Acrylamide exposure induces growth retardation, neurotoxicity, stress, and immune/antioxidant disruption in Nile tilapia (Oreochromis niloticus): The alleviative effects of Chlorella vulgaris diets.

This study looked at the toxic impacts of water-born acrylamide (ACR) on Nile tilapia (Oreochromis niloticus) in terms of behaviors, growth, immune/antioxidant parameters and their regulating genes, biochemical indices, tissue architecture, and resistance to Aeromonas hydrophila. As well as the probable ameliorative effect of Chlorella vulgaris (CV) microalgae as a feed additive against ACR exposure was studied. The 96-h lethal concentration 50 of ACR was investigated and found to be 34.67 mg/L for O. niloticus. For the chronic exposure study, a total of 180 healthy O. niloticus (24.33 ± 0.03 g) were allocated into four groups in tri-replicates (15 fish/replicate), C (control) and ACR groups were fed a basal diet and exposed to 0 and 1/10 of 96-h LC50 of ACR (3.46 mg/L), respectively. ACR+ CV5 and ACR+ CV10 groups were fed basal diets with 5 % and 10 % CV supplements, respectively and exposed to 1/10 of 96-h LC50 of ACR for 60 days. After the exposure trial (60 days) the experimental groups were challenged with A. hydrophila. The findings demonstrated that ACR exposure induced growth retardation (P˂0.01) (lower final body weight, body weight gain, specific growth rate, feed intake, protein efficiency ratio, final body length, and condition factor as well as higher feed conversion ratio). A substantial decrease in the immune/antioxidant parameters (P˂0.05) (lysozyme, serum bactericidal activity %, superoxide dismutase, and reduced glutathione) and neurotransmitter (acetylcholine esterase) (P˂0.01) was noticed with ACR exposure. A substantial increase (P˂0.01) in the serum levels of hepato-renal indicators, lipid peroxidation biomarker, and cortisol was noticed as a result of ACR exposure. ACR exposure resulted in up-regulation (P˂0.05) of the pro-inflammatory cytokines and down-regulation (P˂0.05) of the antioxidant-related gene expression. Furthermore, the hepatic, renal, brain, and splenic tissues were badly affected by ACR exposure. ACR-exposed fish were more sensitive to A. hydrophila infection and recorded the lowest survival rate (P˂0.01). Feeding the ACR-exposed fish with CV diets significantly improved the growth and immune/antioxidant status, as well as modulating the hepatorenal functions, stress, and neurotransmitter level compared to the exposed-non fed fish. In addition, modulation of the pro-inflammatory and antioxidant-related gene expression was noticed by CV supplementation. Dietary CV improved the tissue architecture and increased the resistance to A. hydrophila challenge in the ACR-exposed fish. Noteworthy, the inclusion of 10 % CV produced better results than 5 %. Overall, CV diets could be added as a feed supplement in the O. niloticus diet to boost the fish's health, productivity, and resistance to A. hydrophila challenge during ACR exposure.

Estimating the in vitro cytotoxicity of the newly emerged zinc oxide (ZnO) doped chromium nanoparticles using the human fetal lung fibroblast cells (WI38 cells).

Advances in nanotechnology have been increased for more smart applications and getting the highest level of benefits, recently modification of the surface characters of nanoparticles is a new trend to get the optimal benefits, one of these modification is doping of zinc oxide with chromium nanoparticles (ZnO doped Cr NPs), the present study aimed to identify the surface characters of doped ZnO and their possible cytotoxic effects. The doped NPs were characterized by X-ray diffraction (XRD), Fourier transform infrared (FTIR), Field emission scanning electron microscope (FESEM), and Electromagnetic Data Exchange (EDX). Human fetal lung fibroblast cells (WI38 Cells) was treated with variable concentrations of pure ZnO and ZnO doped Cr (0.01 %, 0.02 %, 0.03 % and 0.04 %) for 24 hr at 37 °C followed by the MTT assay. The cells treated with the obtained half-maximal inhibitory concentration (IC50). The supernatant and cells were collected for oxidant/anti-oxidant and molecular analysis.The observed FESEM features are in line with the reported XRD analysis confirming the hexagonal crystal symmetry of all samples. The findings revealed that pure ZnO exhibited potent cytotoxic effects followed by (0.03 % and 0.04 %). All tested NPs produce lipid peroxidation significantly (0.03 % and 0.04 %). The significant up regulation of Bcl-2-associated X protein (BAX) and apoptotic Caspase (Cas-3) transcription level were reported in ZnO and 0.03 % and 0.04 % in contrast the anti apoptitic B-cell lymphoma 2 (Bcl-2) is elevated in 0.01 % and 0.02 %. Doping of ZnO with Cr causing significant morphological changes which effect on their toxicity especially with 0.03 % and 0.04 %.

Sesame oil ameliorates valproic acid-induced hepatotoxicity in mice: integrated in vivo-in silico study.

Sesame oil (SO) has been exhibited to have anti-inflammatory and antioxidant influences. The goal of this experiment was to look into SO's hepato-protective properties and underlying processes in valproic acid (VPA)-induced hepatotoxicity. Molecular docking was carried out to clarify the functional and structural underlying mechanism of SO ameliorative effect. Mice were given 8 mL/kg/day of SO (orally) and 100 mg/kg/day of VPA (i.p.) for 21 days. The results revealed that VPA caused a considerable increase in hepatic malondialdehyde levels while decreasing the activity of glutathione peroxidase (GPx) enzyme. There was also a significant rise in serum levels of interleukins 1ß and 6 (IL-1ß and IL-6) and a significant decrease in hepatic (PXR) gene expression level. SO co-administration with VPA significantly normalized the antioxidant and anti-inflammatory status and upregulated the gene expression level of PXR. In silico docking analysis results confirmed these results. This study concluded that supplementation of SO attenuated VPA-induced oxidative stress and inflammation. Hence, it was recommended as a dietary supplement for protection against VPA-induced hepatotoxicity.Communicated by Ramaswamy H. Sarma.

Royal Jelly and Chlorella vulgaris Mitigate Gibberellic Acid-Induced Cytogenotoxicity and Hepatotoxicity in Rats via Modulation of the PPARα/AP-1 Signaling Pathway and Suppression of Oxidative Stress and Inflammation.

Gibberellic acid (GA3) is a well-known plant growth regulator used in several countries, but its widespread use has negative effects on both animal and human health. The current study assesses the protective effect of royal jelly (RJ) and Chlorella vulgaris (CV) on the genotoxicity and hepatic injury induced by GA3 in rats. Daily oral administration of 55 mg/kg GA3 to rats for 6 constitutive weeks induced biochemical and histopathological changes in the liver via oxidative stress and inflammation. Co-administration of 300 mg/kg RJ or 500 mg/kg CV with GA3 considerably ameliorated the serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), ALP (alkaline phosphatase), γGT (gamma-glutamyl transferase), total bilirubin, and albumin. Lowered malondialdehyde, tumor necrosis factor α (TNF-α), and nuclear factor κB (NF-κB) levels along with elevated SOD (superoxide dismutase), CAT (catalase), and GPx (glutathione peroxidase) enzyme activities indicated the antioxidant and anti-inflammatory properties of both RJ and CV. Also, they improved the histological structure and reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions along with up-regulating peroxisome proliferator activated receptor α (PPARα) and down-regulating activator protein 1 (AP-1) gene expression. Additionally, chromosomal abnormalities and mitotic index were nearly normalized after treatment with RJ and CV. In conclusion, RJ and CV can protect against GA3-induced genotoxicity and liver toxicity by diminishing oxidative stress and inflammation, and modulating the PPARα/AP-1 signaling pathway.

Targeting Some Key Metalloproteinases by Nano-Naringenin and Amphora coffeaeformis as a Novel Strategy for Treatment of Osteoarthritis in Rats.

Osteoarthritis (OA) represents the highest degenerative disorder. Because cartilage erosion is a common pathological alteration in OA, targeting some key metalloproteinases such as MMP-3, ADAMTS-5 besides their inhibitor TIMP-3 by natural products, could be an effective strategy to protect against osteoarthritis. Forty female Wister rats were categorized into five equal groups. Control, osteoarthritic (OA) (monosodium iodoacetate (MIA) 2 mg/50 µL saline, single intra-articular injection), OA+ indomethacin (2 mg/kg/daily/orally), OA+ nano-naringenin (25 mg/kg/daily/orally), and OA+ Amphora coffeaeformis (772 mg/kg/daily/orally). Treatments were initiated on the 8th day after osteoarthritis induction and continued for 28 days thereafter. Finally, blood and knee joint samples were collected from all rats for biochemical and histopathological evaluations. The current study showed that MIA induced oxidative stress, which resulted in changes in the inflammatory joint markers associated with increased right knee diameter and higher clinical scores for lameness. Amphora coffeaeformis followed by nano-naringenin exhibited a potential anti-arthritic activity by reducing the concentrations of serum MMP-3, ADAMTS-5, and joint MDA and increasing the levels of serum TIMP-3 and joint GSH, similar to indomethacin. The histopathological results confirmed these outcomes. In conclusion, Amphora coffeaeformis and nano-naringenin can be considered as natural therapeutic agents for osteoarthritis owing to their antioxidant and anti-inflammatory activities.