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Protective Effect of Natural and Synthetic Anthocyanins against Tert-butyl-hydroperoxide-induced Oxidative Damages in Normal and β-thalassemic Major Human Erythrocytes In Vitro



Even though β-thalassemia major is a genetic blood disorder, the damages
endured by erythrocytes are mediated in part by oxidative stress. Antioxidants such as anthocyanins
are capable to prevent the pro-oxidant effects induced by reactive oxygen species (ROS).



This study aims to evaluate the in vitro preventive effects of one natural and two synthetic
anthocyanins on normal and β-thalassemic erythrocytes on which toxicity has been induced by the
free radical generator: tert-butyl-hydroperoxide TBHP.



Erythrocytes isolated from fasting blood samples of healthy and β-thalassemic major individuals
were treated either with TBHP alone or with TBHP after being pre-incubated with anthocyanins.
Cell viability, reduced glutathione (GSH) and malondialdehyde (MDA) contents were measured
after 90 minutes of incubation. In parallel, the antiradical scavenging capacities of the investigated
anthocyanins were also estimated by using the 2,2-DiPhenyl-1-PicrylHydrazyl (DPPH•) assay.



The results clearly demonstrate that the treatment of erythrocytes with TBHP induces hemolysis
along with marked redox state alteration (lipid peroxidation concomitant to GSH depletion)
in both normal and β-thalassemia erythrocytes. During the pre-treatment with anthocyanins, erythrocytes
become more resistant to oxidative impairments. Cyanin chloride and 6,7,3’,4’-
tetrahydroxyflavylium chloride effectively prevent from TBHP-induced: hemolysis, lipid peroxidation
and GSH depletion in normal and thalassemic erythrocytes, while 3’4’-dihdroxy-7-methoxyflavylium
chloride had a lesser effect on MDA levels with thalassemic erythrocytes. These results are
in agreement with those derived from the DPPH• assay.



Our study contributes with important insights that tested anthocyanins may exert relevant
potential in the alleviation of oxidative stress, especially the one affecting β-thalassemia erythrocytes.
