Oluwaseun Olanrewaju Esan

Background: Bisphenol A (BPA) is an endocrine‐disrupting chemical, and it is mostly used in plastic industries. Naringin is a potent flavonoid that has been reported to possess several beneficial pharmacological properties such as antioxidant, anti‐inflammatory, and antiapoptotic properties. Objective: The aim of this study was to determine the protective effect of naringin against the damage induced by BPA in the brain and testes of commercial chicken. Methods: Thirty‐day‐old cockerel chickens were purchased and reared for 6 weeks and subsequently divided into six groups: group A (control), group B (100 ppm BPA‐treated), group C (BPA and 100 mg/kg naringin‐treated), Group D (BPA and 200 mg/kg naringin‐treated), group E (100 mg/kg naringin‐treated), and group F (200 mg/kg naringin‐treated). BPA was administered via drinking water, while naringin was administered via oral gavage. Analyses such as biochemical assays, hormonal assays, histopathology, and immunohistochemistry were done. Results: The results showed a decrease in the level of LH, FSH, and testosterone, an increase in the level of oxidative stress markers (MDA and H ₂ O ₂ ), and alteration in the levels of enzymatic and non‐enzymatic antioxidants (GSH, GST, SOD, GPx) in the brain and testes of the BPA‐intoxicated group. Histologically, neuronal necrosis and degeneration were observed in the brain, and degeneration of testicular cells was seen in the testes of BPA‐intoxicated chickens. Immunohistochemical evaluation revealed low expression of myelin basic protein in the brain and increased expression of caspase 3 in the testes of the BPA‐intoxicated group. Conclusions: Naringin reversed the neurotoxicity and reproductive toxicity of BPA by normalizing the values of the altered parameters. Hence, naringin ameliorated the deleterious effects caused by BPA in both the brain and testes by enhancing the antioxidant defence mechanism.

Evaluation of Azadirachta indica's potential on the modulation of blood pressure parameters, antioxidant defense status, as well as immunohistochemical expressions of Peroxisome proliferator-activated receptor α (PPARα) and Bcl-2 (B-cell lymphoma 2) in rats exposed to isoproterenol was the objective of this study. Fifty rats (Rattus norvegicus) of the Wistar strain were used, with myocardial infarction induced by intraperitoneal administration of isoproterenol (ISO) for two consecutive days. Cardiac and renal biomarkers of oxidative stress, blood pressure parameters, electrocardiography, and immunohistochemical staining of PPARα and BCL2 were performed. ISO toxicity heightened blood pressure parameters, aggravated oxidative processes, declined antioxidant defense system, and decreased immunohistochemical expressions of PPARα and BCL2. Interestingly, A. indica improved antioxidant status, lowered free radical generation, mitigated serum myeloperoxidase and xanthine oxidase activities, respectively. Mitigation of oxidative mechanisms and antihypertensive effects of Azadirachta indica suggest a positive modulatory role for the medicinal plant in isoproterenol-induced myocardial infarction.

Objectives: The objective of this study was the assessment of the ameliorative roles of alpha-tocopherol and quercetin on the toxic mechanisms associated with ethanol (EtoH) exposure in the cardiac and renal systems of rats. Material and Methods: Forty male rats were randomly selected and divided into five groups as follows: 0.2 mL distilled water; EtoH 40% v/v; EtoH + 2.5 mg/kg alpha-tocopherol; EtoH + 50 mg/kg quercetin; and EtoH + a cocktail of alpha-tocopherol and quercetin. Results: Treatment with alpha-tocopherol and quercetin significantly (P < 0.05) ameliorated EtoH-induced alterations in hemodynamic and electrocardiographic parameters, kidney function markers, and antioxidant defense status of rats with significantly elevated levels of glutathione, glutathione peroxidase, superoxide dismutase, and glutathione-S-transferase observed in antioxidant-treated rats. Histopathologic lesions induced by EtoH including focal loss of myofiber striation, degeneration, and infiltration of inflammatory cells in the cardiac tissues, as well as patchy tubular necrosis, congestion, and ectasia in renal tissues were absent in the antioxidant treated rats. Heightened immunohistochemical expressions of cardiac-specific troponin and angiotensin converting enzymes induced by EtoH were abated by alpha-tocopherol and quercetin treatment. Conclusion: Alpha-tocopherol and quercetin mitigated oxidative stress-mediated ethanol-induced derangements of the cardiovascular and renal systems in rats.

Introduction: Alterations of antioxidant defense, neuroinflammation, and neurodegeneration are common pathological occurrences associated with neurodegenerative diseases. This study evaluated the neuroprotective effect of Launaea taraxacifolia (LT), popularly known as African Wild lettuce, against neuroinflammation, memory loss, and neurobehavioral deficit. Methods: Adult Wistar rats were used following random assignment into groups 1 to 5. Group one was the normal control. Groups four to five received 40 mg/kg Nω-nitro-l-arginine methyl ester (L-NAME). In addition to L-NAME exposure, groups three and four received 100 and 200 mg/kg LT, whereas group five received 10 mg/kg lisinopril. The experiment lasted for five weeks. Markers of oxidative stress, neurobehavioural studies, histology, and immunohistochemistry of glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin for staining astrocytes, microglia, and Purkinje cells were determined. Results: Malondialdehyde (MDA) and protein carbonyl in the L-NAME alone group were heightened compared to those treated with LT. However, treatment with LT significantly reduced neuronal oxidative stress, neuroinflammation, and neurobehavioural changes. Quantitative analysis of immunohistochemical staining revealed heightened glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin as indicated by astrogliosis, microgliosis, and Purkinje cell degeneration in untreated rats. Moreover, the observed ultrastructural anarchy induced by L-NAME was restored in rats treated with LT (P<0.05). Conclusion: Together, the leaf extract of LT can be effective as a neuroprotective drug candidate.

Objective: Curcuma longa Rhizome (CLR), due to its potent antioxidant phytochemical constituents, was investigated for its effects on bisphenol A (BPA)-induced cardiovascular and renal damage. Materials and Methods: Sixty rats were randomly selected, and grouped as control, BPA (100 mg/ kg), BPA and CLR 100 mg/kg, BPA and CLR 200 mg/kg, CLR 100 mg/kg, and CLR 200 mg/kg for 21 days. Oxidative stress indices, antioxidant status, blood pressure parameters, genotoxicity, and immunohistochemistry were determined. Results: Rats exposed to the toxic effects of BPA had heightened blood pressure, lowered frequency of micronucleated polychromatic erythrocytes, and decreased activities of antioxidant enzymes compared with rats treated with CLR. Moreover, administration of CLR significantly (p < 0.05) lowered malondialdehyde content and reduced the serum myeloperoxidase activity. Immunohistochemical evaluation revealed significantly (p < 0.05) increased expressions of cardiac troponin and Caspase 3 in the BPA group compared with the CLR-treated groups. Conclusion: C. longa ameliorated cardiotoxic and nephrotoxic actions of bisphenol-A via mitigation of oxidative stress, hypertension, and genotoxicity.

Lead (Pb) toxicity constitutes a major health hazard to both humans and animals especially in the developing countries. It is a ubiquitous environmental contaminant found in the air essentially because of unregulated mining and other industrial activities. Lead can be found naturally in the soil thus, contaminating crops for human and animal food, as well as run-off water and air pollution. Intensively and extensively reared domestic chickens are exposed to contamination via inhalation and ingestion of contaminated food materials. Naringin, a product from citrus plant has been described to possess excellent metal chelating ability. Naringin is rich in flavonoid with attendant antioxidant, anti-autophagy, anti-inflammatory, hepatoprotective and cardio-nephroprotective properties. This study was conducted to investigate the hepatoprotective and modulation of oxidative stress in commercial cockerel chickens by Naringin. Thirty-six commercial cockerel chickens were randomly assigned into six groups A-F of six birds each viz: Group A served as control group while groups B, C, and D received Lead acetate at 300 ppm via drinking water continuously till the end of the experiment. In addition, groups C and D were treated with Naringin at 80 mg/kg and 160mg/kg, respectively, via oral gavage for 8 weeks. Groups E and F were administered naringin only at 80mg/kg and 160mg/kg respectively for eight weeks. Pb toxicity induced degenerative changes in the histological sections as well as, higher expression of hepatic caspase 3 as shown by immunohistochemistry. There was increased oxidative stress markers (H2O2, MDA) and depletion of the antioxidant defense system markers SOD, GPx, GSH, and GST. It concluded that Co- treatment with Naringin ameliorated oxidative stress, enhanced antioxidant defense system, reduced the expression of hepatic caspase 3 thus, offering protection against lead acetate-induced derangements in the liver of commercial cockerel chickens

Lead is one of the major pollutants that is harmful to both animals and humans. It is found in every aspect of the environment such as the air, water, and soil. This pollutant affects both wild and domestic birds. Naringin has an active principle called flavonoid that has been found to have medicinal properties, mostly because of its antioxidant and metal chelating properties. This study was carried out to investigate the protective effect of naringin as an antioxidant against lead-induced anemia, cardio and nephrotoxicity, and hypertension. This study also aimed at elucidating the use of naringin as a heavy metal binder in poultry feed. Thirty-six cockerel chicks were used for this study, and randomly grouped into six groups per group; group A served as the control, group B received Pb-only (300 ppm), group C (Pb and naringin; 80 mg/kg), group D (Pb and naringin; 160 mg/kg), group E (naringin 80 mg/kg), and group F (naringin 160 mg/kg), respectively, for 8 weeks. Lead (Pb) was administered via drinking water, while naringin was administered via oral gavage. Lead acetate intoxication precipitated anemia as indicated by significant reductions in the values of PCV, RBC, and Hb concentration in lead-treated chicks when compared with the controls. Also, lead administration induced hypertension together with increased oxidative stress, depletion of the antioxidant defense system, reduced nitric oxide production, and an increase in high blood pressure. Immunohistochemistry indicated high expressions of cardiac troponin, renal angiotensin-converting enzymes, and renal neutrophil gelatinase-associated lipocalin. Treatment with naringin corrected anemia, reduced oxidative stress, improved antioxidant system, reduced high blood pressure, and offered protection against lead acetate-induced cardio-renal dysfunction in cockerel chicks. We recommend that naringin should be incorporated poultry feeds as a metal binder.