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Effect of metallothionein core promoter region polymorphism on cadmium, zinc and copper levels in autopsy kidney tissues from a Turkish population.

Abstract：

:Metallothioneins (MTs) are metal-binding, low molecular weight proteins and are involved in pathophysiological processes like metabolism of essential metals, metal ion homeostasis and detoxification of heavy metals. Metallothionein expression is induced by various heavy metals especially cadmium, mercury and zinc; MTs suppress toxicity of heavy metals by binding themselves to these metals. The aim of this study was to investigate the association between the -5 A/G metallothionein 2A (MT2A) single nucleotide polymorphism (SNP) and Cd, Zn and Cu levels in the renal cortex from autopsy cases. MT2A core promoter region -5 A/G SNP was analyzed by PCR-RFLP method using 114 autopsy kidney tissues and the genotype frequencies of this polymorphism were found as 87.7% homozygote typical (AA), 11.4% heterozygote (AG) and 0.9% homozygote atypical (GG). In order to assess the Cd, Zn and Cu levels in the same autopsy kidney tissues, a dual atomic absorption spectrophotometer system was used and the average levels of Cd, Zn and Cu were measured as 95.54+/-65.58 microg/g, 181.20+/-87.72 microg/g and 17.14+/-16.28 microg/g, respectively. As a result, no statistical association was found between the -5 A/G SNP in the MT2A gene and the Zn and Cu levels in the renal cortex (p>0.05), but considerably high accumulation of Cd was monitored for individuals having AG (151.24+/-60.21 microg/g) and GG genotypes (153.09 microg/g) compared with individuals having AA genotype (87.72+/-62.98 microg/g) (p<0.05). These results show that the core promoter region polymorphism of metallothionein 2A increases the accumulation of Cd in human renal cortex.

journal_name

Toxicol Appl Pharmacol

journal_title

Toxicology and applied pharmacology

authors

Kayaalti Z,Mergen G,Söylemezoğlu T

doi

10.1016/j.taap.2010.03.007

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

252-5

issue

2

eissn

0041-008X

issn

1096-0333

pii

S0041-008X(10)00093-1

journal_volume

245

pub_type

杂志文章

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