This study was undertaken to investigate the protective effects of melatonin against formaldehyde-induced neurotoxicity in prefrontal cortex of rats. For this purpose, 21 male Wistar rats were divided into three groups. The rats in Group I were used as a control, while the rats in Group II were injected every other day with formaldehyde. The rats in Group III received melatonin daily while exposed to formaldehyde. At the end of 14-day experimental period, all rats were killed by decapitation. The brains of the rats were removed and the prefrontal cortex tissues were obtained from all brain specimens. Some of the prefrontal cortex tissue specimens were used for determination of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) levels. The remaining prefrontal cortex tissue specimens were used for immunohistochemical evaluation. The levels of SOD and GSH-Px were significantly decreased, and MDA levels, were significantly increased in rats treated with formaldehyde compared with those of the controls. In the immunohistochemical evaluation of this group, apoptotic cells were observed. However, increased SOD and GSH-Px enzyme activities, and decreased MDA levels, were detected in the rats administered melatonin while exposed to formaldehyde. Furthermore, apoptotic changes caused by formaldehyde were decreased in these rats. The results of our study suggest that melatonin treatment prevents formaldehyde-induced neuronal damage in prefrontal cortex.
This study was designed to investigate the harmful effects of toluene inhalation in the liver of rats and possible protective effects of melatonin on these detrimental effects. For this purpose, 21 adult male Wistar-albino rats were randomly divided into three equal groups. Animals in group I were used as control. The rats in group II were exposed to toluene (3000 ppm/1 hour/day) for 4 weeks, while the rats in group III were treated with melatonin (10 mg/kg/day, intraperitoneally [ip]) plus toluene inhalation. At the end of the experimental period, liver and blood samples were taken from the decapitated animals. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin and albumin levels were determined. Liver tissue sections were stained with routine histological methods and examined under the light microscope. In addition, the sections were immunohistochemically stained using avidin-biotin-peroxidase method for determination of apoptosis. The liver tissue activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) levels were also measured. Toluene inhalation significantly increased serum ALT, AST and tissue MDA, and decreased serum albumin, but did not affect serum ALP, total bilirubin levels and tissue SOD, GSH-Px and CAT activity when compared with controls. The increases in tissue MDA and serum ALT and AST levels induced by toluene inhalation were significantly inhibited by melatonin treatment. In light microscopic observations of tissues from toluene-inhaled rats, massive hepatocyte degeneration, ballooning degeneration and mild pericentral fibrosis were observed. Bax immune reactivity was also increased significantly. Melatonin treatment decreased the balloon degeneration, fibrosis and Bax immune reactivity in the liver of toluene-inhaled rats. In view of the present findings, it is suggested that melatonin has hepatoprotective effects against toluene toxicity via primarily antioxidative properties.
This study was undertaken to investigate the protective effects of melatonin against formaldehyde-induced renal damage in rats. For this purpose, 21 male Wistar rats were divided into three groups. The animals in Group I were used as a control, whereas the rats in group II were injected every other day with formaldehyde. The rats in group III received melatonin daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation, and the kidneys were removed. Some of the renal tissue specimens were used for determination of superoxide dismutase, glutatione peroxidase enzyme activities, and malondialdehyde levels. The remaining kidney tissue specimens were used for light microscopic evaluation. The renal tissue activities of superoxide dismutase and glutatione peroxidase were significantly decreased, and malondialdehyde levels were significantly increased in rats treated with formaldehyde compared with those of the control animals. In the light microscopic evaluation of this group, degenerative glomerules, vacuolization and dilatation of distal tubules, and vascular congestion were detected. However, an increase was observed in activities of superoxide dismutase and glutatione peroxidase enzymes, and a decrease of malondialdehyde levels in animals treated with formaldehyde plus melatonin was observed. Furthermore, the histopathological changes caused by formaldehyde were disappeared except for minimal tubular dilatation in this group. In conclusion, the biochemical and histological findings of our study suggest that melatonin administration prevents formaldehyde-induced oxidative renal damage in rats.
This study aimed to investigate changes in the cerebellum of formaldehyde-exposed rats and the effects of omega-3 fatty acids on these changes. The study involved 21 male Wistar-Albino rats which were divided into three groups. The rats in Group I comprised the control group. The rats in Group II were injected with intraperitoneal 10% formaldehyde every other day. The rats in Group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation and the cerebellum removed. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO), and malondialdehyde (MDA) levels were determined in cerebellum specimens by using spectrophotometric methods. In our study, levels of SOD and CAT were significantly decreased, and GSH-Px, XO, MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Whereas, it was seen that there was an increase in SOD and CAT enzyme activities and decrease in MDA, XO, and GSH-Px levels in rats administered to omega-3 fatty acids with exposure of formaldehyde. It was determined that exposure of formaldehyde increased free radicals in cerebellum of rats and this increase was prevented by administration of omega-3 fatty acids.
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