Sex comparison of oxidative stress, mitochondrial dysfunction, and apoptosis triggers induced by single-dose Abamectin in albino rats.

Abamectin (AB) is widely used in agriculture and has been employed as an insecticide, nematicide, and livestock pest control agent. However, it may also pose a serious threat to mammals. The primary purpose of this research was to compare the sex variations between male and female rats during exposure and to assess the risk of toxicity of abamectin, which are still largely unknown. The twenty albino rats were divided randomly into four groups (n = 5): 1) the male control group; 2) the male treatment group treated with AB (1 mg/kg B.W.); 3) the female control group; and 4) the female treatment group treated with AB (1 mg/kg B.W.). AB administration caused a drop in body weight in females more than males with showing oxidative stress in both sexes of animals, as characterized by an increase in MDA content and a decrease in glutathione (GSH) content and superoxide dismutase (SOD) activity. Reported sex-specific effects suggested that females are more susceptible from males in brain tissues for alteration of antioxidant markers while females' liver and kidney tissues showed more level of lipid peroxidation than males. In addition, mitochondrial dysfunction was associated with a significant decrease in NADH dehydrogenase (Complex I) and a significant decrease in mitochondrial ATPase, which led to apoptosis and histopathological alterations in the targeted tissues, indicating that females are higher sensitive than males to these biological events. In brief, the results of this study led to female rats are generally more sensitive than male rats to neurobehavioral and hepatic complications associated with abamectin treatment. Further evaluation should be performed to determine the adverse outcome pathways involved and to determine the effects of sex on improving the risk assessment of abamectin in both sexes.

Antioxidant and antiapoptotic effects of quercetin against ochratoxin A-induced nephrotoxicity in broiler chickens.

The mycotoxin ochratoxin A (OTA) is produced by the fungi Aspergillus and Penicillium. The flavonoid quercetin (QUE) is distinguished by its antioxidant, anti-inflammatory, and antiapoptotic properties. This study was designed to determine whether QUE can protect broiler chickens against OTA-induced nephrotoxicity. Forty broiler chicks were randomly divided into four equal groups: control, OTA, QUE, and OTA + QUE. For 6 weeks, OTA (0.5 mg/kg) and/or QUE (0.5 g/kg) were added to the diet of chickens. The results demonstrated that OTA exposure increased serum levels of creatinine, uric acid, and blood urea nitrogen. OTA exposure also increased renal malondialdehyde content but decreased renal antioxidants. OTA-exposed chickens exhibited multiple pathological kidney lesions. Moreover, OTA exposure induced apoptosis in renal tissue, which was manifested by the up-regulation of proapoptotic genes and down-regulation of antiapoptotic genes via the suppression of the PI3K/AKT pathway. In addition, coadministration of QUE and OTA mitigated most of these nephrotoxic effects.

Protective Effects of Bacillus Subtilis Fermentation Extract Against Ochratoxin A-induced Nephrotoxicity and Immunotoxicity in Broiler Chickens.

Introduction: Ochratoxin A (OTA) is a mycotoxin notably produced by Aspergillus and Penicillium spp. Bacillus subtilis fermentation extract (BSFE) contains specific enzymes which hydrolyse OTA. This study evaluated the efficiency of BSFE in ameliorating the immunotoxic and nephrotoxic effects of OTA in broiler chickens. Material and Methods: Day-old broiler chicks were divided equally into four groups of ten: control, OTA (0.5 mg/kg feed), BSFE product (1 mL/L water) and OTA + BSFE at the same concentrations. The chicks were vaccinated against avian influenza, Newcastle disease, and infectious bronchitis, and lymphoproliferation was induced in all birds by phytohaemagglutinin-P (PHA-P). Serum samples were taken before sacrifice and organ tissue samples were taken after, in which renal function biomarkers were assayed and the presence of OTA residue was evaluated by high-performance thin-layer chromatography. Protein markers of apoptosis were determined by qPCR, and tissue lesions were examined histopathologically. Results: Exposure to OTA significantly decreased the antibody response to the vaccines and the lymphoproliferative response to PHA-P, and significantly elevated the renal function indicators: serum urea, uric acid and creatinine. It also induced oxidative stress (reduced catalase activity and glutathione concentration), lipid peroxidation (increased malondialdehyde content), apoptosis (increased Bax and Caspase-3 and decreased Bcl-2 gene levels) and pathological lesions in kidney, bursa of Fabricius, spleen and thymus tissue. Residues of OTA were detected in the serum and tissue. BSFE mitigated most of these toxic effects. Conclusion: BSFE counters OTA-induced immunotoxicity and nephrotoxicity because of its content of carboxypeptidase and protease enzymes.

Alterations in reproductive parameters and steroid biosynthesis induced by nickel oxide nanoparticles in male rats: The ameliorative effect of hesperidin.

With recent progress in the manufacture and applications of nickel oxide nanoparticles (NiO NPs), concerns about their adverse effects are increasing. Hesperidin (HSP) is a citrus flavonoid that has a potent anti-inflammatory, antioxidant and free radical scavenging activities. This study aims to investigate the protective effect of HSP against testicular and spermatological damages induced by NiO NPs in male rats. Forty rats were randomly and equally divided into four groups: control, NiO NPs, HSP and NiO NPs + HSP. NiO NPs (100 mg/kg) and/or HSP (100 mg/kg) were given daily by gavage for 60 days. Exposure to NiO NPs induced marked reproductive toxicity in male rats that was manifested by increased sperm abnormalities and deterioration of sperm motility, count and viability. NiO NPs also increased lipid peroxidation and negatively affected the cellular antioxidant defense system in the testis of rats. The level of serum testosterone hormone was increased in NiO NPs-exposed rats. qPCR showed a marked downregulation in expression of steroidogenesis-related genes (CYP11A1, HSD3B and STAR) and a significant upregulation in expression of apoptosis-related gene (caspase-9) in testicular tissue of rats. Various pathological lesions and an increase in the number of PCNA-positive immune-reactive cells were also noticed in the testis of NiO NPs-exposed rats. Co-administration of HSP significantly ameliorated most of the NiO NPs-induced testicular damages and improved male fertility in rats.

Quercetin ameliorates ochratoxin A-Induced immunotoxicity in broiler chickens by modulation of PI3K/AKT pathway.

Ochratoxin A (OTA) is a fungal secondary metabolite produced by certain species of Aspergillus and Penicillium, and exerts immunosuppressive effect on humans and animals. Quercetin (QUE) is one of the flavonoids produced as a plant-secondary metabolite. The present study was designed to evaluate the efficacy of QUE against the immunotoxic hazard of OTA in broiler chickens. Forty one-day-old broiler chicks were randomly and equally allocated into four groups; control, OTA (0.5 mg/kg feed), QUE (0.5 g/kg feed) and OTA + QUE (0.5 mg/kg OTA + 0.5 g/kg QUE). The results revealed that dietary OTA induced a significant decrease in the antibody response to Newcastle Disease (ND), Infectious Bronchitis (IB) and Avian Influenza (AI) vaccination and in the lymphoproliferative response to Phytohemagglutinin-P (PHA-P). Ochratoxin A also induced oxidative stress and lipid peroxidation in the bursa of Fabricius, spleen and thymus tissues of chickens as demonstrated by decreased CAT and GSH levels and increased TBARS content. In addition, administration of OTA resulted in apoptosis, which was evident by the increased expression level of PTEN, Bax and Caspase-3 genes and decreased expression level of PI3K, AKT and Bcl-2 genes. Furthermore, exposure to OTA resulted in various pathological lesions in the bursa of Fabricius, spleen and thymus of chickens. On the other hand, administration of QUE ameliorated most of the immunotoxic effects of OTAby its immunomodulatory, antioxidant and anti-apoptotic activities. Taken together, the results suggested that QUE potentially alleviated the OTA-induced immunotoxicity in broiler chickens, probably through amelioration of oxidative stress and activation of the PI3K/AKT signaling pathway.

Carvacrol ameliorates behavioral disturbances and DNA damage in the brain of rats exposed to propiconazole.

Propiconazole (PCZ) is an ergosterol biosynthesis inhibiting fungicide. Carvacrol (CAR) is a monoterpenoid phenol that has various beneficial health effects. The current research was designed to study the impact of PCZ on the behavior of rats and its ability to induce DNA damage in neurons as well as to clarify the ameliorative effect of CAR against these toxic impacts. Sixty Sprague-Dawley rats were randomly and equally divided into 4 experimental groups and treated daily by oral gavage for 2 months as follows: Group 1 (control); group 2 treated with PCZ (75 mg/kg); group 3 treated with CAR (50 mg/kg) and group 4 treated with both PCZ and CAR. Behavioral tests demonstrated that exposure to PCZ had a deleterious effect on psychological, motor and cognitive neural functions. Additionally, antioxidant enzyme activities, SOD and GSH-Px, were declined in brain tissue following exposure to PCZ. Moreover, comet assay revealed a high percent of DNA damage in the brain of rats exposed to PCZ. On the other hand, CAR administration ameliorated the harmful effects induced by PCZ through a protective mechanism that involved the improvement of neural functions and attenuation of oxidative stress and DNA damage.

Ameliorative effect of carvacrol against propiconazole-induced neurobehavioral toxicity in rats.

Propiconazole (PCZ) is a triazole fungicide extensively used in agriculture. Carvacrol (CAR) is a naturally occurring phenolic monoterpene which has various biological and pharmacological effects. The present study was designed to investigate the neurobehavioral toxic effects of PCZ in albino rats and to evaluate the ameliorative role of CAR against such toxic effects. Sixty adult male rats were used in this investigation; they were randomly and equally divided into 4 groups: control group, PCZ group, CAR group and PCZ + CAR group. PCZ (75 mg/kg) and/or CAR (50 mg/kg) were administered daily by oral gavage for 8 weeks. Behavioral investigation clearly demonstrated the negative impact of PCZ on psychological, motor and cognitive brain functions. Exposure to PCZ also adversely affected the measured oxidative stress and lipid peroxidation parameters in brain tissue. A significant decrease in activity of acetylcholinesterase enzyme in neural tissue was also observed in PCZ-exposed rats. Histopathological examination of the cerebrum, cerebellum, and hippocampus showed various histopathological lesions after exposure to PCZ which were confirmed by immunohistochemical examination. On the other hand, co-administration of CAR ameliorated most of the undesirable effects of PCZ.