Recent advances in particle-forming chemistries used for developing nanotechnology has not only widened novel applications for nanoscale materials but also has provided significant concern regarding their biological effects. The present study investigates the inflammatory responses of RAW 264.7 mouse macrophages exposed to nanoparticles (NPs, 5 μg/ml) of varied sizes including silver (Ag), aluminum (Al), carbon black (CB), carbon-coated silver (CAg) and gold (Au). A significant increase in IL-6, reactive oxygen species (ROS) generation, nuclear translocation of nuclear factor-kappa B (NF-κB), induction of cyclooxygenase-2 (COX-2), and tumor necrosis factor-alpha (TNF-α) expression was observed in macrophages with maximum response found in cells exposed to Ag NPs followed by Al, CB and CAg. These pro-inflammatory effects of NPs were dependent on size and duration of exposure and comparable to those induced by lipopolysaccharide (LPS), a known inflammatory mediator. Au NPs, on the other hand, induced small but significant inflammatory responses in macrophages upon prolonged exposure. These studies reveal that Ag NPs exhibit higher propensity in inducing inflammation, mediated by ROS and NF-κB signaling pathways and leading to the induction of COX-2, TNF-α and IL-6. However, no such prominent pro-inflammatory responses were observed with Au NPs, suggesting their bio-compatibility.

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2-AAF-induced oxidative stress is reduced by C-PC treatment. C-PC inhibited the 2-AAF induced expression of MDR1 by interfering at the level of ROS generation, Akt phosphorylation and NF-kappaB translocation. This study reveals the usefulness of C-PC in preventing oxidative stress and downregulation of MDR1 induced by xenobiotics like 2-AAF.