Minerals in the News Vol. 10, No. 1 (January 2012)

J Cell Biochem. 2011; 112(12):3563-72.

Ikari A; et al.

 

Cell growth is suppressed by lack of magnesium, but the molecular mechanism is not examined in detail. The researchers looked at the effect of extracellular magnesium deficiency on cell cycle progression and the expression of cell cycle regulators in renal epithelial NRK-52E cells. In synchronized cells caused by serum-starved method, over 80% of cells were distributed in G1 phase. Cell proliferation and percentage of the cells in S phase in the presence of MgCl(2) were higher than those without MgCl(2) , suggesting that magnesium is involved in the cell cycle progression from G1 to S phase. After serum addition, the expression levels of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) . The exogenous expression of p21(Cip1) or p27(Kip1) increased the percentage in G1 phase, whereas it decreased that in S phase. The mRNA levels and promoter activities of p21(Cip1) and p27(Kip1) in the absence of MgCl(2) were higher than those in the presence of MgCl(2) . The phosphorylated p53 (p-p53) level was decreased by MgCl(2) addition. Pifithrin-α, a p53 inhibitor, decreased the p-p53, p21(Cip1) and p27(Kip1) levels, and the percentage in G1 phase in the absence of MgCl(2) . Rotenone, a mitochondrial respiratory inhibitor, decreased ATP content and increased the p-p53 level in the presence of MgCl(2) . Together, lack of magnesium may increase p21(Cip1) and p27(Kip1) levels mediated by the decrease in ATP content and the activation of p53, resulting in the suppression of cell cycle progression from G1 to S phase in NRK-52E cells.

 

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Mol Nutr Food Res.; 2011; 55(10):1552-60.

Alcantara EH, et al.

 

Research has pointed to zinc as an activator of bone formation, however, its role in bone calcification has not been reported. This study looks at how zinc regulates the bone matrix calcification in osteoblasts. Two osteoblastic MC3T3-E1 cell subclones (SC 4 and SC 24 as high and low osteogenic differentiation, respectively) were cultured in normal osteogenic (OSM), Zinc deficient (Zn-, 1 μM), or adequate (Zn+, 15 μM) media up to 20 days. Cells (SC 4) were also supplemented with (50 μg/mL) or no ascorbic acid (AA) along with Zinc treatment. Zn- decreased collagen synthesis and matrix accumulation. Although AA is essential for collagen formation, its supplementation could not compensate for Zinc deficiency-induced detrimental effects on extracellular matrix mineralization. Zn- also decreased the medium and cell layer alkaline phosphatase ALP activity. This decreased ALP activity might cause the decrease of Pi accumulation in response to Zn-, as measured by von Kossa staining. Ca deposition in cell layers, measured by Alizarin red S staining, was also decreased by Zn(-) . This study suggests that zinc deprivation inhibits extracellular matrix calcification in osteoblasts by decreasing the synthesis and activity of matrix proteins, type I collagen and ALP, and decreasing Ca and Pi accumulation. Therefore zinc deficiency can be considered as risk factor for poor extracellular matrix calcification.

 

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Syst Biol Reprod Med; 2011 Oct; 57(5):233-43.

Kumari D, et al.

 

This study was conducted in to determine whether prepubertal dietary zinc deficiency in Wistar rats causes apoptotic changes in testes. Prepubertal male Wistar rats (40-50 gm) were divided into 3 groups: zinc control (ZC), pairfed (PF), and zinc deficient (ZD). Control and pairfed groups were given a 100 ppm zinc diet while the deficient groups received 1 ppm zinc diet for 2 and 4 weeks (w), respectively. Cellular structural studies revealed several apoptotic features such as wavy basement membrane, displaced nuclei, chromatin condensation, irregular bulging of plasma membrane, nuclear membrane dissolution, loss of inter-Sertoli cell junctional complexes, and intercellular bridges and deformed mitochondria. A variable spectrum of sperm defects had also been visualized e.g., acrosomal deformities such as decapitation and a ring of condensed chromatin around the nuclear periphery, deformed sperm heads with a condensed nucleus, tail-elements with superfluous cytoplasm, and damage to the mitochondrial sheath and aggregation of spermatozoa within the membrane. This was further supported by TUNEL studies. Apoptotic index, epididymal sperm concentration, motility, and fertility index also revealed a significant (P < 0.05) decrease in zinc deficient groups (2 and 4 w) when compared with their respective control and pairfed groups. These findings indicate that changes observed in the testes after dietary zinc deficiency are due to the onset of apoptosis. Increased apoptotic degeneration in testes may cause irreversible changes in the germ cells associated with decreased epididymal sperm concentration, motility, and fertility index which contributes to the low efficiency of spermatogenesis thereby indicating a possible role of zinc in fertility.

Zinc Supplementation Provides Behavioral Resiliency in a Rat Model of Traumatic Brain Injury

[Peripheral Neuropathy, Myelopathy, Cerebellar Ataxia, and Subclinical Optic Neuropathy Associated with Copper Deficiency Occurring 23 Years After Total Gastrectomy]