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In foundries, various ores are used. Genotoxic assessment of ore-particles was the important aim of this study. In this regard, Ferrochromium, Ferrosilicon, Ferromanganese, and graphite were collected from an iron-casting industry. Also, the analysis has been performed by inductively coupled plasma optical emission spectroscopy (ICP-OES) and Fourier transform-infrared spectroscopy (FT-IR). The effective particle doses for A549-cells and genetic damages were evaluated using MTT and comet assay, respectively. The analysis indicated that, the samples contain Cr, Al, Cu, Fe, Mn, Zn, Ni, Pb, and SiO2. Ferrosilicon was known as the highest toxic ore. Ore particles significantly induced DNA breaks (p < 0.01) in a dose-dependent manner. A mixture of heavy-metals and silica in trace amounts caused genetic impairment. Moreover, the human health risk of the green–melting procedure is still notable in the casting industry. [ABSTRACT FROM AUTHOR]

Alzheimer's disease remains an issue of great controversy due to its pathology. It is characterized by cognitive impairments and neuropsychiatric symptoms. The FDA approved medications for this disease, can only mitigate the symptoms. One reason for the lack of effective medications is the inaccessibility of the brain which is encompassed by the blood-brain barrier, making intranasal (IN) route of administration potentially advantageous. Male Wistar rats underwent stereotaxic surgery to induce an Alzheimer's disease model via intracerebroventricular (ICV) streptozotocin injection, and Carbamylated Erythropoietin-Fc (CEPO-FC), a derivative of Erythropoietin without its harmful characteristics, was administered intranasally for ten consecutive days. Cognition performance for memory and attention was assessed using the Novel Object Recognition Test and the Object-Based Attention Test respectively. Depression like behavior was evaluated using the Forced Swim Test. Western blotting was done on the extracted hippocampus to quantify STIM proteins. Calbindin, PSD-95, Neuroplastin, Synaptophysin and GAP-43 genes were assessed by Realtime PCR. Behavioral tests demonstrated that IN CEPO-FC could halt cognition deficits and molecular investigations showed that, STIM proteins were decreased in Alzheimer's model, and increased after IN CEPO-FC treatment. Calbindin and PSD-95 were downregulated in our disease model and upregulated when treated with IN CEPO-FC. While Neuroplastin, and GAP-43 expressions remained unchanged. This study suggests that IN CEPO-FC in low doses could be promising for improving cognition and synaptic plasticity deficits in Alzheimer's disease and since IN route of administration is a convenient way, choosing IN CEPO-FC for clinical trial might worth consideration. See also the graphical abstract(Fig. 1)., (Copyright © 2024 Mansouri et al.)