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Effect of cadmium on anion exchange capability through Band 3 protein in human erythrocytes
Author(s) -
Rossana Morabito,
Alessia Remigante,
Benedetta Arcuri,
Angela Marino,
Marco Giammanco,
Giuseppina La Spada
Publication year - 2018
Publication title -
journal of biological research - bollettino della società italiana di biologia sperimentale
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.218
H-Index - 6
eISSN - 2284-0230
pISSN - 1826-8838
DOI - 10.4081/jbr.2018.7203
Subject(s) - band 3 , cadmium , oxidative stress , protein expression , antioxidant , membrane , chemistry , homeostasis , cell , metal , enzyme , toxicity , red blood cell , cell membrane , biophysics , biochemistry , membrane protein , biology , microbiology and biotechnology , gene , organic chemistry
The efficiency of Band 3 protein, mediating HCO3-/Cl- exchange across erythrocytes membrane, is reduced by oxidative stress. The aim of the present study was to verify whether Band 3 protein efficiency is compromised by treatment with Cadmium (Cd2+), an extremely toxic heavy metal known to interfere with antioxidant enzymes, energy metabolism, gene expression and cell membranes. To this end, the rate constant for SO4= uptake through Band 3 protein (accounting for velocity of anion exchange) was measured along with membrane –SH groups, Malonyldialdehyde (MDA) and Band 3 protein expression levels in Cd2+ -treated human erythrocytes (300 µM, 1 mM). Our results show that Cd2+ reduced the rate constant for SO4= uptake, with a significant increase in MDA levels at both concentrations and with a reduction in –SH groups observed after 1 mM Cd2+ treatment, whereas Band 3 protein expression levels were unchanged in both conditions. In conclusion: i) Cd2+ reduces Band 3 protein efficiency via different mechanisms depending on metal concentration and with unchanged expression levels; ii) the assessment of Band 3 protein anion exchange capability is a good tool to assay the impact of heavy metals on cell homeostasis and, possibly, useful for diagnosis and monitoring of devalopment of Cd2+ toxicity-related pathologies.

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