 Vol 6, Issue 7 July 2008 |
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| Clinical, Immunological, Anti-inflammatory and Antioxidant Roles of Zinc | ||
| Prasad AS. | ||
| Exp Gerontol May 2008 ; 43(5):370-7. | ||
| The essentiality of zinc for humans was recognized only 40 years ago. Zinc deficiency was suspected to occur in Iranian patients with growth retardation, hypogonadism in males, hepato-splenomegaly, rough and dry skin, geophagia and severe iron deficiency anemia. Later we documented zinc deficiency in similar patients in Egypt. The diet of these patients consisted of mainly cereal proteins which contained high phytate and this led to decreased availability of iron and zinc. These patients had severe immune dysfunctions, inasmuch as they died of intercurrent infections by the time they were 25 years of age. In our studies in experimental human model of zinc deficiency, we documented decreased serum testosterone level, oligospermia, severe immune dysfunctions mainly affecting T helper cells, decreased serum thymulin activity hyperammonemia, neuro-sensory disorders and decreased lean body mass. The basic mechanisms of zinc action on immune cells have been reviewed in this paper. Our studies showed that the activation of many zinc dependent enzymes and transcription factors were affected adversely due to zinc deficiency. The gene expression and production of Th1 cytokines were affected adversely due to zinc deficiency. Zinc is also an antioxidant and has anti-inflammatory actions. We have reported decreased plasma zinc, increased plasma oxidative stress markers and increased generation of inflammatory cytokines in the elderly subjects which were corrected by zinc supplementation. In cell culture studies, we have observed that zinc induces A20 which inhibits NF-kappaB activation resulting in decreased generation of inflammatory cytokines. | ||
| Magnesium Deficiency Accelerates Cellular Senescence in Cultured Human Fibroblasts | ||
| Killilea DW, et al. | ||
| Proc Natl Acad Sci USA: April 2008; 105(15):5768-73. | ||
| Magnesium inadequacy affects more than half of the U.S. population and is associated with increased risk for many age related diseases, yet the underlying mechanisms are unknown. Altered cellular physiology has been demonstrated after acute exposure to severe magnesium deficiency, but few reports have addressed the consequences of long-term exposure to moderate magnesium deficiency in human cells. Therefore, IMR-90 human fibroblasts were continuously cultured in magnesium-deficient conditions to determine the long-term effects on the cells. These fibroblasts did not demonstrate differences in cellular viability or plating efficiency but did exhibit a decreased replicative lifespan in populations cultured in magnesium-deficient compared with standard media conditions, both at ambient (20% 0(2)) and physiological (5% 0(2)) oxygen tension. The growth rates for immortalized IMR-90 fibroblasts were not affected under the same conditions. IMR-90 fibroblast populations cultured in magnesium-deficient conditions had increased senescence associated beta-galactosidase activity and increased p16(1 NK4a) and p21 (WAF1) protein expression compared with cultures from standard media conditions. Telomere attrition was also accelerated in cell populations from magnesium deficient cultures. Thus, the long-term consequence of inadequate magnesium availability in human fibroblast cultures was accelerated cellular senescence, which may be a mechanism through which chronic magnesium inadequacy could promote or exacerbate age-related disease. | ||
| Recent Developments in Intestinal Magnesium Absorption | ||
| Quamme GA. | ||
| Curr Opin Gstroenterol; June 2008; 24(2):230-5. | ||
| Recent identification and characterization of novel Mg transporters have clarified our understanding of intestinal magnesium absorption. The predominant Mg transporters include TRPM6 and TRPM7, members of the transient receptor potential melastatin family of cation channels. Mutations of TRPM6 result in a primary disorder termed hypomagnesemia with secondary hypocalcemia. Both TRPM6 and TRPM7 channels possess an atypical alphakinase domain. Recent studies have shown that TRPM7 channel activity is regulated by intracellular Mg and magnesium-nucleotides and modulated via this phosphotransferase kinase. TRPM6 channel function and intestinal magnesium absorption is altered by a variety of hormones and factors. Although it is apparent that TRPM6 and TRPM7 form heteromeric ion channels, controversy surrounds the nature of this interaction. Some studies show that TRPM6 may function on its own whereas other research concludes that TRPM7 is required for effective trafficking of TRPM6 to the plasma membrane. Finally, a number of other Mg transporters have been identified in intestinal epithelial cells but the role of these proteins is unclear. The recent developments in intestinal magnesium absorption and cellular magnesium homeostasis provide a basis for understanding magnesium deficiency disorders and provide a platform for future investigations. | ||
| Copper Transport and Alzheimer’s Disease | ||
| Macreadie IG. | ||
| Eur Biophys J; June 2008; 37(3):295-300. | ||
| This brief review discusses copper transport in humans, with an emphasis on knowledge learned from one of the simplest model organisms, yeast. There is a further focus on copper transport in Alzheimer's Disease (AD). Copper homeostasis is essential for the well-being of all organisms, from bacteria to yeast to humans: survival depends on maintaining the required supply of copper for the many enzymes, dependent on copper for activity, while ensuring that there is no excess free copper, which would cause toxicity. A virtual orchestra of proteins are required to achieve copper homeostasis. For copper uptake, Cu(lI) is first reduced to Cu(l) via a membrane-bound reductase. The reduced copper can then be internalized by a copper transporter where it is transferred to copper chaperones for transport and specific delivery to various organelles. Of significance are internal copper transporters, A TP7 A and A TP7B, notable for their role in disorders of copper deficiency and toxicity, Menkes and Wilson's disease, respectively. Metallothioneins and Cu/Zn superoxide dismutase can protect against excess copper in cells. It is clear too, increasing age, environmental and lifestyle factors impact on brain copper. Studies on AD suggest an important role for copper in the brain, with some AD therapies focusing on mobilizing copper in AD brains. The transport of copper into the brain is complex and involves numerous players, including amyloid precursor protein, Abeta peptide and cholesterol. | ||
| Copper, Chromium, Manganese, Iron, Nickel, and Zinc Levels in Biological Samples of Diabetes Mellitus Patients | ||
| Kazi TG, et al . | ||
| Biol Trace Elem Res; June 2008; 122(1):1-8. | ||
| There is accumulating evidence that the metabolism of several trace elements is altered in diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. The aim of the present study was to compare the level of essential trace elements, chromium (Cr), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), and zinc (Zn) in biological samples (whole blood, urine, and scalp hair) of patients who have diabetes mellitus type 2 (n = 257), with those of nondiabetic control subjects (n = 166), age ranged (45-75) of both genders. The element concentrations were measured by means of an atomic absorption spectrophotometer after microwave-induced acid digestion. The validity and accuracy was checked by conventional wet-acid-digestion method and using certified reference materials. The overall recoveries of all elements were found in the range of (97.60-99.49%) of certified values. The results of this study showed that the mean values of Zn, Mn, and Cr were significantly reduced in blood and scalp hair samples of diabetic patients as compared to control subjects of both genders (p < 0.001). The urinary levels of these elements were found to be higher in the diabetic patients than in the age-matched healthy controls. In contrast, high mean values of Cu and Fe were detected in scalp hair and blood from patients versus the nondiabetic subjects, but the differences found in blood samples was not significant (p < 0.05). These results are consistent with those obtained in other studies, confirming that deficiency and efficiency of some essential trace metals may play a role in the development of diabetes mellitus. | ||
| Iron and Zinc Deficiencies in China: What Is a Feasible and Cost-effective Strategy? | ||
| HMa G, et al . | ||
| Public Health Nutr; June 2008; 11(6):632-8. | ||
In order to prioritize interventions for micronutrient deficiencies in China, the populations affected by iron and
zinc deficiencies were assessed based on data from the 2002 China National Nutrition and Health Survey. The
costs and cost-effectiveness of supplementation, food diversification and food fortification were estimated using
the standard World Health Organization ingredients approach. Results indicated that 30% of children (60 years),
pregnant and lactating women, and 20% of women of reproductive age were anaemic, some 245 million people.
Approximately 100 million people were affected by zinc deficiency (zinc intake inadequacy and stunting), the
majority living in rural areas. Among interventions on iron and zinc deficiency, biofortification showed the lowest
costs per capita, I$0.01 (international dollars), while dietary diversification through health education represented
the highest costs at I$1148. The cost-effectiveness of supplementation, food fortification and dietary diversification
for iron deficiency alone was I$179, I$66 and I$103 per disability-adjusted life-year (DALY), respectively. Data
for biofortification were not available. For zinc deficiency, the corresponding figures were I$399, I$153 and I$103
per DALY, respectively. In conclusion, iron and zinc deficiencies are of great public health concern in China. Of
the two long-term intervention strategies, i.e. dietary diversification and biofortification with improved varieties,
the latter is especially feasible and cost-effective for rural populations. Supplementation and fortification can be
used as short-term strategies for specific groups. |
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