Showing 3 results for Ajayi
Solomon Umukoro, Mary Apara , Benneth Ben-Azu , Abayomi Mayowa Ajayi , Adegbuyi Olawale Aderibigbe ,
Volume 13, Issue 3 (July 2019)
Abstract
Background: Air fresheners are products with fragrances used to mask unpleasant odor in the environment. However, air fresheners contain diverse chemical substances that pose health challenges to the users; hence are of public health significance. Although previous studies have shown that air fresheners affect the lungs, liver and reproductive organs, the neurobehavioral effects of these agents are yet to be evaluated in details. This study evaluated the neurobehavioral effects and biochemical changes in mice exposed to a solid commercially available air freshener (SAF).
Methods: Male Swiss mice were divided into 6 groups (n = 7). Mice in groups 2-6 were exposed to powdered SAF (10, 25, 50, 100 and 200 g) via inhalation in their cages for 28 days. Mice in group 1 (control) were not exposed to SAF. The neurobehavioral changes: spontaneous motor activity (SMA), memory, anxiety and depression were evaluated on day 28. The mice brains were then proccessed for determination of malondialdehyde, nitrite, glutathione contents, and the activities of catalase and acetyl-cholinesterase.
Results: SAF (25-200g) significantly (p<0.05) impaired SMA compared with control. Mice exposed to SAF exhibited increased anxiety and depression-like symptoms relative to control (p<0.05). It also impaired memory and increased acetylcholinesterase activity (p<0.05). Moreover, SAF increased the levels of nitrite and malondialdehyde accompanied by decreased antioxidant molecules (glutathione and catalase) in mouse brain.
Conclusion: These findings suggest that SAF produced neurobehavioral deficits, increased oxidative stress and altered cholinergic system, posing potential health hazards to the regular consumers.
Taiwo Adekemi Abayomi, Olorunfemi Samuel Tokunbo, Moyinoluwa Ajayi, Olawale Ayobami Abayomi, David A. Ofusori,
Volume 15, Issue 4 (October 2021)
Abstract
Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats.
Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain.
Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment.
Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.
Dr Nathaniel Amedu, Elizabeth Ajayi,
Volume 18, Issue 1 (January 2024)
Abstract
Background: Sodium metabisulfite (SMB) is a frequently utilized as food preservative. While it is generally acknowledged to be safe, there have been concerns regarding its potential impacts. This study aimed to investigate the effects of sodium metabisulfite on the hormonal levels, ovarian and uterine histology, and oxidative stress markers in female Wistar rats.
Methods: Twenty-four adolescent female Wistar rats were randomly allocated into four groups of siz rats each: Group 1 (control) received 0.5mL normal saline; Group 2 was given 100 mg/kg SMB; Group 3 received 300 mg/kg SMB; and Group 4 was administered 500 mg/kg SMB. The administration was done orally over 28 days, followed by euthanasia for tissue collection. Blood samples were collected to assess the serum follicle stimulating hormone (FSH) and luteinizing hormone (LH), while ovary and uterus tissue samples were harvested for malondialdehyde (MDA) assays and histopathology. For histopathology, we used haematoxylin and eosin and periodic acid schiff staining.
Results: The administration of SMB at doses of 300 and 500mg/kg had a notable impact on the hormone levels, particularly FSH and LH. The SMB doses also resulted in disrupted histo-architecture and altered glycogen expression in ovaries and uteri, as observed by histological examinations. Furthermore, SMB at 500mg/kg led to a significant increase in the oxidative stress marker malondialdehyde.
Conclusion: The SMB treatment affected FSH and LH levels, influencing ovarian and uterine structures. Disrupted structure and raised oxidative stress imply reproductive health risks. Further research is needed, including the effects of SMB on glycogen and FSH status.
