Curcumin-functionalized gold nanoparticles attenuate AAPH-induced acute cardiotoxicity via reduction of lipid peroxidation and modulation of antioxidant parameters in a chicken embryo model.

Gold nanoparticles (AuNPs) have gained considerable attention due to their biocompatibility, customizable optical properties and ease of synthesis. In this study, an environmentally friendly method was used for synthesize curcumin-functionalized AuNPs (AuNP-C). AuNP-C exhibited a spherical shape, uniformity, and an average diameter of 6 nm. The in vitro antioxidant activity was analyzed, and cytotoxicity properties of AuNP-C were assessed in fibroblast and macrophage cells. Additionally, the effects of AuNP-C on oxidative stress in chicken embryo liver and hearts were investigated. AuNP-C demonstrated potent free radical scavenging properties without exhibiting cytotoxicity and hepatotoxicity effects. Administration of 300 µg/mL of AuNP-C in chicken embryos, subjected to oxidative damage induced by 2,2'-azobis(2-amidinopropane) dihydrochloride, significantly reduced lipid peroxidation and reactive oxygen species levels in the cardiac tissue. Moreover, the activities of cardiac superoxide dismutase, catalase, and glutathione reductase were restored, accompanied by an increase in overall antioxidant capacity. Furthermore, at higher concentrations, AuNP-C normalized the reduced glutathione content. AuNP-C preserved the normal structure of blood vessels; however, it resulted in an increase in protein carbonylation. This study provides initial evidence for the modulation of antioxidant defense mechanisms by green-synthesized AuNPs and underscores the importance of investigating the in vivo safety of phytoantioxidant-functionalized nanoparticles.

BALB/c mice resistant to Toxoplasma gondii infection proved to be highly susceptible when previously infected with Myocoptes musculinus fur mites.

The immune response induced by Toxoplasma gondii is characterized by Th1 immune mechanisms. We previously demonstrated that C57BL/6 mice infested with Myocoptes musculinus and infected with T. gondii by intraperitoneal route undergo accelerated mortality according to Th2 immune mechanisms induced by the acarian. To evaluate whether infection with M. musculinus influences T. gondii-induced Th1 response in a resistant mouse lineage, BALB/c, which develops latent chronic toxoplasmosis in a way similar to that observed in immunocompetent humans, this study was done. The animals were infected with T. gondii ME-49 strain 1 month after M. musculinus infestation, being the survival and the immune response monitored. The double-infected displayed higher mortality rate if compared with the mono-infected mice. In addition, infection with M. musculinus changed the T. gondii-specific immune response, converting BALB/c host to a susceptible phenotype. Spleen cells had increased the levels of IL-4 in double-infected mice. This alteration was associated with severe pneumonia, encephalitis and wasting condition. In addition, a higher tissue parasitism was observed in double-infected animals. It can be concluded that infection with these two contrasting parasites, M. musculinus and T. gondii, may convert an immunocompetent host into a susceptible one, and such a host will develop severe toxoplasmosis.