Melatonin protects the central nervous system of rats against toluene-containing thinner intoxication by reducing reactive gliosis

Baydaş, Gıyasettin; Reíter, Russel J.; Недзвецкий, В. С.; Yasar, Abdullah; Tuzcu, Mehmet; Ozveren, Faik; Canatan, Halit

doi:10.1016/s0378-4274(02)00400-9

Cited by 86 publications

(61 citation statements)

References 34 publications

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“…The present findings are in agreement with recent reports that clearly show that reactive gliosis occurs in diabetes, possibly as a result of oxidative stress. This is consistent with our previous studies in diabetic rats in which the protective effects of antioxidants against reactive gliosis were attributed to their free radical scavenging properties [15,16] . As we previously described, antioxidant vitamin E [32] and melatonin [15] treatment improved reactive gliosis induced by hyperglycemia via a dramatic reduction in oxidative stress.…”

Section: Discussionsupporting

confidence: 93%

“…The exact mechanism by which GBP inhibits reactive gliosis is not entirely clear; however, one possible explanation is that GBP may reduce oxidative stress via an unknown mechanism. Oxidative stress is known to exacerbate glial reactivity [15,16] . Decreased LPO levels as a result of GBP treatment in the present study supports this explanation.…”

Section: Discussionmentioning

confidence: 99%

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Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Baydaş

Sonkaya

Tuzcu

et al. 2005

Acta Pharmacologica Sinica

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Aim: To investigate the effect of gabapentin on neural [neuron-specific enolase (NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S100B] in different brain regions of diabetic rats. Methods: Diabetes was induced by a single intraperitoneal injection of streptozotocine (50 mg/kg body weight). Rats in one diabetic group received gabapentin (50 mg·kg ) and rats in the other diabetic group received vehicle only for 6 weeks. The levels of GFAP, S100B, and NSE were determined by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid peroxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH) levels were also determined in the same brain parts. Results: Total and degraded GFAP content and S100B protein expression in different areas of brain tissues significantly increased in diabetic rats compared to control rats. Similarly, NSE levels were also significantly elevated in hyperglycemic rats. In addition, there was a significant increase in LPO levels in the diabetic rat brain compared to control rat brains. Pretreatment with gabapentin prevented the upregulation of GFAP, S100B, and NSE in all brain regions of diabetic rats. The level of LPO was reduced, but not completely halted, by treatment with gabapentin. Conclusion: These results suggest that diabetes causes glial and neuronal injury, possibly as a result of elevated oxidative stress, and that gabapentin protects neurons and glial cells. Thus, we predict that gabapentin treatment will attenuate the hippocampal and cortical neurodegeneration observed during diabetes mellitus in rats. Key wordsgabapentin; glial fibrillary acidic protein; neurotrophic protein S100beta; phosphopyruvate hydratase; lipid peroxidation 1 Study supported by the Firat University R esear ch Fou nda t ion ( FUB AP Proj ect number 831).

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Baydaş

Sonkaya

Tuzcu

et al. 2005

Acta Pharmacologica Sinica

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“…In a parallel manner the nerve fibers show edema, irregular thickening and atrophy or disintegration. Baydas et al (38) investigated the effects of melatonin on the glial reactivity induced by the exposure of rats to the fumes of thinner, which due to the presence of toluene (3000 ppm, for 45 days) are known to be neurotoxic. Pathological studies of the effects of toluene inhalation based on biopsies of the sural nerve have shown swelling of the axons and an extremely thin lamella of the myelin sheath (39).…”

Section: Discussionmentioning

confidence: 99%

Ebselen Protects Against Oxidative and Morphological Effects of High Concentration Chronic Toluene Exposure on Rat Sciatic Nerves

et al. 2006

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Aim: Neuroprotective effects of ebselen against free radical damage have been studied extensively. Toluene generates reactive oxygen species (ROS) and the toxic effects relating to these reactants. The aim of this study was designed to investigate the effects of chronic toluene inhalation in high concentration on lipid peroxidation, antioxidant enzyme activities and ultrastructural changes in the sciatic nerves of rats.Methods: We also examined the protective effects of ebselen against toluen exposure. Male Wistar albino rats (150-250 g) were divided in three experimental groups: the control, toluene and toluene+ebselen treated group (n=10 for each). Toluene treatment was performed by inhalation of 3000 ppm toluene, in a 8 hr/day and 6 day/week order for 16 weeks. Control group received 1ml serum physiologic and ebselen was given i.p. (10 mg/kg) to toluene+ebselen treated group just after toluene exposure per day. Blood and tissue samples were obtained for biochemical and histopathological investigation. The blood and sciatic nerves were assayed for toluene by gas chromatography.Results: Toluene significantly increased blood and tissue malondialdehyde (MDA), and decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but not tissue catalase (CAT) levels when compared with controls. Ebselen administration prevented to increase of blood and tissue MDA and decrease to SOD and GSH-Px levels induced by toluene inhalation. Electron micrographs of sciatic nerve in the toluene group shows myelin destructions with onion-bulb and bubble form protrusion on the myelin sheath and axolemma border of myelinated axons. Furthermore, ebselen salvaged the nerve fibers from toluene exposure.Conclusion: Ebselen treatment may provide neuroprotection against toluene neurotoxicity by directly scavenging ROS and by indirectly augmenting their antioxidant capacity.

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“…This process may occur through a free radical-mediated pathway. Tissue damage is observed during untreated diabetes with very high glucose levels, and this is to a great extent attributed to oxidative injury resulting from excessive production of free radicals [20,23]. One of the consequences of such damage is the depletion of a cellular antioxidant, reduced glutathione (GSH).…”

Section: Resultsmentioning

confidence: 99%

“…A sodium dodecylsulfatepolyacrylamide gel electrophoresis (SDS-PAGE) sample buffer containing 2% β-mercaptoethanol was added to the supernatants. Equal amounts of protein were applied in each lane and separated on SDS-PAGE using a 7.5 to 17.5 gradient gel as described previously [19,20]. Proteins were transferred to nitrocellulose filters (Schleich and Schuell Inc., USA) and separated electrophoretically using an electroblotter.…”

Section: Methodsmentioning

confidence: 99%

Astrogliosis in the hippocampus and cortex and cognitive deficits in rats with streptozotocin-induced diabetes: Effects of melatonin

et al. 2008

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We examined, using a Western blot technique, the contents and compositions of a specific neuronal protein, NCAM, and of an astrocyte marker, GFAP, in the hippocampus and cortex of rats with streptozotocin (STZ)-induced diabetes and compared these indices with those in control (intact) animals and STZ-diabetic rats treated with melatonin. Behavioral cognitive indices manifested in the passive avoidance test (PAT) and Morris water maze (MWM) learning performance were also estimated in the above groups of animals. As was found, STZ-diabetic rats demonstrated clear cognitive deficits according to the values of the retention latency in the PAT and time of reaching the escape platform in the MWM performance. In these animals, the GFAP content was elevated, and the amount of degraded products of this protein increased, as compared with the control. Simultaneously, considerable down-regulation of the NCAM expression and modifications of NCAM isoform composition were found in diabetic animals. In addition, significantly increased levels of lipid peroxidation (according to the amounts of malondialdehyde + 4-hydroxyalkenals) were measured in the cortex and hippocampus of rats with stable diabetic hyperglycemia. All the above-mentioned shifts were significantly smoothed or even nearly completely compensated in the case of treatment of STZ-diabetic rats with melatonin (10 mg/kg per day). The role of diabetes-related changes in the amount and composition of specific neural and glial proteins in the development of cognitive deficits, the involvement of oxidative stress in the mechanisms of the respective shifts, and possible mechanisms of the neuroprotective effect of melatonin with respect to diabetes-related pathological biochemical and behavioral shifts are discussed.

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Melatonin protects the central nervous system of rats against toluene-containing thinner intoxication by reducing reactive gliosis

Cited by 86 publications

References 34 publications

Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats1

Ebselen Protects Against Oxidative and Morphological Effects of High Concentration Chronic Toluene Exposure on Rat Sciatic Nerves

Astrogliosis in the hippocampus and cortex and cognitive deficits in rats with streptozotocin-induced diabetes: Effects of melatonin

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