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Index / Bioassays / QuantiChrom™ Zinc Assay Kit / Product Detail : DIZN-250 QuantiChrom™ Zinc Assay Kit
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#DIZN-250 QuantiChrom™ Zinc Assay Kit

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  Price : 515   EUR
585   USD
400   GBP
2166   Zloty
68993   JPY
3976   NOK
4260   SEK
583   CHF

Product name : QuantiChrom™ Zinc Assay Kit

Catalog number : DIZN-250

Quantity: 250

Availability: Yes

Supplier name : Bioassays

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About this Product :

QuantiChrom™ Zinc Assay Kit antibody storage GENTAUR recommends for long therm storage to freeze at -24 C. For short time storage up to 30 days we suggest fridge storage at 1 to 10 C. Prevent multiple freeze taw cycles of QuantiChrom™ Zinc Assay Kit.
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More Details about

For quantitative determination of zinc ion Zn2+ and evaluation of drug effects on zinc metabolism.
Method: OD425nm.
Samples: serum, plasma, urine, saliva, food, beverage and environment.
Species: all.
Procedure: 30 min.
Size: 250 tests.
Detection limit: 0.78 μg/dL (0.12 μM).

DESCRIPTION
Zinc is an essential trace element and plays many key roles in
metabolism. It is required for the activity of more than 300 enzymes, the
structure of many proteins, and control of genetic expression. Zinc status
affects basic processes of cell division, growth, differentiation,
development, performance and aging through its requirement for
synthesis and repair of DNA, RNA and protein. The common causes of
zinc deficiency are low dietary intakes and low bioavailability. Clinical
signs of zinc deficiency include acrodermatitis, low immunity, diarrhea,
poor healing, stunting, hypogonadism, fetal growth failure, teratology and
abortion. Zinc deficiency has now been recognized to be associated with
many diseases such as malabsorption syndrome, chronic liver disease,
chronic renal disease, sickle cell disease, diabetes, malignancy, and
other chronic illnesses.
Simple, direct and automation-ready procedures for measuring zinc
concentration in biological samples are highly desirable in Research and
Drug Discovery. BioAssay Systems' zinc assay kit is designed to
measure zinc directly in biological samples without any pretreatment.
The present method utilizes a chromogen that forms a colored complex
specifically with zinc. The intensity of the color, measured at 425 nm, is
directly proportional to the zinc concentration in the sample.
KEY FEATURES
Sensitive and accurate. Uses 50 μL samples. Linear detection range
0.12 μM (0.78 μg/dL) to 10 μM (65 μg/dL) zinc in 96-well assay format.
Simple and high-throughput. The procedure involves addition of a single
working reagent and incubation for 30 min. Can be readily automated as a
high-throughput assay for thousands of samples per day.
Improved reagent stability and versatility. The optimized formulation has
greatly enhanced reagent and signal stability. Cuvette or 96-well plate
assay formats possible.
Low interference in biological samples. No pretreatments are needed.
APPLICATIONS:
Direct Assays: zinc in serum, plasma (no EDTA), urine, saliva etc.
Drug Discovery/Pharmacology: effects of drugs on zinc metabolism.
Environment: zinc determination in waste water, soil etc.
KIT CONTENTS (for 100 samples in 96-well assay)
Reagent A: 50 mL Reagent B: 1 mL Reagent C: 1 mL
EDTA: 1 mL 100 mM Zinc standard: 1 mL 50 μM
Storage conditions. The kit is shipped at room temperature. Store
Reagents B and C at -20°C and other components at 4°C. Shelf life: 6
months after receipt.
Precautions: reagents are for research use only. Normal precautions for
laboratory reagents should be exercised while using the reagents.

MATERIALS REQUIRED, BUT NOT PROVIDED
Pipeting devices and accessories. Clear bottom 96-well plates (e.g.
Corning Costar) and plate reader, or cuvettes and
spectrophotometer for measuring OD 425nm.

 

Sample Type: serum

Species: mouse

 

References: Knoell, DL et al (2009). Zinc deficiency increases organ damage and mortality in a murine model of polymicrobial sepsis. Crit Care Med 37(4):1380-8.

Pubmed ID: 19242332

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=19242332

Abstract:
OBJECTIVE:
Zinc deficiency is common among populations at high risk for sepsis mortality, including elderly, alcoholic, and hospitalized patients. Zinc deficiency causes exaggerated inflammatory responses to endotoxin but has not been evaluated during bacterial sepsis. We hypothesized that subacute zinc deficiency would amplify immune responses and oxidant stress during bacterial sepsis {lsqb;i.e., cecal ligation and puncture (CLP){rsqb; resulting in increased mortality and that acute nutritional repletion of zinc would be beneficial.

DESIGN:
Prospective, randomized, controlled animal study.

SETTING:
University medical center research laboratory.

SUBJECTS:
Adult male C57BL/6 mice.

INTERVENTIONS:
Ten-week-old, male, C57BL/6 mice were randomized into three dietary groups: 1) control diet, 2) zinc-deficient diet for 3 weeks, and 3) zinc-deficient diet for 3 weeks followed by oral zinc supplementation for 3 days (n = 35 per diet). Mice were then assigned to receive either CLP or sham operation (n = 15 each per diet). CLP and sham-operated treatment groups were further assigned to a 7-day survival study (n = 10 per treatment per diet) or were evaluated at 24 hours (n = 5 per treatment per diet) for signs of vital organ damage.

MEASUREMENTS AND MAIN RESULTS:
Sepsis mortality was significantly increased with zinc deficiency (90% vs. 30% on control diet). Zinc-deficient animals subject to CLP had higher plasma cytokines, more severe organ injury, including increased oxidative tissue damage and cell death, particularly in the lungs and spleen. None of the sham-operated animals died or developed signs of organ damage. Zinc supplementation normalized the inflammatory response, greatly diminished tissue damage, and significantly reduced mortality.

CONCLUSIONS:
Subacute zinc deficiency significantly increases systemic inflammation, organ damage, and mortality in a murine polymicrobial sepsis model. Short-term zinc repletion provides significant, but incomplete protection despite normalization of inflammatory and organ damage indices.

Comment in:

  • Crit Care Med. 2009 Apr;37(4):1513-4.

PMID: 19242332 [PubMed - indexed for MEDLINE] PMCID: PMC2905048

 

Sample Type: saliva

Species: human

 

References: Padiglia, A et al (2010). Sensitivity to 6-n-propylthiouracil is associated with gustin (carbonic anhydrase VI) gene polymorphism, salivary zinc, and body mass index in humans. Am J Clin Nutr 92(3):539-45.

Pubmed ID: 20631203

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=20631203

Abstract:
BACKGROUND:
The individual ability to taste 6-n-propylthiouracil (PROP) may be correlated with body mass index (BMI) and differences in the salivary proteins involved in taste function, such as the zinc-dependent enzyme gustin, which is a trophic factor of taste buds.

OBJECTIVE:
We investigated the possible association of PROP taste responsiveness with gustin gene polymorphism rs2274333 (A/G), salivary ionic zinc concentrations, and BMI.

DESIGN:
We measured cognitive eating behaviors and BMI in 75 volunteers (28 men and 47 women; mean plusmn SEM age: 25 plusmn 3 y). The intensity of taste perception evoked by PROP and sodium chloride solutions was estimated to evaluate PROP taster status. Salivary ionic zinc concentrations were measured, and molecular analyses of the gustin gene polymorphism were performed in individuals classified by PROP status by using polymerase chain reaction techniques.

RESULTS:
We classified subjects as PROP supertasters (n = 27), medium tasters (n = 28), or nontasters (n = 20). Salivary ionic zinc concentrations and BMI were greater in nontasters than in supertasters (P = 0.003 and P = 0.042, respectively). Molecular analyses of gustin DNA showed that allele A and genotype AA were significantly more frequent in supertasters, whereas allele G and genotype GG were significantly more frequent in nontasters (P lt 0.001).

CONCLUSIONS:
These data showed that responsiveness to PROP is inversely related to BMI and salivary ionic zinc concentrations. The gustin gene dimorphism rs2274333 observed in supertaster and nontaster subjects may influence the protein conformation and, thereby, affect zinc ion binding. Our data showed a direct association between PROP sensitivity and a polymorphism in the gustin gene that is hypothesized to affect its function. This trial was registered at clinicaltrials.gov as UNICADBSITB-1.

PMID: 20631203 [PubMed - indexed for MEDLINE]

 

 

Sample Type: serum, urine

Species: human

 

References: Gunasekara, P et al (2011). Effects of zinc and multimineral vitamin supplementation on glycemic and lipid control in adult diabetes. Diabetes Metab Syndr Ob

Pubmed ID: 21448322

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21448322

Abstract:
 AIMS:
To evaluate the effects of zinc with or without other antioxidants on blood glucose, lipid profile, and serum creatinine in adult diabetics on long-term follow-up.

MATERIALS AND METHODS:
Patients (n = 96) were randomly allocated to three groups: group A (n = 29) was supplemented with oral zinc sulfate (22 mg/day) and multivitamin/mineral (zinc+MVM) preparation; group B (n = 31) was given the same preparation without zinc (MVM); and group C (n = 36) was given a matching placebo for a period of 4 months in a single-blinded study. Blood samples were taken at baseline and after 4 months of supplementation to assess blood glucose (fasting and postprandial) and glycosylated hemoglobin (Hb(A1C)%) and serum levels of zinc, creatinine, and lipids.

RESULTS:
The zinc+MVM group had a mean change of fasting blood sugar -0.33 mmol/L (standard error of the mean 0.21 mmol/L) and was significant (P = 0.05) when compared with the other two groups (mean change in the MVM group +0.19 (0.31) mmol/L and +0.43 (0.23) mmol/L in the control group, respectively). The Hb(A1C)% level reduced significantly, irrespective of the baseline level, in zinc+MVM-supplemented individuals. In the other two groups, the change of Hb(A1C)% level was not significant. Serum lipid levels reduced significantly in the zinc+MVM and MVM groups.

CONCLUSIONS:
Zinc+MVM supplementation showed beneficial effects in the metabolic control of adult diabetics in addition to elevating their serum zinc level. Zinc supplementation improved glycemic control measured by Hb(A1C)% and fasting and postprandial glucose. Furthermore, zinc supplementation lowered serum cholesterol and cholesterol/high-density lipoprotein ratio.

PMID: 21448322 [PubMed] PMCID: PMC3064411

 

Sample Type: retinal pigment epithelial cells

 

Species: human

 

References: Leung, KW et al (2011). ZIP2 and ZIP4 Mediate Age-Related Zinc Fluxes Across the Retinal Pigment Epithelium. J Mol Neurosci

Pubmed ID: 21603979

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21603979

Abstract: Decreases in systemic and cellular levels of zinc (Zn(2+)) during normal aging correlate with several age-related pathologies including age-related macular degeneration. Zn(2+) homeostasis in tissues is not only dependent on dietary intake but also on optimal expression and function of its influx (ZIP) and efflux (ZnT) transporters. We recently showed that many of the Zn(2+) transporters are expressed by the retinal pigment epithelial (RPE) cells. In this study, we present evidence that RPE cells contain less endogenous Zn(2+) with increased aging and transport this ion vectorially with greater transport from the basal to apical direction. Expression of two Zn(2+) influx transporters, ZIP2 and ZIP4, is reduced as a function of RPE age. Gene silencing of ZIP2 and ZIP4 in RPE cells from young donors or their overexpression in cells from older donors confirms that these two transporters are essential in controlling Zn(2+) influx and sequestration in RPE cells. Both transporters are distributed on the basal surface of the RPE where they are likely to control Zn(2+) homeostasis in the outer retina.

PMID: 21603979 [PubMed - as supplied by publisher]

 

Sample Type: plasma

Species: rat

 

References: Kelly, E et al (2011). Redistribution of labile plasma zinc during mild surgical stress in the rat. Transl Res 157(3):139-49.

Pubmed ID: 21316030

Pubmed link: http://www.ncbi.nlm.nih.gov/pubmed?term=21316030

Abstract: Zinc is an essential trace element and cofactor for many cellular processes. Uptake of ionized divalent zinc (Zn(2+)) in peripheral tissues depends on its total content in the circulation and on mechanisms facilitating delivery to tissues in its labile form. Understanding mechanisms of Zn(2+) delivery has been hindered by the absence of techniques to detect labile Zn(2+) in the circulation. In this study, we report the use of the fluorescent zinc-binding dye (ZnAF-2) to detect changes in labile Zn(2+) in the circulating plasma of the rat under standardized conditions, including exogenous infusions to increase plasma Zn(2+) and an infusion of the chelator, citrate, to decrease labile Zn(2+) in the plasma without altering total Zn(2+) content. In a model of mild surgical stress (unilateral femoral arterial ligation), plasma levels of total and labile Zn(2+) decreased significantly 24 h after the operation. Ultrafiltration of plasma into high- and low-molecular weight macromolecule fractionations indicated that binding capacity of zinc in the high-molecular weight fraction is impaired for the entire 24-h interval after induction of mild surgical stress. Affinity of the filtrate fraction was rapidly and reversibly responsive to anesthesia alone, decreasing significantly at 4 h and recovering at 24 h; in animals subjected to moderate surgical stress, this responsiveness was lost. These findings are the first reported measurements of labile Zn(2+) in the circulation in any form of mild systemic stress. Zinc undergoes substantial redistribution in the plasma as a response to surgical stress, leading to increased availability in lower molecular weight fractions and in its labile form.

Copyright © 2011 Mosby, Inc. All rights reserved.

PMID: 21316030 [PubMed - indexed for MEDLINE] PMCID: PMC3073749 [Available on 2012/3/1]

 

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