Mahmoud I. M. Darwish

The current study aimed to assess the potential biological and cellular impacts of dietary supplementation with chitosan-flaxseed oil nanocomposite (CFN) in boosting the growth performance indices, digestive enzyme activity, innate immune capacity, economic significance, gene expression, and histopathological alterations in the Nile tilapia exposed to chronic cold stress. Nile tilapia were distributed into six experimental groups, the first three groups were reared under optimum water temperature (25 °C) and fed 0 mg/kg CFN (control), 20 mg/kg CFN or 40 mg/kg -incorporated diets, respectively. However, the other three groups were reared under cold stress conditions (18 °C), and received the same previously mentioned diets, respectively. Growth performance and economic significance analysis were monitored throughout the experiment. Serum and tissue samples were collected after 60 days to evaluate immune indices (lysozyme, nitric oxide, and IgM), glucose, growth hormone (GH), digestive enzymes (amylase and lipase), gene expression (interleukin-8, tumor necrosis factor-alpha, interleukin-1ß, lysozyme-G, lysozyme-C, transforming growth factor-beta, nuclear factor kappa β, myeloperoxidase, and Toll-like receptor-5, and glutathione perioxidase-1), and histopathological changes. A subsequent bacterial challenge with Pseudomonas aeruginosa was carried out, where the clinical disorders and mortalities were monitored. The outcomes showed remarkable declines in various growth metrics, immune variables with dysregulation in the immune-linked genes in fish exposed to chronic cold stress circumstances, compared to fish reared at optimum temperature. Nonetheless, dietary intervention with CFN mitigated the negative impacts induced by cold stress exposure, where the growth, immune indices, and digestive enzymes were notably enhanced in the supplemented groups in relation to the non-supplemented group. The histopathological alterations in the intestine and spleen were also markedly alleviated. Additionally, the expression profiles of both inflammatory cytokines and apoptosis were positively modified. Furthermore, fish resilience to P. aeruginosa infection was triggered, which was evident by the amelioration of the clinical signs and declining mortality rates in CFN-enriched groups. Taken together, CFN is a promising antibacterial dietary additive which promotes the growth, health, and performance of the Nile tilapia.

Background: Plastic is one of the most versatile and widely used materials, but the environmental accumulation of nanoplastics (NPs) poses a risk to human health. Preclinical studies have verified that the liver is one of the main organs susceptible to NPs. Biobran/MGN-3, an arabinoxylan from rice bran, has been shown to have hepatoprotective effects; here, we show Biobran’s ability to alleviate polyethylene nanoplastics (PE-NPs)-induced liver cell toxicity by reversing apoptosis and restoring G2/M cell arrest in mouse liver cells (BNL CL.2). Methods: Toxicological effects were measured using the sulforhodamine B (SRB) assay for cell viability and flow cytometry for cell cycle analysis and apoptosis. An in silico study was also used to demonstrate the docking of PE-NPs to pro-inflammatory mediator proteins (IL-6R, IL-17R, CD41/CD61, CD47/SIRP), cell cycle regulators (BCL-2, c-Myc), as well as serine carboxypeptidase, which is an active ingredient of Biobran. Results: Exposing liver cells to PE-NPs caused a significant decrease in cell viability, with an IC50 value of 334.9 ± 2.7 µg/mL. Co-treatment with Biobran restored cell viability to normal levels, preserving 85% viability at the highest concentration of PE-NPs. Additionally, total cell death observed after exposure to PE-NPs was reduced by 2.4-fold with Biobran co-treatment. The G2/M arrest and subsequent cell death (pre-G0 phase) induced by PE-NPs were normalized after combined treatment. The in silico study revealed that Biobran blocks the nucleophilic centers of PE-NPs, preventing their interaction with pro-inflammatory mediators and cell cycle regulators. Conclusions: These findings highlight the potential use of Biobran as a hepatoprotector against NP toxicity.