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Platinum nanoparticles (PtNPs) are one of the widely used NPs, which contribute to potential risks to the aquatic ecosystem. However, PtNPs toxicity in phytoplankton remains inadequately understood, with significant gaps in knowledge regarding their biochemical bases and species-specific responses. Herein, we investigated the impact of PtNPs on two cyanobacterial species (Anabaena laxa and Nostoc muscorum) to explore the harmful pathways triggered by PtNPs in cyanobacteria, which may help in selecting appropriate biomarkers for PtNPs pollution in aquatic environments. We studied the effect of PtNPs on growth, oxidative stress markers, and antioxidant defense systems of the two species. The obtained results showed that PtNPs reduced the level of chlorophyll. Furthermore, they induced dose-dependent oxidative stress to the two species, expressed by significant increases in H 2 O 2 , malondialdehyde (MDA), and protein oxidation (p < 0.05). Stress-induced oxidative damages were more pronounced in N. muscorum, yet the two cyanobacterial species showed higher levels (p < 0.05) of antioxidant metabolites and antioxidant enzymes to combat oxidative stress. Compared to N. muscorum, A. laxa invested more in the induction of antioxidant metabolites including FRAP, polyphenols, flavonoids, and glutathione (GSH), as well as in antioxidant enzymes such as POX, CAT, GR, and GPX. Overall, A. laxa species could be exploited as efficient biomarkers for monitoring PtNPs-induced ecotoxicology. Further investigation of bio-absorption and uptake of PtNPs by microalgae is recommended for developing algae-based bioremediation technologies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Environmental and occupational exposure to heavy metals, including cadmium (Cd), is associated with extremely adverse impacts to living systems. Antioxidant agents are suggested to eliminate Cd intoxication. In this paper, we investigated the potential neuroprotective effect of protocatechuic acid (PCA) against Cd-induced neuronal damage in rats. Adult male Wistar rats were randomly divided into control, PCA (100 mg/kg)-treated, CdCl 2 (6.5 mg/kg)-treated, and PCA and Cd treatment groups. Pre-treatment with PCA significantly reduced Cd concentrations and increased cortical acetylcholinesterase activity and brain derived neurotrophic factor. Additionally, PCA also prevented CdCl 2 -induced oxidative stress in the cortical tissue by preventing lipid peroxidation and the formation of nitric oxide (NO), and significantly enhancing antioxidant enzymes. Molecularly, PCA significantly up-regulated the antioxidant gene expression (Sod2, Cat, Gpx1, and Gsr) that was down-regulated by Cd. It should be noted that this effect was achieved by targeting the nuclear-related factor 2 (Nfe2l2) mRNA expression. PCA also prevented the Cd-induced inflammation by reducing the pro-inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β. Moreover, PCA supplementation relieved the Cd-induced neuronal death by increasing Bcl-2 and decreasing Bax and Cas-3 levels in the cortical tissue. The improvement of the cortical tissue histopathology by PCA confirmed the biochemical and molecular data. Collectively, our findings indicate that PCA can counteract Cd-induced cortical toxicity by enhancing the antioxidant defense system and suppressing inflammation and apoptosis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020. Published by Elsevier B.V.)

Globally, prostate cancer is among the most threatening and leading causes of death in men. This study, therefore, aimed to search for an ideal antitumor strategy with high efficacy, low drug resistance, and no or few adverse effects. Resistomycin is a natural antibiotic derived from marine actinomycetes, and it possesses various biological activities. Prostate cancer cells (PC3) were treated with resistomycin (IC12.5: 0.65 or IC25: 1.3 µg/mL) or 5-fluorouracil (5-FU; IC25: 7 µg/mL) for 24 h. MTT assay and flow cytometry were utilized to assess cell viability and apoptosis. Oxidative stress, apoptotic-related markers, and cell cycle were also assessed. The results revealed that the IC50 of resistomycin and 5-FU on PC3 cells were 2.63 µg/mL and 14.44 µg/mL, respectively. Furthermore, treated cells with the high dose of resistomycin showed an increased number of apoptotic cells compared to those treated with the lower dose. Remarkable induction of reactive oxygen species generation and lactate dehydrogenase (LDH) leakage with high malondialdehyde (MDA), carbonyl protein (CP), and 8-hydroxyguanosine (8-OHdG) contents were observed in resistomycin-treated cells. In addition, marked declines in glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in PC3 cells subjected to resistomycin therapy were observed. Resistomycin triggered observable cell apoptosis by increasing Bax, caspase-3, and cytosolic cytochrome c levels and decreasing Bcl-2 levels. In addition, notable downregulation of proliferating cell nuclear antigen (PCNA) and cyclin D1 was observed in resistomycin-treated cancerous cells. According to this evaluation, the antitumor potential of resistomycin, in a concentration-dependent manner, in prostate cancer cells was achieved by triggering oxidative stress, mitochondrial apoptosis, and cell cycle arrest in cancer cells. In conclusion, our investigation suggests that resistomycin can be considered a starting point for developing new chemotherapeutic agents for human prostate cancer. [ABSTRACT FROM AUTHOR]

Schistosomiasis is a tropical disease with socioeconomic problems. The goal of this study was to determine the influence of myco-synthesized nano-selenium (SeNPs) as a molluscicide on Biomphlaria alexandrina snails, with the goal of reducing disease spread via non-toxic routes. In this study, Penicillium chrysogenum culture filtrate metabolites were used as a reductant for selenium ions to form nano-selenium. The SeNPs were characterized via UV-Vis spectrophotometer, Fourier transform infrared (FT-IR) spectroscopy, transmission electron microscopy (TEM), dynamic light scattering (DLS), and X-ray diffraction (XRD). Myco-synthesized SeNPs had a significant molluscicidal effect on B. alexandrina snails after 96 h of exposure at a concentration of 5.96 mg/L. SeNPs also had miracidicidal and cercaricidal properties against S. mansoni. Some alterations were observed in the hemocytes of snails exposed to SeNPs, including the formation of pseudopodia and an increasing number of granules. Furthermore, lipid peroxide, nitric oxide (NO), malondialdehyde (MDA), and glutathione s-transferase (GST) increased significantly in a dose-dependent manner, while superoxide dismutase (SOD) decreased. The comet assay revealed that myco-synthesized SeNPs could cause breaks in the DNA levels. In silico study revealed that SeNPs had promising antioxidant properties. In conclusion, myco-synthesized SeNPs have the potential to be used as molluscicides and larvicides. [ABSTRACT FROM AUTHOR]