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Proton release on binding of glutathione to alpha, Mu and Delta class glutathione transferases.

Potentiometric, spectroscopic and stopped-flow experiments have been performed to dissect the binding mechanism of GSH to selected glutathione S-transferases (GSTs), A1-1, M2-2 and Lucilia cuprina GST, belonging to Alpha, Mu and Delta classes respectively. Both Alpha and Mu isoenzymes quantitatively release the thiol proton of the substrate when the binary complex is formed. Proton extrusion, quenching of intrinsic fluorescence and thiolate formation, diagnostic of different steps along the binding pathway, have been monitored by stopped-flow analysis. Kinetic data are consistent with a multi-step binding mechanism: the substrate is initially bound to form an un-ionized pre-complex [k(1)>/=(2-5)x10(6) M(-1).s(-1)], which is slowly converted into the final Michaelis complex (k(2)=1100-1200 s(-1)). Ionization of GSH, fluorescence quenching and proton extrusion are fast events that occur either synchronously or rapidly after the final complex formation. The Delta isoenzyme shows an interesting difference: proton extrusion is almost stoichiometric with thiolate formed at the active site only up to pH 7.0. Above this pH, at least one protein residue acts as internal base to neutralize the thiol proton. These results suggest that the Alpha and Mu enzymes retain not only a similar catalytic outcome and overall three-dimensional structure but also share a similar kinetic mechanism for GSH binding. The Delta GST, which is closely related to the mammalian Theta class enzymes and is distantly related to Alpha and Mu GSTs in the evolutionary pathway, might display a different activation mechanism for GSH.

Animals↗

Glutathione conjugation in male reproductive system: studies on glutathione-S-transferase of bull and boar epididymis.

Male reproductive organs are extremely sensitive to the negative influence of toxic environmental factors as well as drugs, and until now not many attempts have been made at studying the detoxication enzymes and the relationship between the activity of those enzymes and spermatozoa fertility. In the present work we studied cytosolic glutathione-S-transferases (GST, EC 2.5.1.18) from different parts (head, corpus and tail) of bull and boar epididymis. We isolated two molecular forms of GST from each part of epididymis, characterized their biochemical properties and examined the mechanism of the catalyzed reaction. On the basis of their substrate specificity and isoelectric point, the isoforms were found to belong to the near neutral GST class mi. All examined GST forms exhibited higher affinity towards GSH than towards 1-chloro-2,4-dinitrobenzene (CDNB) and bull epididymis GST forms showed biphasic Lineweaver-Burk double reciprocal curves in the presence of GSH as a variable substrate. Boar epididymis anionic GST had the -SH groups both in the GSH and the CDNB binding place, whereas the cationic GST form--arginine residues in the CDNB binding place. Bull epididymis GST forms contained neither thiol nor arginine residues essential for catalytic activity.

Animals↗

Role of glutathione and glutathione S-transferase in chlorambucil resistance.

A chlorambucil (CLB)-resistant cell line, N50-4, was developed from the established mouse fibroblast cell line NIH 3T3, by multistep drug selection. The mutant cells exhibited greater than 10-fold resistance to CLB. Alterations in GSH and glutathione S-transferase (GST) were found in CLB-resistant variants. A 7-10-fold increase in cellular GSH content and a 3-fold increase in GST activity were detected in N50-4 cells, compared with parental cells, as determined by enzymatic assays. An increase in steady state levels of the GST-alpha isozyme mRNA was found in the CLB-resistant cells, as analyzed by Northern blotting. No GST gene amplification or rearrangement was shown by Southern blot analysis. To test the relative roles of GSH and GST in CLB resistance, a number of GSH- and GST-blocking agents were used. The CLB toxicity was significantly enhanced in N50-4 cells by administration of either the GSH-depleting agent buthionine sulfoximine or the GST inhibitors ethacrynic acid or indomethacin. The resistance to CLB cytotoxicity in N50-4 cells, however, was still significantly higher than that of parental cells. The resistance of N50-4 cells to CLB was almost completely abolished by combination pretreatment yielding both GSH depletion and GST inhibition. The results indicate that both increased cellular GSH content and increased GST activity play major roles in CLB resistance in N50-4 mutant cells.

3T3 Cells↗

[Polyphenols and endogenous antioxidant defences: effects on glutathione and glutathione related enzymes].

Among diet antioxidants, polyphenols, naturally occurring in vegetables, fruits and plant-derived beverages such as tea, red wine, and extra virgin olive oil, are the most abundant ones. In vitro cell culture experiments have shown that polyphenols possess antioxidant properties, and it is thought that these activities can contribute to the prevention of several oxidative stress-associated diseases. It has however become clear that the mechanisms of action of polyphenols go beyond their intrinsic reducing capabilities, being able to exert other additional effects that are as yet poorly understood. This article gives an overview of the most recent data on the subject and describe the additional functions that polyphenols can have in biological systems, focusing on their effects on glutathione and its related enzymes. Evidence is provided of a tight connection between exogenous and endogenous antioxidants that appear to act in a coordinated fashion. Experimental data indicate that polyphenols may offer an indirect protection by activating endogenous defense systems. It is reasonable to hypothesize that this is achieved, at least in part, through antioxidant responsive elements (ARE) present in the promoter regions of many of the genes inducible by oxidative and chemical stress. The latest studies strongly suggest that dietary polyphenols can stimulate antioxidant enzyme transcription through ARE.

Animals↗

Glutathione S-transferases YcYfetus and YcYc--kinetic and inhibitor studies relating to their glutathione peroxidase activities.

The kinetic properties of the glutathione (GSH) peroxidase activities of GSH S-transferases YcYfetus and YcYc were compared. The catalytic efficiency of the fetal iso-enzyme with cumene hydroperoxide as substrate was approximately four times higher than the other. The effects of the non-substrate ligand rose-Bengal as well as the substrate ligands sulphobromophthalein and acrolein on the GSH peroxidase activity of these two iso-enzymes were also investigated. Depending on the ligand, the inhibition profiles of these two iso-enzymes when measured with either the peroxidase substrate, cumene hydroperoxide or the standard GSH S-transferase substrate 1-chloro-2,4-dinitrobenzene were found to be either very similar (sulphobromophthalein) or markedly different (rose Bengal and acrolein). Significantly, the GSH peroxidase activity of the fetal iso-enzyme was far less susceptible to inhibition by the teratogen, acrolein, than that of the YcYc isoenzyme. It is therefore attractive to suggest that should a similar situation arise in vivo, this resistance to peroxidase inhibition may play a role in preventing the fetotoxic effects of acrolein.

Acrolein↗

Substrate specificity of rat liver glutathione S-transferase isoenzymes for a series of glutathione analogues, modified at the gamma-glutamyl moiety.

The substrate specificity of purified rat liver glutathione S-transferases (GSTs) for a series of gamma-glutamyl-modified GSH analogues was investigated. GST isoenzyme 3-3 catalysed the conjugation of 1-chloro-2,4-dinitrobenzene with six out of the nine analogues. alpha-L-Glu-L-Cys-Gly and alpha-D-Glu-L-Cys-Gly showed catalytic efficiencies of 40% and 130% that of GSH respectively. The GSH analogue with an alpha-D-glutamyl moiety appeared to be a highly isoenzyme-3-3-specific co-substrate: kcat./Km with GST isoenzyme 4-4 was only about 5% that with GST isoenzyme 3-3, and no enzymic activity was detectable with GST isoenzymes 1-1 and 2-2. GST isoenzyme 4-4 showed some resemblance to GST 3-3: five out of nine co-substrate analogues were accepted by this second isoenzyme of the Mu multigene family. Isoenzymes 1-1 and 2-2, of the Alpha multigene family, accepted only two alternative co-substrates, which indicates that their GSH-binding site is much more specific.

Animals↗

Effects of combined treatments with selenium, glutathione, and vitamin E on glutathione peroxidase activity, ornithine decarboxylase induction, and complete and multistage carcinogenesis in mouse skin.

Several structurally different tumor promoters altered to various degrees both glutathione (GSH) peroxidase (EC 1.11.1.9) and ornithine decarboxylase (ODC, L-ornithine carboxy-lyase, EC 4.1.1.17) activities in mouse epidermis in vivo. At 5 h after their application to the skin, the complete tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) and the stage 2 promoter mezerein were the most potent in inhibiting GSH peroxidase activity and inducing ODC activity. In comparison, the effects of anthralin, phorbol-12,13-didecanoate, benzoyl peroxide, H2O2, and phorbol-12,13-dibenzoate were much smaller, whereas the nontumor promoter phorbol, the hyperplastic agent ethyl phenylpropiolate, and the stage 1 promoter 4-O-methyl TPA did not alter GSH peroxidase and ODC activities. Various treatments including i.p. injections of 40 micrograms of Na2SeO3 and 100 mumol of GSH and/or topical applications of 40 mumol of D-alpha-tocopherol (vitamin E) 20 or 15 min, respectively, before tumor promoter treatment inhibited in an additive manner the effects of either TPA or mezerein on both GSH peroxidase activity and ODC induction. Moreover, these Na2SeO3, GSH, and/or vitamin E treatments inhibited in the same additive manner the tumor-promoting activity of TPA in the initiation-promotion protocol. However, when tested in the 2-stage promotion protocol with 4 doses of TPA followed by twice weekly applications of mezerein, Na2SeO3 plus vitamin E and GSH plus vitamin E treatments inhibited remarkably the tumor-promoting activity of mezerein but were ineffective in the first stage of promotion. The sequence and magnitude for the effects of 7,12-dimethylbenz[alpha]anthracene (DMBA) on GSH peroxidase and ODC activities were very different from those of the tumor promoters. In contrast with their antitumor-promoting activity, the treatments with Na2SeO3 plus vitamin E and GSH plus vitamin E failed to inhibit the carcinogenicity of a single large dose of DMBA and even enhanced the induction of skin tumors by repeated applications of subcarcinogenic doses of DMBA. These results suggest that the promoting component of DMBA carcinogenesis may be different from that of TPA. Moreover, the anticarcinogenicity of Na2SeO3, GSH, and vitamin E may be linked to their ability to facilitate or enhance the activity of the natural GSH-dependent antioxidant protective system of the epidermal cells during the later stages of skin tumor promotion.

9,10-Dimethyl-1,2-benzanthracene↗

Relationship of glutathione depletion and inhibition of glutathione-S-transferase activity to the antimitotic properties of estramustine.

A depletion of intracellular glutathione (GSH) is accompanied by a subsequent inhibition of GSH-S-transferase activity in a DU145 human prostatic carcinoma cell line treated with cytotoxic concentrations of estramustine. When GSH depletion reached approximately 50% of normal (approximately 2 hours after 10 microM estramustine), the mitotic index of logarithmically dividing cultures began to increase. A linear increase from 3.14% to 22.5% occurred during the period of 2-24 hours following 10 microM estramustine. Morphological studies showed that mitotic figures accumulated in metaphase and had abnormalities consistent with spindle malformation. Nocodazole and cytochalasin B also possess anticytoskeletal properties, but had little effect upon the intracellular levels of GSH or its associated transferase enzymes. The constituent moieties of estramustine, estradiol, and nor-mechlorethamine had effects on thiol metabolism which were dissimilar from estramustine, confirming previous findings that the unmetabolized parent drug is responsible for pharmacological activity. Estramustine had no effect upon GSH reductase activity, suggesting that drug toxicity was not a general thiol phenomenon. Buthionine sulfoximine decreased intracellular GSH in DU145 cells and enhanced the cytotoxic potential of estramustine in this cell line. The anticytoskeletal and antimitotic properties of estramustine may be enhanced by the drug-induced GSH imbalance and subsequent effects on GSH-S-transferase enzymes.

Buthionine Sulfoximine↗

The relationship of biliary glutathione disulfide efflux and intracellular glutathione disulfide content in perfused rat liver.

The intracellular glutathione redox state was estimated using newly adapted methods for tissue analysis. Under standard perfusion conditions of rat liver perfused in situ, intracellular GSH content was 5.5 mumol X g of liver-1, and intracellular GSSG content was 18 nmol X g of liver-1, resulting in a GSH/GSSG ratio of 300. GSSG was transported from the cells into bile. The control rate of release amounts to 0.4 nmol X min-1 X g of liver-1 and corresponds to the rate of release previously observed in anesthetized animals (Sies, H., Koch, O., Martino, E., and Boveris, A. (1979) FEBS Lett. 103, 287-290). No GSSG was released into the caval perfusate. In contrast, GSH release occurs both into bile and into the sinusoidal space, the rates of release being 1 and 14 nmol X min-1 X g of liver-1, respectively. Biliary GSH release in very low in isolated perfused liver. The relationship between intracellular GSSG levels and the rate of biliary GSSG transport was studied. This was achieved in experiments in which internal hydrogen peroxide formation was stimulated with substrates for monoamine oxidase (pargyline-sensitive), or by addition of t-butyl hydroperoxide, or of nitrofurantoin. The apparent concentration ratio, GSSG in bile/GSSG intracellular, was about 50 over the range of intracellular GSSG examined.

Animals↗

Dietary vitamin E and levels of reduced glutathione, glutathione peroxidase, catalase and superoxide dismutase in rat blood.

The effects of dietary vitamin E on the important cellular antioxidant defense systems were studied in rat blood. One-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet and supplemented with either none or 45 ppm vitamin E for 4 months. The activity of glutathione (GSH) peroxidase was decreased significantly (p less than 0.05) in the red blood cells and plasma of vitamin E-deficient rats. The level of GSH in the red cells of vitamin E-deficient rats was also significantly decreased. No detectable GSH was found in the plasma of both groups of animals. The activities of catalase and superoxide dismutase were not significantly altered by the status of dietary vitamin E. Similar results were obtained when 2-month-old male rats were fed the respective diets for 3 months. The results suggest that the decreased levels of GSH and GSH peroxidase in the red cells of animals fed a vitamine E-deficient diet may in part contribute to their increased susceptibility to hemolytic agents.

Animals↗

Applications of tandem mass spectrometry to the characterization of derivatized glutathione conjugates. Studies with S-(N-methylcarbamoyl)glutathione, a metabolite of the antineoplastic agent N-methylformamide.

Daughter ion spectra are reported for [M + H]+ ions generated by fast atom bombardment mass spectrometry of S-(N-methylcarbamoyl)glutathione (1) and a series of alkoxycarbonyl methyl ester derivatives thereof. Structurally informative, even-electron fragment ions, which serve to define the nature of both the xenobiotic and peptide components of the conjugate, are observed in the collisionally activated dissociation (CAD) spectra of 1 and its ethoxy- and benzyloxycarbonyl methyl esters. Studies with the t-butyloxycarbonyl (tBOC) methyl ester derivative, on the other hand, indicated that the tBOC group exerts a powerful directing influence on the CAD process, and that the major daughter ions in this case are associated with cleavage of the tBOC functionality itself and are of little diagnostic value. Of the derivatives examined, the benzyloxycarbonyl congener, which may be generated readily from 1 in aqueous media, is judged to be the most useful from the standpoints of ease of formation, desirable high-performance liquid chromatographic properties, and informative mass spectral fragmentation characteristics under CAD conditions.

Animals↗

Glutathione metabolism in newborns: evidence for glutathione deficiency in plasma, bronchoalveolar lavage fluid, and lymphocytes in prematures.

Respiratory distress in premature newborns is associated with deficiency of surfactant in the bronchoalveolar lining fluid; this may be influenced by a local deficiency of antioxidants. Severe L-buthionine-S,R-sulfoximine-induced depletion of glutathione (GSH, a major antioxidant) in rodents is associated with lung type 2 cell lamellar body damage and decreased concentrations in lung and bronchoalveolar lavage fluid (BALF) of phosphatidyl choline (a major component of surfactant). At birth, prematurely born newborns (30-34 weeks) had lower peripheral venous plasma GSH concentrations than term (> 36 weeks) babies; these levels decreased further with increasing prematurity (< 27 weeks, with respiratory distress). On day 2, the peripheral venous plasma GSH concentrations reached a nadir, and the lowest levels were found in the most premature newborns. Lymphocyte GSH concentrations were lowest on day 2 and day 7, and in prematures (< 27 weeks, with respiratory distress) remained below adult lymphocyte GSH levels for at least 4 weeks. At birth, prematures (< 27 weeks, with respiratory distress) had a central plasma arterio-venous (A-V) GSH gradient across the lung (an estimate of lung uptake of GSH) of 0.72 +/- 0.15 (mean +/- SD) mumol/L; on day 2, the A-V gradient did not change significantly (0.49 +/- 0.09 mumol/L). At birth, these prematures had markedly decreased BALF GSH concentrations (compared with adult levels), and they were not significantly changed during the first 4 weeks of life. These results suggest that GSH deficiency is present in prematures and that it increases with the degree of prematurity. At birth, GSH deficiency will compromise the lungs' defense against oxidative stress injury. Oxidative stress is likely to increase if hyperoxic treatment is given for respiratory distress in these infants.

Bronchoalveolar Lavage Fluid↗

Effects of glutathione and chelating agents on copper-mediated DNA oxidation: pro-oxidant and antioxidant properties of glutathione.

The exposure of DNA to H2O2 in the presence of Cu(II) and a reducing agent is known to result in the induction of a variety of oxidative lesions, including DNA strand breaks and base modifications. Since the reducing agent glutathione occurs in cell nuclei at relatively high concentrations, and copper exists in nuclei associated with chromatin, the present study was undertaken to evaluate the ability of GSH to promote copper-mediated free radical damage to DNA. When compared with ascorbate, GSH was found to be inefficient in the promotion of damage to DNA. Parallel ESR spin trapping measurements indicated that GSH inhibits free radical formation by copper ions in the presence of H2O2, ascorbate, and DNA. The protective effect of GSH is attributed to its stabilization of copper in the +1 oxidation state, thereby compromising its ability to participate in free radical generating reactions. Consequently, it is suggested that the GSH in cell nuclei serves to prevent, rather than promote, copper-dependent damage to DNA. In contrast, in the presence of 1,10-phenanthroline, GSH stimulated free radical formation and DNA damage. This is attributed to the failure of GSH to remove copper(I) from 1,10-phenanthroline. Therefore, under these conditions, GSH serves primarily to redox cycle the reactive 1,10-phenanthroline-copper complex.

Ascorbic Acid↗

Guinea pig liver Mu-class glutathione S-transferase M1-2 cross-reacts with antibodies to both rat Mu- and theta-class glutathione S-transferases.

Two novel major heterodimeric Mu-class glutathione (GSH) S-transferases (GSTs), designated M1-2 and M1-3*, were isolated from guinea pig (gp) liver cytosol and purified to homogeneity together with a known major homodimeric Mu-class gpGSTM1-1 (reported as GST b by R. Oshino, K. Kamei, M. Nishioka, and M. Shin, 1990, J. Biochem. 107, 105-110). These three gpGSTs were quantitatively retained on an S-hexyl-GSH affinity column and separated as homogeneous proteins by chromatofocusing. Subunits of the heterodimers were inseparable on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, but could be completely separated by reverse-phase partition high-performance liquid chromatography. A molecular cloning study demonstrated that the gpGST subunit M2 consisted of 217 amino acid residues with a calculated molecular mass of 25,562 and shared 84% identity in overall amino acid sequence with gpGSTM1-1. N-terminal amino acid sequences of peptides from the gpGST subunit M3* with a blocked N-terminus strongly suggested that it should belong to the Mu class. Western blot analysis using antisera raised against purified rat (r) GSTsA1-2 (Alpha), M1-1, P1-1 (Pi), and T2-2 (Theta) indicated that gpGSTsM1-1 and M1-3* cross-reacted only with anti-rGSTM1 antibody. However, gpGSTM1-2 cross-reacted intensely to almost the same extent with antibodies to both rGSTsM1-1 and T2-2. A homodimeric gpGSTM2-2, artificially constructed from native gpGSTM1-2 by treatment with guanidine hydrochloride followed by dialysis, intensely cross-reacted with antibodies to both the rat Mu- and Theta-class GSTs. Thus, the gpGST subunit M2 provided the first evidence for the double immuno-cross-reaction of a GST with polyclonal antibodies to two different classes of GSTs.

Amino Acid Sequence↗

Enrichment and functional reconstitution of glutathione transport activity from rabbit kidney mitochondria: further evidence for the role of the dicarboxylate and 2-oxoglutarate carriers in mitochondrial glutathione transport.

In previous studies, we provided evidence for uptake of glutathione (GSH) by the dicarboxylate and the 2-oxoglutarate carriers in rat kidney mitochondria. To investigate further the role of these two carriers, GSH transport activity was enriched from rabbit kidney mitochondria and functionally reconstituted into phospholipid vesicles. Starting with 200 mg of mitoplast protein, 2 mg of partially enriched proteins were obtained after Triton X-114 solubilization and hydroxyapatite chromatography. The reconstituted proteoliposomes catalyzed butylmalonate-sensitive uptake of [(14)C]malonate, phenylsuccinate-sensitive uptake of [(14)C]2-oxoglutarate, and transport activity with [(3)H]GSH. The initial rate of uptake of 5 mM GSH was approximately 170 nmol/min per mg protein, with a first-order rate constant of 0.3 min(-1), which is very close to that previously determined in freshly isolated rat kidney mitochondria. The enrichment procedure resulted in an approximately 60-fold increase in the specific activity of GSH transport. Substrates and inhibitors for the dicarboxylate and the 2-oxoglutarate carriers (i.e., malate, malonate, 2-oxoglutarate, butylmalonate, phenylsuccinate) significantly inhibited the uptake of [(3)H]GSH, whereas most substrates for the tricarboxylate and monocarboxylate carriers had no effect. GSH uptake exhibited an apparent K(m) of 2.8 mM and a V(max) of 260 nmol/min per mg protein. Analysis of mutual inhibition between GSH and the dicarboxylates suggested that the dicarboxylate carrier contributes a somewhat higher proportion to overall GSH uptake and that both carriers account for 70 to 80% of total GSH uptake. These results provide further evidence for the function of the dicarboxylate and 2-oxoglutarate carriers in the mitochondrial transport of GSH.

Animals↗

On the synthesis and characterization of N-formyl glutathione and N-acetyl glutathione.

Treatment of glutathione (GSH) with formic acid and acetic anhydride leads to preparation of crystalline N-formyl GSH. This is the first characterized preparation of N-formyl GSH; this product was previously erroneously thought to be N-acetyl GSH. Authentic N-acetyl GSH (crystalline) was prepared by treating GSH with acetic acid and acetic anhydride. The N-acylated derivatives were characterized by 1H NMR and mass spectroscopy.

Acetic Anhydrides↗

The role of glutathione in chronic adaptation to oxidative stress: studies in a normal rat kidney epithelial (NRK52E) cell model of sustained upregulation of glutathione biosynthesis.

Reduced glutathione (GSH) is considered to play a central role in protection of cells from oxidant injury. However, the question remains as to whether sustained elevation of intracellular GSH levels, as compared with the ability to rapidly upregulate GSH synthesis, is more important with respect to protection of cell constituents from oxidative stress. To address this question, we conducted studies to evaluate the direct influence of chronically increased endogenous GSH content on chemically induced intracellular free radical formation and oxidative stress using a kidney epithelial cell model adapted to sustain intracellular GSH concentrations in excess of eightfold that observed in unadapted parent kidney cells. Elevated GSH levels in adapted cells were found to be attributable, at least in part, to coordinately increased amounts of both the regulatory and catalytic subunits of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in GSH synthesis. Studies using electron spin resonance (ESR) spectroscopy and scanning laser cytometry demonstrated that cells having sustained elevation of GSH levels did not attenuate free radical formation and associated oxidative stress compared with parent cells when treated with the prooxidant chemicals, menadione or potassium dichromate. In contrast, nonadapted kidney parent cells treated 18 h after initial prooxidant challenge displayed significantly attenuated free radical signals. Additionally, cells adapted to sustain excess GSH were somewhat more sensitive than parent cells in terms of resistance to prooxidant (chromate) toxicity, as determined by cell viability assays. These findings suggest that the capacity of cells to rapidly upregulate GSH synthesis, rather the ability to chronically sustain elevated intracellular GSH levels, may play a more important role in terms of protection from cytotoxicity associated with prooxidant chemical exposures.

Adaptation, Physiological↗

Thioctic acid does not restore glutathione levels or protect against the potentiation of 6-hydroxydopamine toxicity induced by glutathione depletion in rat brain.

Decreased reduced glutathione (GSH) levels are an early marker of nigral cell death in Parkinson's disease. Depletion of rat brain GSH by intracerebroventricular administration of buthionine sulphoximine (BSO) potentiates the toxicity of 6-hydroxydopamine (6-OHDA) to the nigrostriatal pathway. We have investigated whether thioctic acid can replenish brain GSH levels following BSO-induced depletion and/or prevent 6-OHDA induced toxicity. Administration of BSO (2 x 1.6 mg i.c.v.) to rats depleted striatal GSH levels by upto 75%. BSO treatment potentiated 6-OHDA (75 micrograms i.c.v.) toxicity as judged by striatal dopamine content and the number of tyrosine hydroxylase immunoreactive cells in substantia nigra. Repeated treatment with thioctic acid (50 or 100 mg/kg i.p.) over 48h had no effect on the 6-OHDA induced loss of dopamine in striatum or nigral tyrosine hydroxylase positive cells in substantia nigra. Also thioctic acid treatment did not reverse the BSO induced depletion of GSH or prevent the potentiation of 6-OHDA neurotoxicity produced by BSO. Thioctic acid (50 mg or 100 mg/kg i.p.) alone or in combination with BSO did not alter striatal dopamine levels but increased dopamine turnover. Striatal 5-HT content was not altered by thioctic acid but 5-HIAA levels were increased. Under conditions of inhibition of GSH synthesis, thioctic acid does not replenish brain GSH levels or protect against 6-OHDA toxicity. At last in this model of Parkinson's disease, thioctic acid does not appear to have a neuroprotective effect.

Animals↗