Histochemical evaluation of glutathione in brain

Slivka, Adam; Mytilineou, Catherine; Cohen, Gerald

doi:10.1016/0006-8993(87)90712-8

Cited by 258 publications

(126 citation statements)

References 8 publications

Supporting

Mentioning

118

Contrasting

Order By: Relevance

“…By contrast, these tissues do not possess very high concentrations of antioxidants vitamins E and C (Hornig, 1975;Kornbrust and Mavis, 1979). In particular, neurons contain very low levels of reduced glutathione, an antioxidant responsible for removal of cytosolic peroxides (Slivka et al, 1987), and their membranes contain a high proportion of freeradical-susceptible polyunsaturated fatty acids (see Evans, 1993). Interestingly enough, several studies demonstrated a significative antioxidant activity for carnosine-related dipeptides, both in muscle and brain tissue (see for example Boldyrev et al, 1987Boldyrev et al, , 1988Boldyrev et al, , 1997Kohen et al, 1988;Boldyrev, 1993).…”

Section: Antioxidant Effectmentioning

confidence: 99%

Carnosine-related dipeptides in the mammalian brain

Bonfanti

Peretto

Marchis

et al. 1999

Progress in Neurobiology

186

107

View full text Add to dashboard Cite

-Carnosine and structurally related dipeptides are a group of histidine-containing molecules widely distributed in vertebrate organisms and particularly abundant in muscle and nervous tissue. Although many theories have been proposed, the biological function(s) of these compounds in the nervous system remains enigmatic. The purpose of this article is to review the distribution of carnosine-related dipeptides in the mammalian brain, with particular reference to some cell populations wherein these molecules have been demonstrated to occur very recently. The high expression of carnosine in the mammalian olfactory receptor neurons led to infer that this dipeptide could play a role as a neurotransmitter/modulator in olfaction. This prediction, which has not yet been fully demonstrated, does not explain the localization of carnosine-related dipeptides in other cell types, such as glial and ependymal cells. A recent demonstration of high carnosine-like immunoreactivity in the subependymal layer of rodents, an area of the forebrain which shares with the olfactory neuroepithelium the occurrence of continuous neurogenesis during adulthood, supports the hypothesis that carnosine-related dipeptides could be implicated in some forms of structural plasticity. However, the particular distribution of these molecules in the subependymal layer, along with their expression in glial/ependymal cell populations, suggests that they are not directly linked to cell migration or cell renewal. In the absence of a unified theory about the role of carnosine-related dipeptides in the nervous system, some common features shared by different cell populations of the mammalian brain which contain these molecules are discussed.

show abstract

Section: Antioxidant Effectmentioning

confidence: 99%

Carnosine-related dipeptides in the mammalian brain

Bonfanti

Peretto

Marchis

et al. 1999

Progress in Neurobiology

186

107

View full text Add to dashboard Cite

show abstract

“…GSH is produced by GSH peroxidase in culture (Raps et al, 1989). GSH peroxidase is mainly a mitochondrial enzyme (Victonica et al, 1984) exclusively located in the human midbrain within glial cells (Slivka et al, 1987;Damier et al, 1993). GSH levels decrease with age in neurons but remain stable in astrocytes in culture (Sagara et al, 1996).…”

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

“…The ability of astrocytes to withstand oxidative stress is currently thought to be high (100,117,118 Given that nitroaromatic chemicals readily form free radicals, the apparent lack of neuronal protection provided by reduced glutathione is interesting (86 The severity of lesions produced by 1,3-dinitrobenzene is linked to the activity of neurons in susceptible regions (104,110). The severity of lesions elicited is enhanced by pretreatment of rats with pyrethroid (105 Figure 5).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Injury in the Central Nervous System

2000

View full text Add to dashboard Cite

Neurotoxicants with similar structural features or common mechanisms of chemical action frequently produce widely divergent neuropathologic outcomes. Methylmercury (MeHg) (CNS). The severity of lesions produced by DNB is modulated by the activity of neurons in the affected pathways. The inherent discrepancy between susceptibility of neuronal and glial cell populations is likely mediated by differential control of the mitochondrial permeability transition in astrocytes and neurons. Lessons learned in the mechanistic investigation of neurotoxicants suggest caution in the evaluation and interpretation of structure-activity relationships, eg, TMT, MeHg, and DNB all induce oxidative stress, whereas TMT and triethyltin produce neuronal damage and myelin edema, respectively. The precise CNS molecular targets of cell-specific lipophilic neurotoxicants remain to be determined.

show abstract

Histochemical evaluation of glutathione in brain

Cited by 258 publications

References 8 publications

Carnosine-related dipeptides in the mammalian brain

Carnosine-related dipeptides in the mammalian brain

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

Mechanisms of Injury in the Central Nervous System

Contact Info

Product

Resources

About