Silver has been used for years in medicine; it has known antimicrobial properties. Additionally, silver has been used in water and air filtration to eliminate microorganisms, and, more recently, as a biocide to prevent infections in burns. In contact with the human body, nanoparticles can elicit a spectrum of tissue responses such as the generation of reactive oxygen species, decreased function of mitochondria and even cell death. Mitochondries are intracellular organelles that play a crucial role in ATP production. In the present work, we evaluate the in vitro effect of silver nanoparticles (AgN) on the activities of mitochondrial respiratory chain complexes from the brain, skeletal muscle, heart, and liver of rats. Our results demonstrated that AgN (10, 25, and 50 mg l(-1)) decreases the activity of mitochondrial respiratory chain complexes I, II, III, and IV from all tissues.

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The bacterial lipopolysaccharide (LPS) is a highly toxic molecule derived from the outer membrane of gram-negative bacteria. LPS endotoxin affects the lungs and is used as a model of acute pulmonary inflammation affecting the cellular morphology of the organ. Previously, gold nanoparticles (GNPs) have been shown to demonstrate anti-inflammatory and antioxidative activity in muscle and epithelial injury models.The objective of this study was to investigate the effect of the intraperitoneal treatment using GNPs on the inflammatory response and pulmonary oxidative stress induced by LPS. Wistar rats were divided into four groups (N = 10): Sham; Sham + GNPs 2.5 mg/kg; LPS; and LPS + GNPs 2.5 mg/kg. Treatment with LPS upregulated the levels of markers of cellular and hepatic damage (CK, LDH, AST, and alanine aminotransferase); however, the group treated with only GNPs exhibited no toxicity.Treatment with GNPs reversed LPS-induced changes with respect to total peritoneal leukocyte count and the pulmonary levels of pro-inflammatory cytokines (IFN-γ and IL-6). Histological analysis revealed that treatment with GNPs reversed the increase in alveolar septum thickness due to LPS-induced fibrosis. In addition, treatment with GNPs decreased production of oxidants (nitrite and DCFH), reduced oxidative damage (carbonyl and sulfhydryl), and downregulated activities of superoxide dismutase and catalase. Treatment with GNPs did not showed toxicity; however, it exhibited anti-inflammatory and antioxidative activity that reversed morphological alterations induced by LPS. K E Y W O R D S gold nanoparticles, inflammation, lipopolysaccharide, lung, oxidative stress

PURPOSE. This study evaluates the effects of the gold nanoparticle in endotoxin-induced uveitis in rats.METHODS. Adult male Wistar rats were divided into five groups: saline þ saline, lipopolysaccharide (LPS) þ saline, LPS þ prednisolone, LPS þ gold salt (GS) and LPS þ gold nanoparticle (GNP). Two hours after LPS administration, prednisolone acetate 1%, GS, and GNP were topically applied to both eyes of rats and repeated every 6 hours for 24 hours. After 24 hours, rats were anesthetized and aqueous humor was sampled and the irides were removed. Aqueous humor TNF-a, myeloperoxidase activity were determined. Irides oxidative damage and content of toll-like receptor 4 (TLR4) and nuclear factor-jB (NF-jB) were determined.RESULTS. The administration of LPS-induced eye inflammatory response characterized by an increase in aqueous humor TNF-a, myeloperoxidase, and by irides oxidative damage. All these parameters were decreased by the administration of GNP. Since the inflammatory response secondary to LPS administration depends, in part, to the activation of the TLR4-NF-jB pathway we demonstrated here that a potential mechanism to explain the GNP effects was the decrease on TLR4 content and NF-jB activation.CONCLUSIONS. These findings suggest that topical GNP decreases intraocular inflammation and oxidative damage by interfering in the TLR4-NF-jB pathway. Oxidative stress is also suggested to be pathogenic by inducing inflammation in the eye. 10,11Endotoxin-induced uveitis (EIU) is an established animal model for ocular inflammation. These animals develop acute bilateral anterior inflammation, characterized by a breakdown of the blood-ocular barrier and accumulation of inflammatory cells. 12 Oxidative biomarkers are shown to be elevated in EIU, suggesting that inflammation and oxidative stress cooperatively contribute to its pathogenesis. 13Over the past few decades, gold nanoparticles (GNP) have become the object of special interest due to their antiinflammatory activity.14 Gold compounds have been used as anti-inflammatory treatment against rheumatoid arthritis for more than 50 years. [15][16][17] The molecular mechanisms of gold actions include modulation of pro-inflammatory, as well as inactivation of phagolysosomal enzymes and inhibition of NF-jB. 18,19 In view of these anti-inflammatory properties of gold compounds, the present study investigates the potential applications of GNP in the modulation of the inflammatory response in an animal model of uveitis. MATERIALS AND METHODS GNPs PreparationGNP were prepared as described by Turkevich et al. 20 In brief, glass vials were washed in aqua regia and rinsed in ultrapure water, then aurochloric acid solution (0.2 mM) was gently warmed up to 908C and sodium citrate (39 mM) was added. After 20 minutes of vigorous stirring and refluxing, the solution was cooled at room temperature (20 6 28C) and the GNP were purified by serial centrifugations at 9000g for 10 minutes, followed by supernatant removing and ultra pure water rinsing. The resulting powder was resuspended in s...

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This study evaluated the parameters of oxidative stress and energy metabolism after the acute and long-term administration of gold nanoparticles (GNPs, 10 and 30 nm in diameter) in different organs of rats. Adult male Wistar rats received a single intraperitoneal injection or repeated injections (once daily for 28 days) of saline solution, GNPs-10 or GNPs-30. Twenty-four hours after the last administration, the animals were killed, and the liver, kidney, and heart were isolated for biochemical analysis. We demonstrated that acute administration of GNPs-30 increased the TBARS levels, and that GNPs-10 increased the carbonyl protein levels. The long-term administration of GNPs-10 increased the TBARS levels, and the carbonyl protein levels were increased by GNPs-30. Acute administration of GNPs-10 and GNPs-30 increased SOD activity. Long-term administration of GNPs-30 increased SOD activity. Acute administration of GNPs-10 decreased the activity of CAT, whereas long-term administration of GNP-10 and GNP-30 altered CAT activity randomly. Our results also demonstrated that acute GNPs-30 administration decreased energy metabolism, especially in the liver and heart. Long-term GNPs-10 administration increased energy metabolism in the liver and decreased energy metabolism in the kidney and heart, whereas long-term GNPs-30 administration increased energy metabolism in the heart. The results of our study are consistent with other studies conducted in our research group and reinforce the fact that GNPs can lead to oxidative damage, which is responsible for DNA damage and alterations in energy metabolism.

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Introduction Tendinitis affects a substantial number of people in several occupations involving repetitive work or direct trauma. Iontophoresis is a therapeutic alternative used in the treatment of injury during the inflammatory phase. In recent years, gold nanoparticles (GNP) have been studied due to their therapeutic anti-inflammatory capacity and as an alternative to the transport of several proteins. Purpose This study evaluates the therapeutic effects of iontophoresis using GNPs and diclofenac diethylammonium on inflammatory parameters in rats challenged with traumatic tendinitis. Methods Wistar rats were divided in three treatment groups (n = 15): (1) iontophoresis + diclofenac diethylammonium; (2) iontophoresis + GNP; and (3) iontophoresis + diclofenac diethylammonium + GNP. External control was formed by challenged tendons without treatment (n = 15). Iontophoresis was administered using 0.3 mA direct current on 1.5 cm 2 electrodes. Results The levels of both inflammatory cytokines were significantly higher in untreated challenged rats, when compared with the control (5.398 ± 234 for interleukin 1 beta and 6.411 ± 432 for tumor necrosis factor alpha), which confirms the occurrence of an inflammatory stage in injury ( P < 0.05). A significant decrease was observed in expression of cytokines interleukin 1 beta in the three treatment groups, in comparison with untreated challenged tendons, although, in the group treated with diclofenac and GNP, results were similar to the control (1.732 ± 239) ( P < 0.05). Concerning tumor necrosis factor alpha, only the group treated with the association diclofenac and GNPs presented decreased levels, compared with the control (3.221 ± 369) ( P < 0.05). Conclusion The results show the efficacy of drug administration using direct current to treat tendinitis in an animal model, and the potential anti-inflammatory, carrier, and enhancing effects of GNPs in iontophoresis.