Interaction of cadmium sulfide quantum dots capped with dextrin with rats red cells in vitro : hemolytic and morphology effect

Multiple advantages and biomedical applications are displayed for theragnostic purposes of quantum dots (QD). However, its potential toxicity restricts them for use in humans as a tool for detection, as biosensors, for bioimaging and as a vehicle for controlled drug release, to name a few. The hemolytic effect (erythrocyte lysis) and eryptosis (loss of its functionality due to deformation) are considered as indicative of toxicity for a nanomaterial. The aim of this study is to evaluate dextrin‐coated cadmium sulphide QD (CdS‐dex) with rats blood erythrocytes in vitro. The hemolytic test is used to evaluate the toxicity of QDs to erythrocytes. Blood was obtained from male Wistar rats (healthy) and placed in a tube with 3.2% sodium citrate anticoagulant (0.109 M). Then, we separated the erythrocytes and the count was performed in the Neubauer chamber with the help of an erythrocyte “Thoma” pipette. All the treatments evaluates of quantum dots was at [0.01, 0.1, 1, 10, 100 and 1000 µg/mL]. After 30 minutes of exposition the supernatant was collected, and was measured (λ=550 nm). An XE‐Bio Atomic Force Microscope (ATM) from Park Systems, South Korea, was used to obtain topographic images of erythrocyte at 30 and 60 minutes of time exposure of CdS‐dex at different concentration [0.01 at 1000 µg/mL]. XEP and XEI software from Park Systems were used to obtain and analyze data respectively. The CdS‐dex QD on erythrocytes caused hemolysis from the concentration of 0.01 to 1000 µg/mL. However, this effect did not exceed 10% of red cell lysis, respectively. Even so, there were significant changes in the morphology of erythrocytes treated with CdS‐dex QD, from the concentration of 0.01 to 1000 µg/mL both incubated at 30 and 60 minutes. That is, they have lost their classic biconcave shape, their size was reduced and they have lost their defined edges with respect to untreated erythrocytes. These findings could suggest that the deformation and structural changes could be caused by the QD in a concentration‐dependent manner. What could cause eryptosis, a type of erythrocytes programmed death that responded in a specialized way to the CdS‐dex QD. Although the erythrocytes did not lysate, we cannot assure that the deformation of their membrane does not cause the partial or total loss of their function and is the trigger to cause greater damage. In conclusion, our results suggest that the interaction of CdS‐Dex NPs has effects on erythrocytes in a concentration and incubation time dependent manner.