The Pseudomonas putida strain was primarily identified and tested in vitro against antibiotic sensitivity for several antibiotics using the disc diffusion method. This isolate was also tested against sensitivity to carvacrol oil (c) and formic acid (f). The genotyping of Pseudomonas spp. and virulotyping for P. putida isolate was carried out and verified by 16S rDNA-PCR amplification. Furthermore, we assessed the efficacy of carvacrol oil and formic acid in vivo for treatment of P. Putida infection. For the in vivo challenge, 180 fish (Nile tilapia, Oreochromis niloticus) were divided into six groups: (G1: control (unchallenged), G2: carvacrol prophylaxis (3 g/kg), G3: formic acid prophylaxis (5 mL/kg), G4: control positive (challenged), G5: carvacrol treatment (3 g/kg), and G6: formic acid treatment (5 mL/kg); 30 fish per group) with three replicates. Following the challenge, nitric oxide and lysozyme activity were measured as essential indicators for fish immunity. The antioxidant parameters including SOD and catalase were computed to reflect the antioxidant status. Furthermore, relative percent survival (RPS) and mortality percent were evaluated to indicate functional immunity. The findings of the antibiotic sensitivity test showed that ciprofloxacin exhibited the largest inhibition zone. Additionally, formic acid (f) displayed the greatest inhibition zone compared to carvacrol oil (c) and was more effective in stimulating the immune-antioxidant response compared to carvacrol oil. The tested exotoxin A (tox A), exoenzyme S (exo S), and the nan1 associated-virulence genes were identified in the P. putida isolate. Overall, the current study verified the virulence of P. putida and highlighted the promising role of dietary addition of formic acid for enhancing the immune-antioxidant indicators and for mitigating P. putida infection. Future studies could be devoted to this field.

The present study aimed to investigate the protective effect of argan oil (AO) against nephrotoxic effects following overdose and long-term administration of betamethasone (BM). The phytochemical compositions of AO were assessed using GC/MS. Forty eight male Wister albino rats were divided into six groups and treated for 3 successive weeks. The control group was orally administrated distilled water daily, the BM group received BM (1 mg/kg, IM, day after day), AO/0.5 and AO/1 groups received AO (0.5 mL/kg, 1 mL/kg, orally, daily, respectively), BM + AO/0.5 group and BM + AO/1 group. The results revealed that BM induced hematological changes, including reduction of red blood cells with leukocytosis, neutrophilia, monocytosis, lymphocytopenia, and thrombocytopenia. Moreover, BM caused a significant increase of serum urea and creatinine levels, and renal malondialdehyde and nitric oxide contents with significant decrease of reduced glutathione content. BM also caused vascular, degenerative, and inflammatory histopathological alterations in kidney, along with an increase in the Bax/Bcl-2 ratio, activation of caspase-3, and decrease of proliferating cell nuclear antigen expression. Conversely, the concomitant administration of AO (0.5, 1 mL/kg) with BM ameliorated the aforementioned hematological, biochemical, pathological, and histochemical BM adverse effects. In conclusion, AO has protective effects against BM-induced renal damage, possibly via its antioxidant, anti-apoptotic, and proliferative properties.

The current study is a pioneer trial to verify the effectiveness of Petroselinum crispum (parsley) nanoparticles (PNPs) for fortifying physiological and biochemical biomarkers in female African catfish postexposure to bisphenol A (BPA) toxicity. The aim of this experiment is to verify the influence of PNPs for mitigating serum hemato‐biochemical alterations as well as antioxidant enzyme, and hormonal changes induced by BPA toxicity in the hepatic and ovarian tissues. Fish were equally allocated into four groups: group I as a control without any treatments, group II received a commercial diet + PNPs (4 g/kg diet). In group III, fish were subjected to 1/10 LC50 (BPA) (1.43 µg/L), while in group IV, fish got 1/10 LC50 BPA (1.43 µg/L) + PNPs (4 g/kg diet) for 60 consecutive days. Exposure to BPA showed macrocytic hypochromic anemia and leukopenia, and a noticeable elevation in glucose, alanine amino‐transferase (ALT), aspartate aminotransferase (AST), ALP, urea, creatinine, cortisol, cholesterol, and testosterone (T) hormone. Furthermore, serum AchE, estradiol (E2), follicle‐stimulating hormone (FSH), luteinizing hormone (LH), globulin, albumin, and total proteins were significantly decreased in a BPA‐exposed group. Alternatively, activities of superoxide dismutase (SOD), lipid peroxidation (LPO), and catalase (CAT) were notably augmented in the hepatic tissue and ovaries of the BPA‐supplemented fish. While total antioxidant capacity (TAC) and reduced glutathione (GSH) levels decreased in the equal tissues of exposed fish. PNPs‐supplemented diets in combination with BPA alleviated its destructive effects on the tested parameters. In conclusion, the results proved that BPA is an endocrine hormonal disruptor that induces imbalances in blood profile, hepato–renal indicators, and stress parameters, besides the occurrence of oxidative damage and reproductive dysfunction. Interestingly, PNPs have a protective role in attenuating BPA toxicity and modulating all the measured biomarkers, as well as improving the fertility of female Clarias gariepinus .