This study evaluated the ameliorative and prophylactic effects of 2 different doses of polyphenolic-rich fraction of Garcinia kola (PPRFGk) seeds on the histology and hormones of pituitary–testicular axis of male Wistar rats. Thirty-five male Wistar rats (150-200 g) were divided into 7 groups of 5 rats each. Groups I and II were given distilled water (0.5 mL/day) for 8 days followed by propylene glycol (0.2 mL/d) and 600 mg/kg of PPRFGk, respectively, for 21 days. Group III received sodium arsenate (8 days), left untreated for 21 days. Groups IV and V received sodium arsenate (20 mg/kg) for 8 days followed by PPRFGk (300 and 600 mg/kg, respectively) for 21 days. Groups VI and VII received PPRFGk (300 and 600 mg/kg, respectively) for 21 days followed by sodium arsenate (20 mg/kg) for 8 days. Rats were killed by cervical dislocation 24 hours after the last dose and their blood collected through cardiac puncture. Blood sera were assayed for the levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone using immunoassay techniques. Histology of the pituitary gland and testes was carried out. A significant reduction was observed in the concentration of FSH in groups IV, V, VI, and VII in comparison with groups I and II. The concentrations of both LH and testosterone showed significant decreases in groups IV, V, VI, and VII in comparison with group I. Group III presented with the lowest serum hormonal concentrations. Photomicrographs of the pituitary gland revealed greatly reduced basophils in group III and mildly reduced basophils in groups IV, VI, and VII in comparison with groups I and II. Group V revealed hypercellularized and distorted basophils. Photomicrographs of the testes showed detachment of the seminiferous tubules from the basement membrane and disruption of the interstitial space which was worse in group III, moderate in groups V and VI, and mild in group VII. In conclusion, PPRFGk effected a dose-dependent reversal and prevention of the perturbations caused by arsenate in rats.
Background: Oligodendrocytes are critical to the function of the brain. They generate the myelin sheath which ensures saltatory conduction, which is a more energy saving and efficient means of axonal impulse transmission. Ventriculomegaly results in neuronal degeneration and astrogliosis. Purpose: The effect of the degree of ventriculomegaly on oligodendrocyte in kaolin-induced hydrocephalus and the timeline have not been extensively documented, hence this study. Methods: A total of 81 rats that were 3 weeks old were divided into 4 groups each consisting of control and experimental subgroups. Kaolin suspension was intracisternally injected to induce hydrocephalus and the animal sacrificed post-induction at 1, 2, 3, and 4 weeks. Two 1-mm-thick coronal slices at optic chiasma level were fixed in 10% buffered formal-saline and Karnovsky's fixative for light and transmission electron microscopy (TEM), respectively. The former slices were processed and stained with hematoxylin and eosin for glial density, cortical thickness, and oligodendrocyte evaluations. Subcortical white matter region of the latter were processed by conventional techniques for TEM. Results: Compared with their corresponding control rats, thickness of the dorsolateral cortex was significantly reduced across the 2-4 week post-induction (WPI), glial density was significantly increased in the mild and moderate ventriculomegaly subgroups 1 WPI but only in mild ventriculomegaly subset 2 WPI. In the 4 WPI group, there was significant increase in glial density across the 3 ventriculomegaly subsets. Early hydropic changes of oligodendrocytes were noted in the inner pyramidal layer mostly in the 4 WPI experimental rats. Dilation of the endoplasmic reticulum precedes that of mitochondria, while mitochondrial crista disruption was noted in the 3 and 4 WPI rats. The nuclear membrane of the oligodendrocytes was progressively deformed from the 2nd to 4th WPI. Conclusion: This study reported degenerative changes of oligodendrocytes and its organelles in kaolin-induced hydrocephalus. Degeneration was worse with duration and in the deep cortical layers.
Background: In hydrocephalus, the impairment of cognitive and motor functions is thought to be partly due to injury to the myelin sheath of axons in the central nervous system. The exact nature of this injury is not completely understood. Methods: We induced hydrocephalus in 3-week-old rats with an intracisternal injection of kaolin suspension (0.04 ml of 200 mg/ml) and examined paraffin and ultrathin sections of the subcortical white matter from coronal slices of the cerebrum obtained at the level of the optic chiasm after sacrifice at weekly intervals for 4 weeks. Results: Over time, there was a progression of injury to the myelin sheath consisting of attenuation, lamella separation and accumulation of myelin debris, focal degeneration, and the appearance of casts and loops. Conclusion: The results suggest that myelin injury in kaolin-induced hydrocephalus progresses with the duration and severity of ventriculomegaly.
The role of age and concomitant exposure to trace elements on Wistar rats was investigated in this study. Fifteen 12 weeks old rats divided into groups A, B and C, and fifteen 36 weeks old rats divided into groups D, E and F were acclimatised for 2 weeks. Groups A and D served as the control groups and were administered distilled water. Groups B and E were administered 1 mL each of 5 ppm, while groups C and F were administered 1 mL each of 10 ppm of lead, cadmium, copper and zinc solutions daily for 1 week. Rats were sacrificed by cervical dislocation and the harvested cerebrum was digested in HNO 3 and HClO 4 . Quantification of metals was done using Flame Atomic Absorption Spectrophotometer. A 5 µm thick paraffin section of the cerebrum obtained at the level of the optic chiasma was stained with H&E and evaluated.Zinc concentration was markedly reduced while cadmium and lead concentrations were increased in both experimental groups across the age groups in a dose-dependent fashion. Copper concentration was reduced in rats with 5 ppm exposure while in those with 10 ppm exposure it was similar to the control. Pyknotic glial cells were more and widespread in the younger rats but few and restricted to the mid-cortical region in older rats. Early neuronal necrosis was widespread in older rat group but restricted to internal granular layer in young rats. Central neuronal chromatolysis was noted in both groups of younger rats but restricted to the 5 ppm group of older rat group.Cerebral concentration of zinc was reduced in cadmium and lead exposure. Glial cells pyknosis were widespread in older rats, but early neuronal necrosis was more widespread in younger rats, showing that the cellular effect of heavy metal is age dependent.
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