Little research has been conducted on the toxicity of aluminium oxide nanoparticles (Al-NPs) on aquatic organisms. In this context, the purpose of this study was to determine some mechanistic pathways underlying the toxicological impact of Al-NPs on growth performance, oxidative status, some pro-inflammatory gene expression, and the histological alterations in the gills and liver of Nile tilapia fish ( Oreochromis niloticus ). In addition, the beneficial role of two different doses of selenium nanoparticles (Se-NPs) dietary supplementation in antagonizing these effects was studied. Fish ( n =  180) were allotted into six groups: Control, 10 mg/L Al-NPs, 1 mg/kg Se-NPs + 10 mg/L Al-NPs, 2.5 mg/kg Se-NPs + 10 mg/L Al-NPs, 1 mg/kg Se-NPs, and 2.5 mg/kg Se-NPs for 28 days. Findings revealed that Al-NPs caused a substantial decrease ( P < 0.05) in growth indices (weight gain and feed efficiency ratio), plus oxidative damage demonstrated by decreased glutathione levels from 230.2 μM/g tissue to 130.1 μM/g tissue in liver tissue and from 260.4 μM/g tissue to 129.2 μM/g tissue in the gills. The levels of malondialdehyde elevated in the liver from 31,316.6 μM/g tissue to 48,180 μM/g tissue and in the gills from 16,650.3 μM/g tissue to 34,266.6 μM/g tissue along with the overexpression of pro-inflammatory genes, such as Tumor Necrosis Factor-β to 7.28-fold and 7.61-fold and Interleukin-1β to 9.54-fold and 8.08-fold in the gills and liver tissue, respectively. The dietary supplementation of both low and high doses of Se-NPs significantly (P < 0.05) reduced these negative impacts of Al-NPs, with the high dose having more noticeable mitigative effects. Furthermore, Al-NPs induced severe hepatocellular vacuolization, congestion and dilatation of the central veins and hepatic sinusoids, gill hyperplasia, and extensive fusion of secondary lamellae with massive inflammatory cell infiltration. This suggests that Se-NPs have growth-promotive, antioxidant, and anti-inflammatory properties in fish that encourage their usage as a great supplement to the fish diet.

Polyethylene terephthalate nanoplastics (PET-NPs) are utilized in the production of medical bionic materials and the packaging of beverages. Betaine is a ubiquitous natural constituent present in organisms such as plants, animals, and microorganisms. So, the current investigation tries to find out if PET-NPs could seriously harm mice's kidneys and whether betaine could have any ameliorative effects. In this study, a total of 40 mice were separated into four groups (ten mice in each): Group I (performed as the control group), Group II (received 1000 mg/kg betaine intraperitoneally), Group III (received 200 mg/kg PET-NPs orally), and Group IV (was given betaine first, and after 1 hour, PET-NPs were given at dosages that were the same as those given to groups II and III, respectively) daily for a month. Serum and kidney samples were collected and processed for biochemical and histological assessments. The current study found that PET-NPs significantly increased blood urea nitrogen (BUN), creatinine, and malondialdehyde levels (MDA), while reducing glutathione (GSH) levels. The histological examination revealed multiple histopathological alterations. The PET-NPs-exposed group demonstrated renal corpuscle hypotrophy, a loss of cellular structure in some proximal convoluted tubules (PCT) and distal convoluted tubules (DCT). The renal medulla exhibits hyalinization, congestion, and degeneration of collecting tubules. Conversely, the pre-administration of betaine results in a decline in BUN, creatinine, and MDA concentrations. Furthermore, there is a rise in GSH levels, and the group pretreated with betaine showed significant improvement in kidney architecture, with the renal cortex showing almost normal architecture and the collecting tubules in the renal medulla slightly improving. In conclusion, betaine showed a promising nephroprotective effect against PET-NP-induced toxicity

Background: Gold nanoparticles (AuNPs) have been considered as an ideal candidate in various biomedical applications due to their ease of tailoring into different size, shape, and decorations with different functionalities. The current study was conducted to investigate the epigenetic alteration in the lung in response to AuNPs administration regarding microRNA-155 (miR-155) gene which can be involved in AuNP-induced lung pathogenesis. Methods: Thirty-two Wister rats were divided into two equal groups, control group and AuNPs treated group which received a single intravenous (IV) injection of plain spherical AuNPs (0.015 mg/kg body wt) with an average diameter size of 25±3 nm. Lung samples were collected from both the control and injected groups at one day, one week, one month and two months post-injection. The alteration of relative expression of miR-155 gene and two of its putative target genes; tumor protein 53 inducible nuclear protein 1 (TP53INP1) and protein S (PROS1) was investigated by real time PCR and protein S (PS) expression was analyzed by Western blotting technique. Results: The obtained results revealed that AuNPs administration significantly increases the expression level of miR-155 and reduce relative mRNA expression of TP53INP1 and PROS1 genes at one day post-injection. In contrast, a significant down-regulation of miR-155 level of expression concurrent with up-regulation of expression level of TP53INP1 and PROS1 genes were shown at one week, one month and two months post-injection. PS levels were mirrored to their PROS1 mRNA levels except for two month post-injection time point. Conclusions: These findings indicate epigenetic modulation in the lung in response to AuNPs administration regarding the miR-155 gene which can be involved in AuNP-induced lung pathogenesis.