation of (ROS) production and the improvement of human health. In this article, we will discuss the molecular mechanisms of zinc as an anti-oxidative stress agent or mediator in the body. We will also discuss the applications of zinc supplementation as an anti-oxidative stress agent or mediator in human health and disease.
Highlights
The earliest clinical cases of human zinc deficiency, as manifested by dwarfism, sexual development delay in males, depressed immune response, and cognitive dysfunction, were observed by Dr Prasad and his team in the Middle East in the 1960s [1]
In our earlier human subject study in healthy adults, we found that oral zinc supplementation (45 mg zinc as gluconate per day for eight weeks) in normal healthy volunteers resulted in the significant decrease in the blood lipid peroxidation products malonyl dialdehyde (MDA)
Another animal study revealed that the protective role of zinc in Alcohol-related liver disease (ALD) might contribute to the activation of the hepatocyte nuclear factor-4α (HNF-4α) and peroxisome proliferator-activated receptor (PPAR) signaling pathways by zinc [118]
Summary
The earliest clinical cases of human zinc deficiency, as manifested by dwarfism, sexual development delay in males, depressed immune response, and cognitive dysfunction, were observed by Dr Prasad and his team in the Middle East in the 1960s [1]. Zinc supplementation in elderly subjects improves their zinc and health status, for example through decreased incidence of infections [5,6,7]. Zinc supplementation suppresses or attenuates these adverse effects [5,6,7]. These findings suggest that zinc might have a protective role as a pro-antioxidant agent or mediator by the down-regulation of ROS production and accumulation. We will summarize the biological functions of zinc as a ROS/oxidative suppressor or pro-antioxidant agent through several molecular mechanisms including anti-inflammatory effects and zinc-binding proteins such as nuclear factor κB (NF-κB), zinc containing transcription factor (A20), peroxisome proliferator-activated receptor (PPAR), tristetraprolin (TTP), hepatocyte nuclear factor-4α (HNF-4α), nuclear factor erythroid 2-related factor 2 (Nrf2), Kruppel-associated box domain (KRAB), and metallothionein (MT)/metal regulatory transcription factor 1 (MTF-1) in human health and diseases
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