Antioxidant and hepatoprotective role of selenium against silver nanoparticles

Abstract

Silver nanoparticles (AgNPs) have attracted the most interest in terms of their potential biomedical and industrial applications. However, these nanoparticles have shown their toxic behavior toward environment, living tissues, and organisms. Selenium (Se), an essential trace element, is necessary for various metabolic processes, including protection against oxidative stress and immune function. The present study was undertaken to evaluate the effect of Se against AgNP-induced hepatic oxidative stress. AgNPs were synthesized and then prepared nanoparticles were characterized using various analytical techniques such as UV-visible spectroscopy, X-ray diffraction, and transmission electron microscopy. Rats were administered AgNPs intraperitoneally (5 mg/kg/day) and Se (0.2 mg/kg) was given by gavage. AgNP administration induced hepatic damage as indicated by the serum marker enzymes with reduction in levels of glutathione, and decrease in activities of SOD, CAT, and GSH-peroxidase (P<0.05). Decrease in levels of total antioxidant capacity (TAC) and increase in level of C-reactive protein (CRP) was also observed in AgNP-treated group compared to control group. However, Se markedly attenuated AgNP-induced biochemical alterations, levels of TAC, CRP, and serum transaminases (AST, ALT) (P<0.05). Taken together, these findings suggest that administration of AgNPs produces hepatotoxicity in rats, whereas Se supplementation attenuates these effects.

Keywords: antioxidant enzymes; hepatotoxicity; oxidative stress; selenium; silver nanoparticles.

Figure 1

(A) UV-visible spectra of AgNPs, (B) XRD pattern of AgNPs. Abbreviations: AgNPs, silver nanoparticles; UV, ultraviolet; XRD, X-ray diffraction.

Figure 2

(A, B) TEM images of AgNPs, (C) HRTEM of AgNPs, (D) SAED pattern of AgNPs. Abbreviations: TEM, transmission electron microscopy; AgNPs, silver nanoparticles; HRTEM, high-resolution transmission electron microscopy; SAED, selected area (electron) diffraction.

Figure 3

(A) Effect of Se on AgNP-induced GSH levels, the data represent means ± SEM. (B–D) Influence of Se on AgNP-induced antioxidant levels in the liver compared with their respective control groups, the data represent means ± SEM. a: P<0.05 with respect to the control group (significant). b: P<0.05 with respect to AgNP group (significant). Abbreviations: Se, selenium; AgNP, silver nanoparticle; Cont, control; GSH, glutathione; prot, protein.

Figure 4

(A, B) Influence of Se on AgNP-induced TAC and CRP levels in serum compared with their respective control groups. The data represent means ± SEM. a: P<0.05 with respect to the control group (significant). b: P<0.05 with respect to AgNP group (significant). Abbreviations: Se, selenium; AgNP, silver nanoparticle; TAC, total antioxidant capacity; CRP, C-reactive protein; Cont, control; prot, protein.

Figure 5

Histological evaluation of Se and AgNPs treatment of rats. (A) Control group, normal liver architecture showing portal area (circle), hepatic strands of eosinophils (arrows), and central vein. (B) AgNPs treated group showing portal tract expansion (square), dense infiltration of mononuclear cells (star), increase in Kupffer cells (Kc), proliferated bile duct (Bd), and accumulation of cells around central vein. (C) Section of rat liver (Se-treated) showing normal hepatocytes and central vein similar to control. (D) Section of rat livers (Se + AgNPs treated) showing normal cellular appearance and decrease in toxicity (arrows). Scale bar 50 μm. Abbreviations: Se, selenium; AgNPs, silver nanoparticles; CV, central vein.