Bioaccumulation of CdSe Quantum Dots Show Biochemical and Oxidative Damage in Wistar Rats

Abstract

Cadmium selenium quantum dots (CdSe QDs) with modified surfaces exhibit superior dispersion stability and high fluorescence yield, making them desirable biological probes. The knowledge of cellular and biochemical toxicity has been lacking, and there is little information on the correlation between in vitro and in vivo data. The current study was carried out to assess the toxicity of CdSe QDs after intravenous injection in Wistar male rats (230 g). The rats were given a single dose of QDs of 10, 20, 40, and 80 mg/kg and were kept for 30 days. Following that, various biochemical assays, hematological parameters, and bioaccumulation studies were carried out. Functional as well as clinically significant changes were observed. There was a significant increase in WBC while the RBC decreased. This suggested that CdSe quantum dots had inflammatory effects on the treated rats. The various biochemical assays clearly showed that high dose induced hepatic injury. At a dose of 80 mg/kg, bioaccumulation studies revealed that the spleen (120 g/g), liver (78 g/g), and lungs (38 g/g) accumulated the most. In treated Wistar rats, the bioretention profile of QDs was in the following order: the spleen, liver, kidney, lungs, heart, brain, and testis. The accumulation of these QDs induced the generation of intracellular reactive oxygen species, resulting in an alteration in antioxidant activity. It is concluded that these QDs caused oxidative stress, which harmed cellular functions and, under certain conditions, caused partial brain, kidney, spleen, and liver dysfunction. This is one of the most comprehensive in vivo studies on the nanotoxicity of CdSe quantum dots.

In Vivo Assessment of Hepatic and Kidney Toxicity Induced by Silicon Quantum Dots in Mice

“…Although the significant decrease in CAT activity could indicate a high amount of hydrogen peroxide, we should take into consideration that the increase in GPx activity after the first 6 h of exposure could actually suggest that the hydrogen peroxide was maintained at a low level based on the difference in K M for this substrate between these two enzymes. Similar results regarding the hepatic CAT activity after QDs administration have also been reported by Das et al [ 42 ]. The transient increase in SOD activity at 6 h after administration might be due to either indirect activation by SiQDs, stimulating the production of superoxide anion in the cells and activating the antioxidant defense mechanisms in order to counteract the radicals; or due to the alteration of gene expression involved in SOD synthesis.…”

“…After a dose-dependent decrease in SOD activity after the first hour, an increase in this enzyme’s activity compared with the control was measured after 6 h, suggesting that SOD was vulnerable at the beginning of exposure due to superoxide anion generation; however, antioxidant defense mechanisms were further activated to neutralize the free radicals. Nevertheless, this mechanism was not enough to counteract the oxidative stress as we could observe a decrease in SOD activity after 24 and 72 h. A previous report of Das et al [ 42 ] showed the same reduction in renal SOD activity after CdSe QD administration at a high dose to rats. This pattern of activity dynamics was also evidenced in the case of Gred and GPx, showing that the balance between GSH utilization and regeneration was perturbed, as it was confirmed by the dose- and time-dependent decrease in GSH levels.…”

“…However, the liver successfully neutralized the toxicity after 24 h, and the MDA level returned to the control values. No changes in MDA levels were also measured in the liver of mice that were injected with non-toxic near infrared QD800 linked to peptides containing arginine–glycine–aspartic acid [ 17 ] and Mn-doped ZnS QDs and QDs-PEG [ 18 ]; however, significant higher lipid peroxidation in hepatic cells was previously obtained for the toxic CdTe QDs [ 19 , 20 ] and CdSe QDs [ 42 , 43 ].…”

“…The decrease in CAT activity in a dose-dependent manner could indicate a reduction in its function due to hydrogen peroxide generation and accumulation. In contrast, more toxic QDs, such as CdTe and CdSe QDs, induced higher CAT activities in mice [ 19 ] and rats [ 42 ], respectively, compared with the control. After a dose-dependent decrease in SOD activity after the first hour, an increase in this enzyme’s activity compared with the control was measured after 6 h, suggesting that SOD was vulnerable at the beginning of exposure due to superoxide anion generation; however, antioxidant defense mechanisms were further activated to neutralize the free radicals.…”

A Review of in vivo Toxicity of Quantum Dots in Animal Models

“…These newly developed non-Cd QDs exhibit improved blood half-life and minimal reticuloendothelial system (RES) uptake. 25 QDs toxicity has also been studied by using different animal models, such as zebrafish, 26 xenopus, 27 mouse, 28 rat 29 , 30 and macaque. 31 …”