Cytoarchitectural differences in reproductive organs of some polycystic ovary-like induced animal models.

Polycystic ovary syndrome (PCOS) is the most common gynaecological, endocrine disorder that occurs during reproductive age and is a significant cause of anovulatory infertility. Letrozole is an aromatase inhibitor which negates the action of the aromatase enzyme, which results in the buildup of male hormones (testosterone) in the females, causing hyperandrogenism, which is a hallmark of Polycystic Ovarian Syndrome. Mifepristone (RU486) is a progestin antagonist that acts to arrest the actions of the progesterone hormone, resulting in follicular atresia and anovulation. DHEA is an androgen which was also administered in a bid to cause hyperandrogenism in the rats.This study aimed to evaluate the effects of these hormones on the cytoarchitecture of the ovaries and uterus to assess their various PCOS-like histological features.Animals were grouped mainly into three: Letrozole, Mifepristone and DHEA groups, which were further divided into two subgroups each, administered low and high doses of letrozole orally, Mifepristone and Dehydroepiandosterone (DHEA) subcutaneously. Each of the subgroups also had a comparison control group. Following the completion of administration, the Wistar rats were euthanized, and their ovaries and uterus were collected for histological analysis.Increased proliferation of ovarian follicles was noted in the treated groups compared to control, as well as thickening of the endometrial layer.

Phoenix dactylifera and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.

Monosodium glutamate (MSG) has been known to cause neurodegeneration, due to its ability to trigger excitotoxicity, and the hippocampus is one of the most affected regions. Therefore, Phoenix dactylifera (P. dactylifera) and polyphenols was employed in this study to mitigate on the deleterious effect of monosodium glutamate on the dentate gyrus of Wistar rats. Forty-eight male Wistar rats weighing between 120-150g was used for the study. The Wistar rats were grouped into eight, (n=6). Groups 1-8 received 1.6mL/kg normal saline, 4000mg\kg monosodium glutamate for 7-days, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg caffeic-acid for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg Phoenix dactylifera for 14-days concurrently, 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days concurrently, 100mg\kg. caffeic-acid for 14-days followed by 4000mg\kg monosodium glutamate for 7-days, 100mg\kg Phoenix dactylifera for 14-days followed by 4000mg\kg monosodium glutamate for 7-days and 100mg\kg luteolin for 14-days followed by 4000mg\kg monosodium glutamate for 7-days respectively. After the treatments, the rats underwent behavioural tests, and subsequently, the brain tissues were processed for histological and biochemical analyses. The activities of P. dactylifera and polyphenols ameliorated the deleterious effect of monosodium glutamate, through increased spontaneous alternation of the experimental animals, dominant matured granule cells of the dentate gyrus and modulated the activities of superoxide dismutase, glutathione peroxidase and malondialdehyde in the of male Wistar rats. Therefore, this study revealed that P. dactylifera and polyphenols ameliorated monosodium glutamate toxicity in the dentate gyrus of Wistar rats.

D-Ribose-LCysteine attenuates manganese-induced cognitive and motor deficit, oxidative damage, and reactive microglia activation.

Due to overexposure, manganese (Mn) accumulation in the brain can trigger the inhibition of glutathione synthesis and lead to increased generation of reactive oxygen species (ROS) and oxidative stress. D-Ribose-L-Cysteine (RibCys) has been demonstrated to effectively support glutathione synthesis to scavenge ROS and protect cells from oxidative damage. In the present study, we examined the effects of RibCys on weight changes, cognitive and motor associated activities, oxidative stress markers, striatal and cortical histology, and microglia activation following Mn exposure. Rats were exposed to either saline, Mn or/and RibCys for two weeks. The Mn exposed rats received RibCys either as pre-, co-, or post-treatments. Mn caused a significant decrease in weight, memory and motor activities, increased lactate dehydrogenase level, overexpression of IBA1 reflecting microglia activation, and distortion of the neuronal cytoarchitecture of the striatum and motor cortex, respectively. Interventions with RibCys mitigated Mn-induced neurotoxic events. Our novel study demonstrates that RibCys effectively ameliorates the neurotoxicity following Mn treatment and maybe a therapeutic strategy against the neurological consequences of Mn overexposurec.

Oral thymoquinone modulates cyclophosphamide-induced testicular toxicity in adolescent Wistar rats.

Cyclophosphamide (CYP) is an effective anti-cancer drug that is widely accepted, but it is not devoid of unintended toxic effects. Gonadal toxicity is reported as one of the side effects of its long-time use. This study examined the effects of thymoquinone (TQ) on the biological integrities of the testes after cyclophosphamide exposure. Thirty adolescent male Wistar rats (100-110 g) were divided into six groups (n = 5), receiving normal saline (NS), 20 mg/kg of CYP (CYP), 5 mg/kg of TQ (TQ5), 10 mg/kg of TQ (TQ10), 20 mg/kg of CYP and 5 mg/kg of TQ (CTQ5), and 20 mg/kg of CYP and 10 mg/kg of TQ (CTQ10) respectively. On the 22nd day, blood, semen and testicular samples were collected for the assay of serum reproductive hormones (follicle-stimulating (FSH) and luteinizing (LH) hormones), semen analysis and testicular histology and proliferating cell nuclear antigen (PCNA) expression. The results revealed that CYP exposure affected functional and structural integrities of the testes, by depleting sperm count and motility, testosterone, LH, spermatogenic and mature sperm cell population, Leydig cells and PCNA immunoreactive proliferating cells. TQ interventions were able to reverse all cytotoxic CYP impacts, but with differential activities on the hormonal concentrations, specifically LH and FSH. Cumulatively, thymoquinone may be a potent agent against cyclophosphamide effects on the physiological, regeneration and histological integrities of the testes, as observed in this study.

D-Ribose-L-Cysteine Improves Glutathione Levels, Neuronal and Mitochondrial Ultrastructural Damage, Caspase-3 and GFAP Expressions Following Manganese-Induced Neurotoxicity.

Repeated manganese (Mn) exposure may cause increased production of reactive oxygen species (ROS), with a consequent imbalance in the glutathione (GSH) antioxidant defence system, resulting in cellular dysfunctions, and eventually cell death, particularly in the brain. D-ribose-L-cysteine (RibCys) has been demonstrated to effectively promote the synthesis of glutathione, a potent neutralizer of ROS. In the present study, we examined the effects of RibCys on glutathione levels, apoptotic and astrocytic responses, neuronal ultrastructural integrity, following Mn exposure. Wild-type rats were exposed to either saline, Mn, or/and RibCys for 2 weeks. The Mn-exposed rats received RibCys either as pre-, co-, or post-treatments. Mn caused a marked decrease in GSH levels, overexpression of GFAP and caspase-3, reflecting astrocytosis and apoptosis, and altered ultrastructural integrities of the neuronal nuclei, mitochondria, and myelin sheath of the striatum and motor cortex respectively, while all interventions with RibCys minimized and prevented the neurotoxic events. Our study demonstrates that RibCys effectively attenuates the neurotoxic effects of Mn and may be useful as a therapeutic strategy against neurological consequences of Mn overexposure.