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  1. Home
  2. Browse by Author

Browsing by Author "Imam, Aminu"

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    Exogenous melatonin ameliorates pontine histoarchitecture and associated oxidative damage in sodium fluoride-induced toxicity
    (Published by Nepalese Society of Neurosurgeons., 2020) SULAIMON, Fatimo; Okesina, Akeem; Imam, Abubakar; Usman, Rukayyah; Ibrahim-Abdulkareem, Ruqoyyah; Imam, Aminu; Adana, Misturah; Shehu, Monsur; Abioye, Adeshola; Ajao, Moyosore
    Background: Sodium fluoride (NaF) is a highly consumed food additive, that is capable of disrupting the activities of several brain areas. It is unclear whether this compound affects the autonomic activities of the brain. Objective: Therefore, this study was designed to investigate the ameliorative potentials of exogenous melatonin on sodium fluoride-induced pontine toxicity in adult male Wistar rats, as melatonin has been implicated to have a high concentration in the cerebrospinal fluid of injured brains. Method: Thirty-two rats were randomly divided into 4 groups (n=8, per group). Groups I, II, III and IV received 0.2 ml of normal saline (NS), 500 ppm of sodium fluoride (NaF) via their drinking water, 10 mg/kg melatonin (MLT), and melatonin with sodium fluoride concurrently (MLT+NaF) respectively for fourteen days. At the end of these treatments, the rats were euthanized and brainstem tissues were excised for histological, histochemical, and biochemical analyses. Results: There were shreds of evidence of DNA fragmentation, vacuolation, dispersion of the Nissl bodies, and axonal disruption in the cells of the basilar pons of the sodium fluoride-treated animals. This was coupled with high concentrations of malondialdehyde and low-level concentrations of glutathione reductase. Melatonin, however, was observed to limit neuronal injury in the cells of the basilar pons in the experimental animals by reducing the extent of cells undergoing process pyknosis, chromatolysis, and demyelination. Also, melatonin was able to reduce the concentration of malondialdehyde and increase glutathione reductase activities in the pons. Conclusion: This study revealed that sodium fluoride injured the pontine histoarchitecture, and induced oxidative damage which were ameliorated by exogenous melatonin treatments. Key words: Histoarchitecture, Melatonin, Oxidative damage, Pontine, Sodium fluoride, Wistar rats
  • Item
    Hippocampal-dependent spatial memory and histoarchitectural integrities of the ca regions of wistar rats following administration of rauwolfia vomitoria and chlorpromazine
    (Neuroscience Society of Nigeria, 2015) Ajao, Moyosore Saliu; Imam, Aminu; Ajibola, Musa Iyiola; Abdulmumin, Ibrahim; Amin, Abdulbasit; Adana, Misturah Yetunde; Olawepo, Ayokunle; Abdulmajeed, Wahab Imam
    Psychotic patients demonstrate poor spatial memory, ascribed to impaired hippocampal functions, and bodies of evidences have attributed cognitive impairments to the poor functional outcomes in psychosis management. The efficacy of chlorpromazine and Rauwolfia vomitoria on spatial memory performance and differential histoarchitecture of the hippocampi of adult Wistar rats was examined in this study. Twenty five adult male Wistar rats weighing between 200 - 230 g were randomly grouped to five (Normal, low and high dose chlorpromazine and low and high dose R. vomitoria) of five animals each. 2 ml of normal saline was given to Control animals daily, 5mg/kg of chlorpromazine was given as low dose, 10 mg/kg of chlorpromazine was given as moderate dose, 150 mg/kg of R. vomitoria was given as low dose and 300 mg/kg of R. vomitoria was given as high dose orally. All the medications were given daily for 21 days. A Y-maze apparatus was used to assess the spatial memory performance in the rats at days 14 and 21 of the experiment. All the animals were euthanized using 20 mg/kg of intramuscular ketamine, cardially perfused with 4% paraformaldehyde, the brains and the hippocampus removed for histological analysis. Results from this study show that Rauwolfia at 150 and 300 mg/kg improved the correct decision (right triplet alternation) and reduced wrong decision (wrong triplet alternation) in the treated rats at days 14 and 21 respectively with an unaltered hippocampal histoarchitecture. While chlorpromazine at 5 and 10 mg/kg induced an increased wrong decision (wrong triplet alternation) and reduced correct decision (right triplet alternation) across treatment periods and caused an apparent distortion in the hippocampus. In conclusion, R. vomitoria could be a better alternative agent with more therapeutic potential in the treatment of psychosis and could possibly remediate cognitive impairments in psychosis.
  • Item
    Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam
    (Hindawi, 2021-05-18) Badmus, Olufunto; Areola, Emmanuel; Benjamin, Eleojo; Obekpa, Matthew; Adegoke, Tolulope; Elijah, Oluwatobi; Imam, Aminu; Olajide, Olayemi; Olatunji, Lawrence
    Objective. We tested the hypothesis that postpartum combined oral contraceptive (COC) treatment would induce oxidative stress via the adenosine deaminase-xanthine oxidase pathway in the kidney. We also sought to determine whether mineralocorticoid receptor (MR) or glucocorticoid receptor (GR ) blockade would suppress the activities of ADA and xanthine oxidase caused by postpartum COC treatment in the kidney. Methods. Twenty-four Wistar dams were randomly assigned to 4 groups (n = 6/group). Dams received vehicle (po), COC (1.0 μg ethinylestradiol and 5.0 μg levonorgestrel; po), COC with GR blockade (mifepristone; 80.0 mg/kg; po), and COC with MR blockade (spironolactone; 0.25 mg/kg; po) daily between 3rd and 11th week postpartum. Results. Data showed that postpartum COC caused increased plasma creatinine and urea, increased renal triglyceride/high-density lipoprotein ratio, free fatty acid accumulation, alanine aminotransferase, gamma-glutamyltransferase, uric acid, and activities of renal XO and ADA. On the other hand, postpartum COC resulted in decreased plasma albumin, renal glutathione, and Na+ -K+-ATPase activity with no effect on lactate production. However, MR or GR blockade ameliorated the alterations induced by postpartum COC treatment. The present results demonstrate that MR or GR blockade ameliorates postpartum COC-induced increased activities of ADA and xanthine oxidase and restores glutathione-dependent antioxidative defense. Conclusion. These findings implicate the involvements of GR and MR in renal dysfunctions caused by COC in dams via disrupted glutathione antioxidative barrier.

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