Palladium Nanoparticles and Lung Health: Assessing Morphology-Dependent Subacute Toxicity in Rats and Toxicity Modulation by Naringin - Paving the Way for Cleaner Vehicular Emissions.

The release of palladium nanoparticles (PdNPs) from autocatalytic converters has raised concerns regarding public health and the environment due to their emergence as anthropogenic contaminants. With growing vehicular population, there is an urgent need for comprehensive toxicological studies of PdNPs to mitigate their risk. The present study aims to investigate the effects of spherical PdNPs with average sizes of 20 and 80 nm, as well as Pd nanorods, on the lung function of female Wistar rats following oral exposure to environmentally relevant doses (1 and 10 µg/kg) over a period of 28 days. Various biological parameters were evaluated, including liver and kidney biochemical changes, lung oxidative stress markers (SOD, CAT, GSH, LPO), lung inflammatory markers (IL-1ß, IL-8, IL-6, and TNF-α), and histopathological alterations in the lungs. Additionally, the potential mitigating effects of naringin on PdNPs-induced toxicity were examined. The results demonstrate a significant increase in oxidative stress, the onset of inflammation, and histological changes in lung alveolar sacs upon exposure to all tested particles. Specifically, 20@PdNPs and PdNRs exhibited higher cytotoxicity and pro-inflammatory properties compared to 80@PdNPs. Naringin effectively attenuated the pulmonary toxicity induced by PdNPs by modulating oxidative and inflammatory pathways. These findings contribute to the sustainable development of PdNPs for their future applications in the biomedical and environmental sectors, ensuring the advancement of safe and sustainable nanotechnology.

GABAergic implications in anxiety and related disorders.

Evidence indicates that anxiety disorders arise from an imbalance in the functioning of brain circuits that govern the modulation of emotional responses to possibly threatening stimuli. The circuits under consideration in this context include the amygdala's bottom-up activity, which signifies the existence of stimuli that may be seen as dangerous. Moreover, these circuits encompass top-down regulatory processes that originate in the prefrontal cortex, facilitating the communication of the emotional significance associated with the inputs. Diverse databases (e.g., Pubmed, ScienceDirect, Web of Science, Google Scholar) were searched for literature using a combination of different terms e.g., "anxiety", "stress", "neuroanatomy", and "neural circuits", etc. A decrease in GABAergic activity is present in both anxiety disorders and severe depression. Research on cerebral functional imaging in depressive individuals has shown reduced levels of GABA within the cortical regions. Additionally, animal studies demonstrated that a reduction in the expression of GABAA/B receptors results in a behavioral pattern resembling anxiety. The amygdala consists of inhibitory networks composed of GABAergic interneurons, responsible for modulating anxiety responses in both normal and pathological conditions. The GABAA receptor has allosteric sites (e.g., α/γ, γ/ß, and α/ß) which enable regulation of neuronal inhibition in the amygdala. These sites serve as molecular targets for anxiolytic medications such as benzodiazepine and barbiturates. Alterations in the levels of naturally occurring regulators of these allosteric sites, along with alterations to the composition of the GABAA receptor subunits, could potentially act as mechanisms via which the extent of neuronal inhibition is diminished in pathological anxiety disorders.