Surf Redfish-Based ZnO-NPs and Their Biological Activity with Reference to Their Non-Target Toxicity.

The marine environment is a rich source of bioactive compounds. Therefore, the sea cucumber was isolated from the Red Sea at the Al-Ain Al-Sokhna coast and it was identified as surf redfish (Actinopyga mauritiana). The aqueous extract of the surf redfish was utilized as an ecofriendly, novel and sustainable approach to fabricate zinc oxide nanoparticles (ZnO-NPs). The biosynthesized ZnO-NPs were physico-chemically characterized and evaluated for their possible antibacterial and insecticidal activities. Additionally, their safety in the non-target organism model (Nile tilapia fish) was also investigated. ZnO-NPs were spherical with an average size of 24.69 ± 11.61 nm and had a peak at 350 nm as shown by TEM and UV-Vis, respectively. XRD analysis indicated a crystalline phase of ZnO-NPs with an average size of 21.7 nm. The FTIR pattern showed biological residues from the surf redfish extract, highlighting their potential role in the biosynthesis process. DLS indicated a negative zeta potential (-19.2 mV) of the ZnO-NPs which is a good preliminary indicator for their stability. ZnO-NPs showed larvicidal activity against mosquito Culex pipiens (LC50 = 15.412 ppm and LC90 = 52.745 ppm) and a potent adulticidal effect to the housefly Musca domestica (LD50 = 21.132 ppm and LD90 = 84.930 ppm). Tested concentrations of ZnO-NPs showed strong activity against the 3rd larval instar. Topical assays revealed dose-dependent adulticidal activity against M. domestica after 24 h of treatment with ZnO-NPs. ZnO-NPs presented a wide antibacterial activity against two fish-pathogen bacteria, Pseudomonas aeruginosa and Aeromonas hydrophila. Histopathological and hematological investigations of the non-target organism, Nile tilapia fish exposed to 75-600 ppm ZnO-NPs provide dose-dependent impacts. Overall, data highlighted the potential applications of surf redfish-mediated ZnO-NPs as an effective and safe way to control mosquitoes, houseflies and fish pathogenic bacteria.

Neuroprotective and therapeutic effects of calcitriol in rotenone-induced Parkinson's disease rat model.

Parkinson's disease (PD) is the second most common neurodegenerative disease. Treatment of PD is challenging, as current treatment strategies are only symptomatic and do not stop disease development. Recent studies reported neuroprotective effects of calcitriol in PD through its antioxidant and anti-inflammatory properties. The exact pathomechanisms of PD are not yet fully understood. So, investigation of different molecular pathways is challenging. Sirtuin-1 (Sirt1) modulates multiple physiological processes, including programmed cell death, DNA repair, and inflammation. Furthermore, defective autophagy is considered a key pathomechanism in PD as it eliminates protein aggregation and dysfunctional cell organelles. The present study investigated the involvement of autophagy and Sirt1/NF-κB molecular pathway in rotenone-induced PD and explored the protective and restorative effects of calcitriol through these mechanisms. Therefore, behavioral tests were used to test the effect of calcitriol on motor disability and equilibrium. Furthermore, the histological and neuronal architecture was assessed. The expression of genes encoding neuroinflammation and autophagy markers was determined by qPCR while their protein levels were determined by Western blot analysis and immune-histochemical staining. Our results indicate that behavioral impairments and dopaminergic neuron depletion in the rotenone-induced PD model were improved by calcitriol administration. Furthermore, calcitriol attenuated rotenone-induced neuroinflammation and autophagy dysfunction in PD rats through up-regulation of Sirt1 and LC3 and down-regulation of P62 and NF-κB expression levels. Thus, calcitriol could induce a neuro-protective and restorative effect in the rotenone-induced PD model by modulating autophagy and Sirt1/NF-κB pathway.

Dietary Aspergillus oryzae Modulates Serum Biochemical Indices, Immune Responses, Oxidative Stress, and Transcription of HSP70 and Cytokine Genes in Nile Tilapia Exposed to Salinity Stress.

Nile tilapia Juveniles (19.50 ± 0.5 g) were fed on a basal diet (control group (CTR)) and a diet supplemented with 1 g Aspergillus oryzae (ASP) per kg diet for 12 weeks. Fish were then subjected to different salinity levels (0, 10, 15, and 20 practical salinity units (psu)) for another 15 days. Two-way ANOVA analysis revealed that the individual effects of ASP in Nile tilapia exposed to salinity levels presented a significant decrease (p < 0.05) in values of haemato-biochemical indices (such as glucose, cortisol, alanine transaminase, aspartate transaminase, and malondialdehyde) compared to those in the CTR group exposed to the same salinity levels. Moreover, significant increases (p < 0.05) of blood protein profile (albumin, globulin, and total protein), non-specific immune responses (lysozyme activity, phagocytic activity, and phagocytic index), and antioxidant enzymes activities (glutathione peroxidase, catalase, and superoxide dismutase) were observed in ASP-supplemented groups. Interestingly, there was significant (p < 0.05) downregulation of the mRNA expression values of heat shock protein 70 and interferon-gamma genes, alongside upregulation of the mRNA expression values of interleukin 1 beta and interleukin 8 genes, in the hepatic tissues of Nile tilapia in ASP-supplemented groups exposed to different salinities compared to those in the CTR group exposed to the same salinity levels. Taken together, these findings supported the potential efficacy of dietary supplementation with ASP in alleviating salinity stress-induced haemato-biochemical alterations, immune suppression, and oxidative stress in the exposed Nile tilapia.

Trial for use nanoselenium particle with different dietary regime in Oreochromis niloticus and Mugil cephalus polyculture ponds: Growth efficiency, haematological, antioxidant, immunity and transcriptional analysis.

BACKGROUND: Fish farming is one of the most productive economies in the world. One of the essential goals in fish production is to minimize processing costs while maintaining and increasing the vital functions, weight and immunity of fish. OBJECTIVE: We conducted this study to explore nanoselenium (Nano-Se) particles in various feeding schemes. MATERIAL AND METHOD: Nano-Se particles incorporated in the basal diet at (0.5 mg/kg diet), and the fish was divided into six groups after adaptation as the follows: The first group was feed daily with a diet containing Nano-Se (0.5 mg/kg diet); the second group was exposed to a feeding programme in which it has day feeding followed by day of starvation with a diet containing Nano-Se (0.5 mg/kg diet); the third group was day feeding followed by 2 days of starvation; the fourth group served as a negative control group in which this group was continuous feeding with a basal diet without Nano-Se; the fifth group was day feeding with the basal diet followed by a day of starvation; and the sixth group was day feeding with basal diet followed by 2 days of starvation. RESULT: Our result revealed that Group 2 showed significant improvement in haematological parameters, red blood cells and haemoglobin with a substantial increase in total protein (p < 0.05) as well as lysosomal and phagocytic activity with considerable upregulation of growth hormone and insulin growth factor 1 in addition to markedly increase in the pro-inflammatory cytokines. Finally, this study offers the first-time dietary regime with Nano-Se supplementation that saves the feeding cost and increases fish welfare and growth.

Modulation of vigabatrin induced cerebellar injury: the role of caspase-3 and RIPK1/RIPK3-regulated cell death pathways.

Vigabatrin is the drug of choice in resistant epilepsy and infantile spasms. Ataxia, tremors, and abnormal gait have been frequently reported following its use indicating cerebellar involvement. This study aimed, for the first time, to investigate the involvement of necroptosis and apoptosis in the VG-induced cerebellar cell loss and the possible protective role of combined omega-3 and vitamin B12 supplementation. Fifty Sprague-Dawley adult male rats (160-200 g) were divided into equal five groups: the control group received normal saline, VG200 and VG400 groups received VG (200 mg or 400 mg/kg, respectively), VG200 + OB and VG400 + OB groups received combined VG (200 mg or 400 mg/kg, respectively), vitamin B12 (1 mg/kg), and omega-3 (1 g/kg). All medications were given daily by gavage for four weeks. Histopathological changes were examined in H&E and luxol fast blue (LFB) stained sections. Immunohistochemical staining for caspase-3 and receptor-interacting serine/threonine-protein kinase-1 (RIPK1) as well as quantitative real-time polymerase chain reaction (qRT-PCR) for myelin basic protein (MBP), caspase-3, and receptor-interacting serine/threonine-protein kinase-3 (RIPK3) genes were performed. VG caused a decrease in the granular layer thickness and Purkinje cell number, vacuolations, demyelination, suppression of MBP gene expression, and induction of caspases-3, RIPK1, and RIPK3 in a dose-related manner. Combined supplementation with B12 and omega-3 improved the cerebellar histology, increased MBP, and decreased apoptotic and necroptotic markers. In conclusion, VG-induced neuronal cell loss is dose-dependent and related to both apoptosis and necroptosis. This could either be ameliorated (in low-dose VG) or reduced (in high-dose VG) by combined supplementation with B12 and omega-3.

Protective effect of rapamycin against acrylamide-induced hepatotoxicity: The associations between autophagy, apoptosis, and necroptosis.

Acrylamide (ACRL) was demonstrated to induce hepatotoxicity and programmed cell death (PCD). Rapamycin (RAPA)-induced autophagy had been reported to limit the progression of hepatocellular injury in experimental models. This research was designed to study two death pathways involved in ACRL-induced hepatotoxicity and the modulating effect of RAPA on the resulting hepatic injury. Thirty-six adult male rats were divided into three groups: control group, ACRL-treated group (20 mg kg/day), and the last group co-treated with ACRL plus RAPA (0.5 mg kg/day). Drugs were administered for 21 days via oral gavage. Blood samples were collected to assess alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Livers were dissected; parts were used for detection of superoxide dismutase (SOD) and malondialdehyde (MDA) tissue levels. Other parts were processed for hematoxylin and eosin, Masson's trichrome staining, immunostaining for microtubule-associated proteins 1A/1B light chain 3B (LC3), ubiquitin-binding protein (p62), caspase-3, and receptor-interacting protein kinase 1 (RIPK1). ACRL induced a significant elevation in ALT, AST, MDA levels, and reduction in the SOD level. ACRL also induced hepatocellular injury, fibrosis, and defective autophagy indicated by elevation of LC3 and p62 and increased p62/LC3 ratio. Moreover, it increased the apoptotic (caspase-3) and necroptotic (RIPK1) markers expression. RAPA significantly reduced liver enzymes, oxidative stress, fibrosis, and improved liver histology. Moreover, RAPA decreased p62/LC3 ratio indicated enhanced autophagy, and significantly reduced caspase-3 and RIPK1 expression. In conclusion, RAPA maintained autophagic activity which may save the hepatocytes from PCD and enhance cell viability.

Selenium Nanoparticles Act Potentially on the Growth Performance, Hemato-Biochemical Indices, Antioxidative, and Immune-Related Genes of European Seabass (Dicentrarchus labrax).

The current study investigated the role of selenium (Se) nanoparticles on the growth performance, hemato-biochemical indices, antioxidative, and immune-related genes of European seabass (Dicentrarchus labrax). Therefore, fish with initial weight of 20.53 ± 0.10 g/fish were fed diets with 0, 0.25, 0.5, and 1 mg Se nanoparticles/kg diet for 90 days. The final body weight, weight gain, and specific growth rate of fish fed dietary nano-Se varying levels were significantly higher than the control with the highest performances and lowest FCR in the group of fish fed nano-Se at 0.5 mg/kg. The values of Hb, PCV, RBCs, and WBCs were significantly higher in fish fed varying levels of Se nanoparticles than fish fed the basal diets. The values of total serum protein and globulin were significantly higher in fish fed varying levels of Se nanoparticles than fish fed the basal diets. Additionally, globulin had higher value in the group of fish fed 0.25 and 0.5 mg nano-Se/kg than fish fed 1 mg nano-Se/kg (P < 0.05). No significant alterations were observed on albumin, ALT, and AST variables (P > 0.05). Phagocytic index, phagocytic, lysozyme activities were significantly higher in fish fed varying levels of Se nanoparticles than fish fed the basal diets in a dose dependent manner (P < 0.05). Further, SOD activity had higher value in the group of fish fed 0.25 and 0.5 mg nano-Se/kg than fish fed 1 mg nano-Se/kg, whereas CAT was increased in the group of fish fed dietary 0.5 mg nano-Se/kg diet (P < 0.05). The level of MDA was significantly lowered by dietary nano-Se where the group of fish fed 0.25 mg/kg had the lowest level followed by those fed 0.5 and 1 mg/kg. The expression of GH, IGF-1, IL-8, and IL-1ß genes had the highest mRNA levels in the group of fish fed 0.25 and 0.5 mg/kg followed by those fed 1 mg/kg, whereas HSP70 was downregulated. Based on the overall results, Se nanoparticles are recommended at the rate of 0.5-1 mg/kg diet to maintain the optimal growth performance, hemato-biochemical indices, antioxidative status, and immune-related genes in European seabass.

Comparative nephroprotective effects of curcumin and etoricoxib against cisplatin-induced acute kidney injury in rats.

OBJECTIVE: Although cisplatin (CIS) acts as potent chemotherapy, nephrotoxicity still its major life-threatening side effect. The purpose of this study was to discuss and compare the renoprotective effects of curcumin (CUR) and etoricoxib (ETB) against CIS-induced nephrotoxicity. MATERIALS & METHODS: Thirty six adult female rats were divided equally into 6 groups: Group I (control), Group II (CIS) received cisplatin (7.5 mg/kg i.p), Group III (CUR) and group IV (ETB) received curcumin (200 mg/kg/day) or etoricoxib (10 mg/kg/day) respectively via gavage for seven continuous days. Group V (CIS + CUR) and Group VI (CIS + ETB) received curcumin (200 mg/kg/day) or etoricoxib (10 mg/kg/day) via gavage for seven continuous days. On the 4th day, the rats received cisplatin (7.5 mg/kg i.p) as a single injection 1 h after last curcumin or etoricoxib administration. At the assigned time, blood and tissue samples were collected for biochemical, histochemical, histopathological, immunohistochemical, and RT-PCR gene expression studies. RESULTS: Curcumin administration significantly decreased CIS-induced elevation of serum creatinine and blood urea nitrogen (BUN), and reversed oxidative stress markers; glutathione (GSH) and malondialdehyde (MDA) to control level. Suppression of inflammatory and apoptotic responses by CUR co-treatment was evidenced by decreased iNOS and BAX immunohistochemical reactions, and TNF-α and Caspase3 gene expressions which were detected by RT-PCR in kidney tissues. To our knowledge, this is the first time to discuss the effect of ETB on CIS induced nephrotoxicity. Although ETB reduced the previously mentioned inflammatory and apoptotic markers, its effect was less than that of CUR. Administration of ETB couldn't modify the disturbed levels of creatinine, BUN, GSH, and MDA. CONCLUSION: In conclusion, CUR provided a promising renoprotective effect against CIS induced nephrotoxicity. Further studies are recommended to approve or disapprove the protective role of ETB in CIS induced nephrotoxicity.