Mitochondrial administration alleviates lead- and cadmium-induced toxicity in rat renal cells.

The role of heavy metals such as lead (Pb) and cadmium (Cd) in the etiology of many diseases has been proven. Also, these heavy metals can affect the normal mitochondrial function. Mitochondrial administration therapy is one of the methods used by researchers to help improve mitochondrial defects and diseases. The use of isolated mitochondria as a therapeutic approach has been investigated in in vivo and in vitro studies. Accordingly, in this study, the effects of mitochondrial administration on the improvement of toxicity caused by Pb and Cd in renal proximal tubular cells (RPTC) have been investigated. The results showed that treatment to Pb and Cd caused an increase in the level of free radicals, lipid peroxidation (LPO) content, mitochondrial and lysosomal membrane damage, and also a decrease in the reduced glutathione content in RPTC. In addition, reports have shown an increase in oxidized glutathione content and changes in energy (ATP) levels. Following, the results have shown the protective role of mitochondrial administration in improving the toxicity caused by Pb and Cd in RPTC. Furthermore, the mitochondrial internalization into RPT cells is mediated through actin-dependent endocytosis. So, it could be suggested that the treatment of Pb- and Cd-induced cytotoxicity in RPTC could be carried out through mitochondria administration.

Phytohormone abscisic acid ameliorates cognitive impairments in streptozotocin-induced rat model of Alzheimer's disease through PPARß/δ and PKA signaling.

Aim: Alzheimer's disease (AD) is characterized by oxidative stress, neuroinflammation and progressive cognitive decline. Abscisic acid (ABA) is produced in a variety of mammalian tissues, including brain. It has anti-inflammatory and antioxidant effects and elicits a positive effect on spatial learning and memory performance. Here, the possible protective effect of ABA was evaluated in streptozotocin (STZ)-induced AD rat model which were injected intracerebroventriculary (i.c.v.) with STZ (3 mg/kg). Material and Methods: The STZ-treated animals received ABA (10 µg/rat, i.c.v.), ABA plus PPARß/δ receptor antagonist (GSK0660, 80 nM/rat) or ABA plus selective inhibitor of PKA (KT5720, 0.5 µg/rat) for 14 d. Learning and memory were determined using Morris water maze (MWM) and passive avoidance (PA) tests. Results: The data showed that STZ produced a significant learning and memory deficit in both MWM and PA tests. ABA significantly prevented the learning and memory impairment in STZ-treated rats. However, ABA effects were blocked by GSK0660 and KT5720. Conclusion: The data indicated that ABA attenuates STZ-induced learning and memory impairment and PPAR-ß/δ receptors and PKA signaling are involved, at least in part, in the ABA mechanism.

Mechanisms Involved in the Formation of Biocompatible Lipid Polymeric Hollow Patchy Particles.

Patchy polymeric particles have anisotropic surface domains that can be remarkably useful in diverse medical and industrial fields because of their ability to simultaneously present two different surface chemistries on the same construct. In this article, we report the mechanisms involved in the formation of novel lipid-polymeric hollow patchy particles during their synthesis. By cross-sectioning the patchy particles, we found that a phase segregation phenomenon occurs between the core, shell, and patch. Importantly, we found that the shear stress that the polymer blend undergoes during the particle synthesis is the most important parameter for the formation of these patchy particles. In addition, we found that the interplay of solvent-solvent, polymer-solvent, and polymer-polymer-solvent interactions generates particles with different surface morphologies. Understanding the mechanisms involved in the formation of patchy particles allows us to have a better control on their physicochemical properties. Therefore, these fundamental studies are critical to achieve batch control and scalability, which are essential aspects that must be addressed in any type of particle synthesis to be safely used in medicine.

Closing the gap: accelerating the translational process in nanomedicine by proposing standardized characterization techniques.

On the cusp of widespread permeation of nanomedicine, academia, industry, and government have invested substantial financial resources in developing new ways to better treat diseases. Materials have unique physical and chemical properties at the nanoscale compared with their bulk or small-molecule analogs. These unique properties have been greatly advantageous in providing innovative solutions for medical treatments at the bench level. However, nanomedicine research has not yet fully permeated the clinical setting because of several limitations. Among these limitations are the lack of universal standards for characterizing nanomaterials and the limited knowledge that we possess regarding the interactions between nanomaterials and biological entities such as proteins. In this review, we report on recent developments in the characterization of nanomaterials as well as the newest information about the interactions between nanomaterials and proteins in the human body. We propose a standard set of techniques for universal characterization of nanomaterials. We also address relevant regulatory issues involved in the translational process for the development of drug molecules and drug delivery systems. Adherence and refinement of a universal standard in nanomaterial characterization as well as the acquisition of a deeper understanding of nanomaterials and proteins will likely accelerate the use of nanomedicine in common practice to a great extent.