NGF restores decrease in catalase activity and increases superoxide dismutase and glutathione peroxidase activity in the brain of aged rats

Nisticò, Giuseppe; Ciriolo, Maria Rosa; Fışkın, Kayahan; Iannone, Michelangelo; Martino, Angelo; Rotilio, Giuseppe

doi:10.1016/0891-5849(92)90024-b

Cited by 147 publications

(56 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This may result in hampered dismutation of superoxide anions and inefficient detoxification of H 2 O 2 which results in formation of OH · ions enhancing the peroxidation of membrane lipids thereby leading to oxidative damage in many tissues [43]. However, vitamin E supplementation was observed to increase the levels of GSH, SOD and catalase significantly in the LPS-challenged animals in the present investigation.…”

Section: Discussioncontrasting

confidence: 46%

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Bharrhan¹,

Chopra²,

Rishi³

2010

Am. J. Biomed. Sci.

View full text Add to dashboard Cite

Vitamin E (-Tocopherol [-Toc]) is the primary membrane bound, lipid-soluble, chain-breaking antioxidant that has been reported to protect against lipid peroxidation-induced tissue damage. Therefore, the present study was designed to investigate the protection afforded by α-Tocopherol (vitamin E), if any, on LPS-induced liver injury in Wistar rats and to study the underlying mechanism of protection. Bacterial endotoxin (10 mg/Kg body weight-prestandardized dose) was injected intraperitoneally and animals were sacrificed 8 h post-challenge. Vitamin E (35 mg/Kg body weight) was administered orally for 15 days prior to endotoxin challenge. Challenge with LPS resulted in a significant increase in the activities of serum transaminases and alkaline phosphatase along with histological alterations in the liver. These responses were associated with elevated levels of malondialdehyde (MDA) and reduced levels of glutathione, superoxide dismutase and catalase along with increased levels of tumor necrosis factor alpha (TNF-α) in the liver homogenates. However, vitamin E supplementation attenuated the oxidative stress by reducing the levels of MDA, restoring the levels of glutathione, superoxide dismutase and catalase and decreasing the levels of TNF-α. Decreased TNF-α levels after vitamin E supplementation might have resulted into the modulation of above mentioned biochemical changes resulting into amelioration of hepatic architecture. Vitamin E, therefore, seems to have a promising role for clinical manifestations due to oxidative stress.

show abstract

Section: Discussioncontrasting

confidence: 46%

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Bharrhan¹,

Chopra²,

Rishi³

2010

Am. J. Biomed. Sci.

View full text Add to dashboard Cite

show abstract

“…Ethanol induces lipid peroxidation through iron that is present in certain regions of brain which catalyses the generation of oxygen derived free radicals (Nistico et al, 1992). Hydroxyethyl free radicals from ethanol having long half life produce damage to the membrane due to an increase in lipid peroxidation (Guochuan et al, 1998).…”

Section: Tanzania Journal Of Health Researchmentioning

confidence: 99%

Protective effect of the leaves of Vitex negundo against ethanol-induced cerebral oxidative stress in rats

Umamaheswari

Asokkumar

Umamageswari

et al. 2012

Tanzania J Hlth Res

View full text Add to dashboard Cite

The present study investigated the effect of the various fractions of hydromethanolic extract of the leaves of Vitex negundo (Verbenaceae) against ethanol-induced cerebral oxidative stress in rats. Cerebral oxidative stress was induced by the administration of 20% ethanol (5 ml/100gbw) for a period of 28 days. The petroleum ether (PEF), chloroform (CF), ethylacetate (EAF) and residual (RF) fractions at a dose of 200 mg/kgbw orally were simultaneously administered with ethanol for 28 days. α-tocopherol at a dose of 100 mg/kg orally was used as the standard. Administration of ethanol resulted in a significant elevation in serum biochemical parameters like aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), uric acid, triglycerides and lipoprotein levels. In addition there was a significant (P<0.01) elevation in malondialdehyde (MDA) and lipid hydroperoxide (LH) levels and a significant (P<0.01) reduction in enzymatic and non-enzymatic antioxidants in the brain tissue. Histopathological examination of the brain tissue of the ethanol treated animals showed marked gliosis. Simultaneous administration of the fractions prevented the enzymatic leakage and elevation of serum uric acid, triglycerides and lipoprotein levels. All the fractions (except the residual fraction) prevented the rise in lipid peroxidation and enhanced the antioxidant enzymes. Further, histopathological examination revealed that the fractions of V. negundo offered a significant protection against ethanol toxicity in rat brain. The activity exhibited by the chloroform fraction is comparable to that of the standard. The present study reveals that the leaf of V. negundo has protective action on the brain, which could be attributed to its antioxidant potential. __________________________________________________________________________________________

show abstract

“…Among the systems identified are a glutamate uptake activity that protects against excitotoxicity (Rosenberg et al, 1991) and stimulation of GSH synthesis and enzymes involved in GSH metabolism (Nisticè et al, 1992). GSH plays a major role in protection against oxidative stress (Meister, 1988;Makar et al, 1994) and functions to remove the H 202 generated by monoamine oxidase (Werner and Cohen, 1993).…”

Section: Effect Of L-dopa On Glutathione Levelsmentioning

confidence: 99%

Neurotrophic Effects of l‐DOPA in Postnatal Midbrain Dopamine Neuron/Cortical Astrocyte Cocultures

Mena

Davila

Sulzer

1997

Journal of Neurochemistry

118

View full text Add to dashboard Cite

L-DOPA IS toxic to catecholamine neurons in culture, but the toxicity is reduced by exposure to astrocytes. We tested the effect of L-DOPA on dopamine neurons using postnatal ventral midbrain neuron/cortical astrocyte cocultures in serum-free, glia-conditioned medium. L-DOPA (50 tiM) protected against dopamine neuronal cell death and increased the number and branching of dopamine processes. In contrast to embryonically derived glia-free cultures, where L-DOPA is toxic, postnatal midbrain cultures did not show toxicity at 200 1iM L-DOPA. The stereoisomer D-DOPA (50-400 btM) was not neurotrophic. The aromatic amino acid decarboxylase inhibitor carbidopa (25~zM) did not block the neurotrophic effect. These data suggest that the neurotrophic effect of L-DOPA is stereospecific but independent of the production of dopamine. However, L-DOPA increased the level of glutathione. Inhibition of glutathione peroxidase by Lbuthionine sulfoximine (3 1iM for 24 h) blocked the neurotrophic action of L-DOPA. N-Acetyl-L-cysteine (250 1iM for 48 h), which promotes glutathione synthesis, had a neurotrophic effect similar to that of L-DOPA. These data suggest that the neurotrophic effect of L-DOPA may be mediated, at least in part, by elevation of glutathione content. Key Words: L-DOPA-Glia-Glutathione-Parkinson's disease-Dopamine neurons.

show abstract

NGF restores decrease in catalase activity and increases superoxide dismutase and glutathione peroxidase activity in the brain of aged rats

Cited by 147 publications

References 23 publications

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Vitamin E Supplementation Modulates Endotoxin-induced Liver Damage in a Rat Model

Protective effect of the leaves of Vitex negundo against ethanol-induced cerebral oxidative stress in rats

Neurotrophic Effects of l‐DOPA in Postnatal Midbrain Dopamine Neuron/Cortical Astrocyte Cocultures

Contact Info

Product

Resources

About