Zinc Deficiency and Microtubule Function in Prostate Cells

2006 ◽  
Author(s):  
Bruce N. Ames
2009 ◽  
Vol 297 (5) ◽  
pp. C1188-C1199 ◽  
Author(s):  
Chung-Ting Han ◽  
Norberta W. Schoene ◽  
Kai Y. Lei

Phosphorylated Akt (p-Akt), a phosphoinositide-3-OH-kinase-activated protein kinase, is highly expressed in prostate tumors. p-Akt can indirectly hinder p53-dependent growth suppression and apoptosis by phosphorylating Mdm2. Alternatively, p-Akt can directly phosphorylate p21 and restrict it to the cytoplasm for degradation. Because the prostate is the highest zinc-accumulating tissue before the onset of cancer, the effects of physiological levels of zinc on Akt-Mdm2-p53 and Akt-p21 signaling axes in human normal prostate epithelial cells (PrEC) and malignant prostate LNCaP cells were examined in the present study. Cells were cultured for 6 days in low-zinc growth medium supplemented with 0 [zinc-deficient (ZD)], 4 [zinc-normal (ZN)], 16 [zinc-adequate (ZA)], or 32 [zinc-supplemented (ZS)] μM zinc. Zinc status of both cell types was altered in a dose-dependent manner, with LNCaP cells reaching a plateau at >16 μM zinc. For both cell types, p-Akt was higher in the ZD than in the ZN cells and was normalized to that of the ZN cells by treatment with a PI3K inhibitor, LY-294002. PTEN, an endogenous phosphatase targeting Akt dephosphorylation, was hyperphosphorylated (p-PTEN, inactive form) in ZD PrEC. Nuclear p-Mdm2 was raised, whereas nuclear p53 was depressed, by zinc deficiency in PrEC. Nuclear p21 and p53 were lowered by zinc deficiency in LNCaP cells. Higher percentages of ZD, ZA, and ZS than ZN LNCaP cells were found at the G0/G1 phase of the cell cycle, with proportionally lower precentages at the S and G2/M phases. Hence, the increased p-PTEN in ZD PrEC would result in hyperphosphorylation of p-Akt and p-Mdm2, as well as reduction of nuclear p53 accumulation. For ZD LNCaP cells, Akt hyperphosphorylation was probably mediated through p21 phosphorylation and degradation, thus restricting p21 nuclear entry to induce cell cycle arrest. Thus zinc deficiency differentially modulated the Akt-Mdm2-p53 signaling axis in normal prostate cells vs. the Akt-p21 signaling axis in malignant prostate cells.


2010 ◽  
Vol 9 (3) ◽  
pp. 65-67
Author(s):  
Yu. V. Yeschenko ◽  
V. V. Novitsky ◽  
V. D. Bovt ◽  
V. A. Yeschenko ◽  
O. I. Urazova

It was shown in experiments on rats, that dithizone induced zinc deficiency in prostate cells. Three phase type of fluctuations of cytochemically detected zinc concentration was observed in the cells: phase of primary decrease, phase of temporary partial restoration and the phase of secondary decrease. Sodium diethyldithiocarbamate unlike to dithizone didn’t induce damage of cells and secondary decrease zinc content in its.


2009 ◽  
Vol 40 (5) ◽  
pp. 28
Author(s):  
BRUCE JANCIN
Keyword(s):  

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
A Kiss ◽  
K Krupa ◽  
B Galambosi ◽  
A Shikov

2008 ◽  
Vol 70 (4) ◽  
pp. 402-405 ◽  
Author(s):  
Chie HIRABE ◽  
Chisato HOSOKAWA ◽  
Masakazu TAKAHARA ◽  
Satoko SHIBATA ◽  
Satoshi TAKEUCHI ◽  
...  

2019 ◽  
Vol 31 (3) ◽  
pp. 251-256

Cirrhosis of liver is one of the common medical problem in daily clinical practice and one of the leading causes of morbidity and mortality. Zinc is an essential trace elements for human and plays in many biological roles in the body. Among them, zinc deficiency is thought to be involved in metabolism of ammonia and causes hyperammonia that worsen hepatic encephalopathy. This study aimed to find out the severity of cirrhosis of liver was by Child Turcotte Pugh score and to investigate the associations between serum zinc level and severity of cirrhosis. A hospital-based cross-sectional descriptive study was performed on 78 patients with different underlying causes of cirrhosis of liver at the Medical Units of Yangon General Hospital and Yangon Specialty Hospital. Among the study population, Child grade A was found to be 28.21%, Child grade B was 30.77% and Child grade C was 41.03%. Regarding result of serum zinc level, 62.8% were low level, 28.2% were within normal level and 8.9% were high level. Mean value of serum zinc level in grade A was 0.68 mg/l, grade B was 0.54 mg/l and grade C was 0.48 mg/l (p=0.00). It was found out that there was a high prevalence of zinc deficiency in severe cirrhotic patients. The zinc level was significantly lowest among patients with Child-Pugh C as compare to those with Child-Pugh B and C. Severity of zinc deficiency should be requested for supplementation therapy in cirrhotic patients as to prevent complications such as hepatic encephalopathy, hepatocellular carcinoma and liver failure. Screening for zinc deficiency may need in these patients with more advanced cirrhosis because it seems to be a marker of advanced liver disease and it can be deducted that awareness of serum zinc level among cirrhotic patients is very important in clinical practice.


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