Background Silver nanoparticles (AgNPs) can accumulate in various organs after oral exposure. The main objective of the current study is to evaluate the renal toxicity induced by AgNPs after repeated oral exposure and to determine the relevant molecular mechanisms. Methods In this study, 40 male Wistar rats were treated with solutions containing 30, 125, 300, and 700 mg/kg of AgNPs. After 28 days of exposure, histopathological changes were assessed using hematoxylin-eosin (H&E), Masson’s trichrome, and periodic acid-Schiff (PAS) staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and the level of expression of the mRNAs of growth factors was determined using RT-PCR. Results Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border, and interrupted tubular basal laminae. These changes were more noticeable in groups treated with 30 and 125 mg/kg. The collagen intensity increased in the group treated with 30 mg/kg in both the cortex and the medulla. Apoptosis was much more evident in middle-dose groups (i.e., 125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in the treated groups (p < 0.05). Moreover, the data related to EGF, TNF-α, and TGF-β1 revealed that AgNPs induced significant changes in gene expression in the groups treated with 30 and 700 mg/kg compared to the control group. Conclusion Our observations showed that AgNPs played a critical role in in vivo renal toxicity.

Background: Silver nanoparticles have antibacterial properties and their use is growing in different industries. Since the toxicity of nanosilver is not well known, it is essential to examine its safety.

Currently, many corneal diseases are treated by corneal transplantation, artificial corneal implantation or, in severe cases, keratoprosthesis. Owing to the shortage of cornea donors and the risks involved with artificial corneal implants, such as infection transmission, researchers continually seek new approaches for corneal regeneration. Corneal tissue engineering is a promising approach that has attracted much attention from researchers and is focused on regenerative strategies using various biomaterials in combination with different cell types. These constructs should have the ability to mimic the native tissue microenvironment and present suitable optical, mechanical and biological properties. In this article, we review studies that have focused on the current clinical techniques for corneal replacement. We also describe tissue-engineering and cell-based approaches for corneal regeneration.

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Background: Silver nanoparticles (AgNPs) can accumulate in various organs after orally exposure. This study evaluated the toxicity of AgNPs in vivo on histological changes, apoptosis and expression of growth factor genes in kidney. Methods: The male Wistar rats were treated orally with 30,125,300, and 700 mg/kg silver nanoparticles solution. After 28 days of exposure, histopatological changes were assessed by hematoxylin-eosin, trichrome Masson, and Pas staining. Apoptosis was quantified by TUNEL and immunohistochemistry of caspase-3, and level of expression of growth factors mRNAs were determined using RT-PCR. Results: Histopathologic examination revealed degenerative changes in the glomeruli, loss of tubular architecture, loss of brush border and interrupted tubular basal laminae. These changes were more noticeable in 30, and 125 mg/kg groups. The collagen intensity was increased in 30 treated groups in both cortex and medulla. Apoptosis was much more evident in middle dose groups (125 and 300 mg/kg). The results of RT-PCR indicated that Bcl-2 and Bax mRNAs upregulated in treated groups (p<0.05) and data of the EGF, TNF-α, and TGF-β1 revealed that AgNPs induced more enormous changes in gene expression in 30 and 700 mg/kg groups compared to control. Conclusion: Our observations showed that the AgNPs played a critical role in their in vivo renal toxicity.