Cinnamon nanoemulsion mitigates acetamiprid-induced hepatic and renal toxicity in rats: biochemical, histopathological, immunohistochemical, and molecular docking analysis.

Acetamiprid (ACDP) is a widely used neonicotinoid insecticide that is popular for its efficacy in controlling fleas in domestic settings and for pets. Our study aims to offer a comprehensive examination of the toxicological impacts of ACDP and the prophylactic effects of cinnamon nanoemulsions (CMNEs) on the pathological, immunohistochemical, and hematological analyses induced by taking ACDP twice a week for 28 days. Forty healthy rats were divided into four groups (n = 10) at random; the first group served as control rats; the second received CMNEs (2 mg/Kg body weight); the third group received acetamiprid (ACDP group; 21.7 mg/Kg body weight), and the fourth group was given both ACDP and CMNEs by oral gavage. Following the study period, tissue and blood samples were extracted and prepared for analysis. According to a GC-MS analysis, CMNEs had several bioactive ingredients that protected the liver from oxidative stress by upregulating antioxidant and anti-inflammatory agents. Our findings demonstrated that whereas ACDP treatment considerably boosted white blood cells (WBCs) and lymphocytes, it significantly lowered body weight gain (BWG), red blood cells (RBCs), hemoglobin (Hb), hematocrit (HCT), and platelets (PLT). ACDP notably reduced antioxidant enzyme activities: superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) and elevated hydrogen peroxide and malondialdehyde levels compared with other groups. ACDP remarkably raised alanine aminotransferase (ALT), aspartate amino transaminase (AST), and alkaline phosphatase (ALP) levels.Moreover, the histopathological and immunohistochemistry assays discovered a severe toxic effect on the liver and kidney following ACDP delivery. Furthermore, cyclooxygenase 2 (COX-2) + immunoexpression was enhanced after treatment with CMNEs. All of the parameters above were returned to nearly normal levels by the coadministration of CMNEs. The molecular docking of cinnamaldehyde with COX-2 also confirmed the protective potential of CMNEs against ACDP toxicity. Our findings highlighted that the coadministration of CMNEs along with ACDP diminished its toxicity by cutting down oxidative stress and enhancing antioxidant capacity, demonstrating the effectiveness of CMNEs in lessening ACDP toxicity.

Enhancing the Toxicity of Cypermethrin and Spinosad against Spodoptera littoralis (Lepidoptera: Noctuidae) by Inhibition of Detoxification Enzymes.

The extensive use of wide-ranging insecticides in agricultural activities may develop resistance in insects. The dipping technique was utilized for examining changes in detoxifying enzyme levels in Spodoptera littoralis L. induced by cypermethrin (CYP) and spinosad (SPD) with and without a combination of three enzyme inhibitors: triphenyl phosphate (TPP), diethyl maleate (DEM), and piperonyl butoxide (PBO), at 70 µg/mL. PBO, DEM, and TPP showed 50% mortality against larvae at 236.2, 324.5, and 245.8 µg/mL, respectively. The LC50 value of CYP on S. littoralis larvae reduced from 2.86 µg/mL to 1.58, 2.26, and 1.96 µg/mL, while the LC50 value of SPD declined from 3.27 µg/mL to 2.34, 2.56, and 2.53, with the addition of PBO, DEM, and TPP, respectively, 24 h after treatment. Moreover, the activity of carboxylesterase (CarE), glutathione S-transferase (GST), and cytochrome P450 monooxygenase (Cyp 450) was significantly inhibited (p < 0.05) by TPP, DEM, PBO plus CYP, and SPD in S. littoralis larvae in comparison with tested insecticides alone. These findings suggested that three enzyme inhibitors play a major role in increasing the toxicity of CYP and SPD in S. littoralis and will provide insight into how to overcome insecticide resistance in insects.

Ameliorating effect of the biological Zinc nanoparticles in abamectin induced hepato-renal injury in a rat model: Implication of oxidative stress, biochemical markers and COX-2 signaling pathways.

Extensive use of abamectin (ABM) as an anthelmintic in veterinary systems adversely affects the health and welfare of animals and humans. Zinc nanoparticles (ZnNPs) have therapeutic benefits and ameliorate the effect of environmental pollutants. In this study, we assessed the ameliorative effect of ZnNPs against the sub-lethal toxicity of ABM in rats. Forty healthy rats were randomly selected into four groups (n = 10); the control received normal saline and test rats were treated orally twice weekly with ABM (1 mg/kg bwt), ZnNPs (10 mg/kg bwt) and ABM + ZnNPs for 28 days. Upon completion of the study period, blood and tissue samples were collected and prepared for hematological, biochemical, pathological, and immunohistochemical analysis. Our results showed that ABM treatment significantly decreased body weight gain (BWG), red blood cells (RBCs), hemoglobin (Hb), hematocrit (HC), and platelet (PLT); while it significantly increased white blood cells (WBCs) and lymphocytes. ABM also significantly decreased antioxidant enzyme activities: superoxide dismuthase (SOD), glutathione peroxidase (GPx), and catalase (CAT) and increased hydrogen peroxide and malondialdehyde levels compared with other groups. ABM significantly raised alanine aminotransferase (ALT), aspartate amino transaminase (AST), and alkaline phosphatase (ALP) levels, which was restored by co-administration of ZnNPs. Moreover, ZnNPs ameliorated ABM-mediated negative histopathological changes in the liver and kidney tissues, exhibiting a significant protective effect. Cyclooxygenase 2 (COX-2) + immuno-expression were reduced after pretreatment with ZnNPs. These findings suggested that co-administration of ZnNPs with ABM mitigated its toxicity by combating oxidative stress and boosting antioxidant capacity, indicating the efficacy of ZnNPs in attenuating ABM toxicity.