title: Melatonin ameliorates blood-brain barrier permeability, glutathione, and nitric oxide levels in the choroid plexus of the infantile rats with kaolin-induced hydrocephalus.
abstract: Hydrocephalus is a disabling disease for children, but current data concerning the effects of melatonin on ventricular enlargement are still limited. We have investigated the changes in the choroid plexuses (CPs) of ventricles and blood-brain barrier (BBB) of hydrocephalic rats. Forty-five Swiss Albino rats at age 2 weeks were divided into three equal groups: control, hydrocephalus, and melatonin-treated hydrocephalus groups. Hydrocephalus was induced by kaolin injection into the cisterna magna of all pups except control group and melatonin was given at a daily dose of 0.5 mg/100 g body weight for 4 weeks. At the end of the study, one animal from each group was examined using a gamma camera to study the disruption of BBB due to hydrocephalus. All animals were then killed for assay of glutathione (GSH) and nitric oxide (NO), as well as histological study of the CPs during the hydrocephalus. We observed an increased BBB activity was found in hydrocephalus group, while melatonin reversed these changes. It was found that NO concentration was elevated in hydrocephalus group and melatonin partly abolished the increased levels of NO. In contrast, GSH levels were significantly decreased in hydrocephalus group, while melatonin increased the tissue GSH level (p<0.01). Histologically, there was a significant alteration in the CPs of the ventricles of hydrocephalic animals, but it was regressed after melatonin treatment in consistent with the gross morphological changes related to hydrocephalus. In conclusion, our results clearly demonstrated for the first time the neuroprotective effects of melatonin upon hydrocephalus-induced CP changes in infantile rats, but further studies are needed to suggest melatonin as a candidate protective drug in children.
authors: Department of Neurosurgery, Adnan Menderes University School of Medicine, TR-09100 Aydin, Turkey. drmturgut@yahoo.com
authors: Mehmet
authors: M
authors: Turgut
authors: Serpil
authors: S
authors: Erdogan
authors: Kemal
authors: K
authors: Ergin
authors: Mukadder
authors: M
authors: Serter
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001812:Blood-Brain Barrier / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D002831:Choroid Plexus / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006849:Hydrocephalus / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D020547:Lateral Ventricles / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008550:Melatonin / Q000494:pharmacology* / Q000627:therapeutic use; D009421:Nervous System Malformations / Q000473:pathology* / Q000503:physiopathology*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D016896:Treatment Outcome
chemical_list: D018696:Neuroprotective Agents; D009569:Nitric Oxide; D005978:Glutathione; D008550:Melatonin