Oxidative stress has been reported to induce cognitive impairment in Parkinson's disease. This paper aimed to determine the effect of quercetin, a substance possessing antioxidant activity, on the cognitive function in a rat model of Parkinson's disease. Male Wistar rats, weighing 200–250 g, were orally given quercetin at doses of 100, 200, 300 mg/kg BW once daily for a period of 14 days before and 14 days after the unilateral lesion of right substantia nigra induced by 6-hydroxydopamine (6-OHDA). Their spatial memory was assessed at 7 and 14 days of treatment and neuron density was determined, malondialdehyde (MDA) level, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were evaluated at the end of the experiment. In addition, the activity of acetylcholinesterase (AChE) was also measured. It was found that all doses of quercetin enhanced spatial memory. Therefore, it is suggested that the cognitive-enhancing effect of quercetin occurs partly because of decreased oxidative damage resulting in increased neuron density.

Objective. is study aimed to investigate the sensitivity of the testis, epididymis, seminal vesicle, and sperm acrosome reaction (AR) to monosodium L-glutamate (MSG) in rats. Materials and methods. Rats were divided into four groups and fed with non-acidic MSG at 0.25, 3 or 6 g/kg body weight for 30 days or without MSG. e morphological changes in the reproductive organs were studied. e plasma testosterone level, epididymal sperm concentration, and sperm AR status were assayed. Results. Compared to the control, no signi cant changes were discerned in the morphology and weight of the testes, or the histological structures of epididymis, vas deferens and seminal vesicle. In contrast, signi cant decreases were detected in the weight of the epididymis, testosterone levels, and sperm concentration of rats treated with 6 g/kg body weight of MSG. e weight loss was evident in the seminal vesicle in MSG-administered rats. Moreover, rats treated with MSG 3 and 6 g/kg exhibited partial testicular damage, characterized by sloughing of spermatogenic cells into the seminiferous tubular lumen, and their plasma testosterone levels were signicantly decreased. In the 6 g/kg MSG group, the sperm concentration was signi cantly decreased compared with the control or two lower dose MSG groups. In AR assays, there was no statistically signi cant di erence between MSG-rats and normal rats. Conclusion. Testicular morphological changes, testosterone level, and sperm concentration were sensitive to high doses of MSG while the rate of AR was not affected. erefore, the consumption of high dose MSG must be avoided because it may cause partial infertility in male.

Endoscopic sinus surgery in patients who have an Onodi cell (sphenoethmoid cell) carries a high risk f or optic nerve injury. We meticulously dissected 65 embalmed cadaver adult half-heads and attempted to identify an optic canal bulge in each with a nasal endoscope. Our aims were to determine the prevalence ofan Onodi cell in adult Thai cadavers, to ascertain the prevalence of an overriding ethmoid cell, and to measure the length ofan overriding ethmoid cell's superio r and posterior extensions in relation to the anterior sphenoid wall. Moreover, we attempted to determine the minimum amount ofbone thickness betwee n an Onodi cell and the optic nerve. We fo und that an Onodi cell was present in 39 of the 65 specimens (60.0 %). We also fo und that an overriding ethmoid cell was present in 14 spec imens, which accounted f or 21.5 % of the total numb er of specimens and 36.8% of38 Onodi cell-pos itive speci mens (the presence or absence of an overriding ethmoid cell was not recorded in one of the 39 Onodi cell-pos itive specimens). The distance of the overriding ethmoid cell 's superior and posterior extensions f rom the anterior sphenoid wall rangedfro m 3 to 13 mm (median: 7) andfrom 4 to 16mm (median: 9.5), respectively. Measurements of the minimum amount ofbone thicknesses between each Onodi cell and optic nerve ranged fro m 0.03 to 0.54 mm (median: 0.08). Our study demonstrated that the prevalence ofan Onodi cell in adult Thai cadavers was as great as the

Oxidative stress plays an important role in brain dysfunctions induced by alcohol. Since less therapeutic agent against cognitive deficit and brain damage induced by chronic alcohol consumption is less available, we aimed to assess the effect of Tiliacora triandra extract, a plant possessing antioxidant activity, on memory impairment, neuron density, cholinergic function, and oxidative stress in hippocampus of alcoholic rats. Male Wistar rats were induced ethanol dependence condition by semivoluntary intake of alcohol for 15 weeks. Alcoholic rats were orally given T. triandra at doses of 100, 200, and 400 mg·kg−1BW for 14 days. Memory assessment was performed every 7 days while neuron density, activities of AChE, SOD, CAT, and GSH-Px and, MDA level in hippocampus were assessed at the end of study. Interestingly, the extract mitigated the increased escape latency, AChE and MDA level. The extract also mitigated the decreased retention time, SOD, CAT, and GSH-Px activities, and neurons density in hippocampus induced by alcohol. These data suggested that the extract improved memory deficit in alcoholic rats partly via the decreased oxidative stress and the suppression of AChE. Therefore, T. triandra is the potential reagent for treating brain dysfunction induced by alcohol. However, further researches are necessary to understand the detail mechanism and possible active ingredient.

Due to the crucial role of oxidative stress on the pathophysiology of autism and the concept of synergistic effect, the benefit of the combined extract of purple rice and silkworm pupae (AP1) for autism disorder was the focus. Therefore, we aimed to determine the effect of AP1 on autistic-like behaviors, oxidative stress status, and histopathological change of cerebellum in valproic acid (VPA) rat model of autism. VPA was injected on postnatal day (PND) 14 and the animals were orally given AP1 at doses of 50, 100, and 200 mg·kg−1 BW between PND 14 and PND 40. The autism-like behaviors were analyzed via hot-plate, rotarod, elevated plus-maze, learning, memory, and social behavior tests. Oxidative stress and the histological change in the cerebellum were assessed at the end of study. AP1 treated rats improved behaviors in all tests except that in hot-plate test. The improvement of oxidative stress and Purkinje cell loss was also observed in the cerebellum of VPA-treated rats. Our data suggest that AP1 partially reduced autism-like behaviors by improving oxidative stress and Purkinje cell loss. Further research is required to identify the active ingredients in AP1 and gender difference effect.