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Manivasakan Sabesan - One of the best experts on this subject based on the ideXlab platform.
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inhibition of monoamine oxidase b by the polyphenolic compound curcumin and its metabolite tetrahydrocurcumin in a model of parkinson s disease induced by mptp neurodegeneration in mice
Inflammopharmacology, 2008Co-Authors: A. Rajeswari, Manivasakan SabesanAbstract:We investigated the effects of the polyphenolic compound curcumin and its metabolite tetrahydrocurcumin (ThC), in the model of Parkinson’s disease induced in mice by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In this model depletion of dopamine(DA) and DOPAC (3,4-dihydroxy phenyl acetic acid)) occurs with increased monoamine oxidase (MAO-B) activity. We used HPLC with electrochemical detection to measure DA and DOPAC respectively while MAO-B was assayed by spectroflourimetry using the conversion of the fluorogenic substrate, kyuramine. Systemic administration of curcumin (80 mg/kg i. p.) and tetrahydrocurcumin (60 mg/kg i. p.) significantly reversed the MPTP-induced depletion of DA and DOPAC. The MAO-B activity was also significantly inhibited by these compounds. The results showed that curcumin and tetrahydrocurcumin reversed the MPTP induced depletion of DA and DOPAC which may in part be due to inhibition of MAO-B activity. In conclusion, both curcumin and its metabolite ThC exert neuroprotection against MPTP induced Neurotoxicity.
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enhanced neuroprotective effect by combination of bromocriptine and hypericum perforatum extract against mptp induced Neurotoxicity in mice
Journal of the Neurological Sciences, 2006Co-Authors: M Mohanasundari, Sivasamy Sethupathy, M. S. Srinivasan, Manivasakan SabesanAbstract:Abstract The present study has been designed to evaluate the combined effect of bromocriptine (BRC) and Hypericum perforatum extract (HPE) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease in male Swiss Albino mice, which were randomly divided into seven groups of six animals each. Group I served as control. Groups II and III were given 300 mg/kg HPE (po) and 10 mg/kg BRC (i.p.) respectively, once daily for 7 days. The four doses of MPTP (20 mg/kg) were administered intraperitoneally with an interval of 2 h to the groups IV, V, VI and VII. The drug treatment was given to fifth group (10 mg/kg BRC; i.p), sixth group (300 mg/kg HPE; po) and seventh group (300 mg/kg HPE; po and 10 mg/kg BRC; i.p.) once in a day for 7 days and the dose on the first day was given 30 min prior to first MPTP injection. The rotarod test, hang test and forepaw stride length revealed significant improvement by the combined treatment. Dopamine and DOPAC levels were significantly improved ( p p
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the effect of hypericum perforatum extract against the neurochemical and behavioural changes induced by 1 methyl 4 phenyl 1 2 3 6 tetrahydropyridine mptp in mice
Indian Journal of Pharmacology, 2006Co-Authors: M Mohanasundari, Sivasamy Sethupathy, Manivasakan SabesanAbstract:Objective: Hypericum perforatum extract (HPE), known for its antidepressant effect, has been explored in the present study for its protective role against MPTP induced Neurotoxicity. Materials and Methods: Mice were treated with 20 mg/kg of MPTP, four injections i.p., at 2 h intervals within 24 h. HPE was administered at different doses of 100, 200 and 300 mg/kg (p.o) in different groups once a day for seven days and the dose on the first day was given 30 min prior to first MPTP injection. Striatal dopamine (DA) and its metabolites, antioxidant status were analysed. The behavioural changes were studied using the rotarod test, hang test and narrow beam test. Results: HPE significantly ( P <0.05) improved the behavioural activities, striatal neurotransmitter levels and striatal antioxidant status in a dose dependent manner and significantly ( P <0.05) reduced TBARS levels. Conclusion: HPE possesses significant antioxidant activity and renders neuroprotection which was more pronounced at the dose of 300 mg/kg against MPTP induced Neurotoxicity.
Wenshih Huang - One of the best experts on this subject based on the ideXlab platform.
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Retraction Note to: Hericium erinaceus mycelium and its isolated erinacine A protection from MPTP-induced Neurotoxicity through the ER stress, triggering an apoptosis cascade.
Journal of translational medicine, 2021Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Wenshih Huang, Shuiyi Tung, Techuan ChenAbstract:Background Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
Hsingchun Kuo - One of the best experts on this subject based on the ideXlab platform.
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Retraction Note to: Hericium erinaceus mycelium and its isolated erinacine A protection from MPTP-induced Neurotoxicity through the ER stress, triggering an apoptosis cascade.
Journal of translational medicine, 2021Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Wenshih Huang, Shuiyi Tung, Techuan ChenAbstract:Background Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
Shuiyi Tung - One of the best experts on this subject based on the ideXlab platform.
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Retraction Note to: Hericium erinaceus mycelium and its isolated erinacine A protection from MPTP-induced Neurotoxicity through the ER stress, triggering an apoptosis cascade.
Journal of translational medicine, 2021Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Wenshih Huang, Shuiyi Tung, Techuan ChenAbstract:Background Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved.
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hericium erinaceus mycelium and its isolated erinacine a protection from mptp induced Neurotoxicity through the er stress triggering an apoptosis cascade
Journal of Translational Medicine, 2016Co-Authors: Hsingchun Kuo, Chin-chu Chen, Chihchuan Teng, Chienheng Shen, Mengchiao Hsieh, Kochao Lee, Liya Lee, Shuiyi Tung, Wenshih HuangAbstract:Hericium erinaceus is an edible mushroom; its various pharmacological effects which have been investigated. This study aimed to demonstrate whether efficacy of oral administration of H. erinaceus mycelium (HEM) and its isolated diterpenoid derivative, erinacine A, can act as an anti-neuroinflammatory agent to bring about neuroprotection using an MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson’s disease, which results in motor disturbances, in addition to elucidating the mechanisms involved. Mice were treated with and without HEM or erinacine A, after MPTP injection for brain injuries by the degeneration of dopaminergic nigrostriatal neurons. The efficacy of oral administration of HEM improved MPTP-induced loss of tyrosine hydroxylase positive neurons and brain impairment in the substantia nigra pars compacta as measured by brain histological examination. Treatment with HEM reduced MPTP-induced dopaminergic cell loss, apoptotic cell death induced by oxidative stress, as well as the level of glutathione, nitrotyrosine and 4-hydroxy-2-nonenal (4-HNE). Furthermore, HEM reversed MPTP-associated motor deficits, as revealed by the analysis of rotarod assessment. Our results demonstrated that erinacine A decreases the impairment of MPP-induced neuronal cell cytotoxicity and apoptosis, which were accompanied by ER stress-sustained activation of the IRE1α/TRAF2, JNK1/2 and p38 MAPK pathways, the expression of C/EBP homologous protein (CHOP), IKB-β and NF-κB, as well as Fas and Bax. These physiological and brain histological changes provide HEM neuron-protective insights into the progression of Parkinson’s disease, and this protective effect seems to exist both in vivo and in vitro.
Serge Przedborski - One of the best experts on this subject based on the ideXlab platform.
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blockade of microglial activation is neuroprotective in the 1 methyl 4 phenyl 1 2 3 6 tetrahydropyridine mouse model of parkinson disease
The Journal of Neuroscience, 2002Co-Authors: Vernice Jacksonlewis, Miquel Vila, Kim Tieu, Peter Teismann, Caryn Vadseth, Dongkug Choi, Harry Ischiropoulos, Serge PrzedborskiAbstract:1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) damages the nigrostriatal dopaminergic pathway as seen in Parkinson's disease (PD), a common neurodegenerative disorder with no effective protective treatment. Consistent with a role of glial cells in PD neurodegeneration, here we show that minocycline, an approved tetracycline derivative that inhibits microglial activation independently of its antimicrobial properties, mitigates both the demise of nigrostriatal dopaminergic neurons and the formation of nitrotyrosine produced by MPTP. In addition, we show that minocycline not only prevents MPTP-induced activation of microglia but also the formation of mature interleukin-1beta and the activation of NADPH-oxidase and inducible nitric oxide synthase (iNOS), three key microglial-derived cytotoxic mediators. Previously, we demonstrated that ablation of iNOS attenuates MPTP-induced Neurotoxicity. Now, we demonstrate that iNOS is not the only microglial-related culprit implicated in MPTP-induced toxicity because mutant iNOS-deficient mice treated with minocycline are more resistant to this neurotoxin than iNOS-deficient mice not treated with minocycline. This study demonstrates that microglial-related inflammatory events play a significant role in the MPTP neurotoxic process and suggests that minocycline may be a valuable neuroprotective agent for the treatment of PD.
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role of neuronal nitric oxide in 1 methyl 4 phenyl 1 2 3 6 tetrahydropyridine mptp induced dopaminergic Neurotoxicity
Proceedings of the National Academy of Sciences of the United States of America, 1996Co-Authors: Serge Przedborski, Vernice Jacksonlewis, Rina Yokoyama, Toshihiro Shibata, Valina L Dawson, Ted M DawsonAbstract:Abstract 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic pathway damage similar to that observed in Parkinson disease (PD). To study the role of NO radical in MPTP-induced Neurotoxicity, we injected MPTP into mice in which nitric oxide synthase (NOS) was inhibited by 7-nitroindazole (7-NI) in a time- and dose-dependent fashion. 7-NI dramatically protected MPTP-injected mice against indices of severe injury to the nigrostriatal dopaminergic pathway, including reduction in striatal dopamine contents, decreases in numbers of nigral tyrosine hydroxylase-positive neurons, and numerous silver-stained degenerating nigral neurons. The resistance of 7-NI-injected mice to MPTP is not due to alterations in striatal pharmacokinetics or content of 1-methyl-4-phenylpyridinium ion (MPP+), the active metabolite of MPTP. To study specifically the role of neuronal NOS (nNOS), MPTP was administered to mutant mice lacking the nNOS gene. Mutant mice are significantly more resistant to MPTP-induced Neurotoxicity compared with wild-type littermates. These results indicate that neuronally derived NO mediates, in part, MPTP-induced Neurotoxicity. The similarity between the MPTP model and PD raises the possibility that NO may play a significant role in the etiology of PD.
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transgenic mice with increased cu zn superoxide dismutase activity are resistant to n methyl 4 phenyl 1 2 3 6 tetrahydropyridine induced Neurotoxicity
The Journal of Neuroscience, 1992Co-Authors: Serge Przedborski, Vernice Jacksonlewis, Vladimir Kostic, Ali Naini, S Simonetti, Stanley Fahn, E Carlson, C J Epstein, Jean Lud CadetAbstract:Administration of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mammals causes damage to the nigrostriatal dopaminergic pathway similar to that observed in Parkinson9s disease. It has been suggested that the mechanism by which MPTP kills dopamine (DA) neurons involves an energy crisis due to the inhibition of mitochondrial complex I. In addition, superoxide radicals (O2-), generated subsequent to the blockade of mitochondrial complex I, may also be involved in MPTP- induced Neurotoxicity. Superoxide dismutase (SOD) is a scavenger enzyme that protects cells from the hazard of O2- radicals. To evaluate further the role of O2- radical in MPTP-induced toxicity, we tested the effects of MPTP in transgenic mice with increased SOD activity. In nontransgenic littermates with normal SOD activity, MPTP injection causes a marked reduction in striatal levels of DA and its metabolites as well as in striatal and nigral 3H-DA uptake; these findings are consistent with a loss in dopaminergic neurons. In contrast, in transgenic mice with increased SOD activity, MPTP injection does not cause any significant changes either in levels of DA and metabolites or in 3H-DA uptake. We show that this lack of toxicity is not due to a lower delivery of MPTP to the brain following its intraperitoneal injection, to reduced brain biotransformation of MPTP to N-methyl-4- phenylpyridinium ion (MPP+), to diminished striatal mitochondrial monoamine oxidase B activity, to decreased synaptosomal uptake of MPP+, to lower potency of MPP+ to inhibit the complex I of the mitochondrial electron transport chain, or to faster brain elimination of MPP+. These results suggest that increased SOD activity is, most likely, the protective factor that confers resistance to transgenic mice against MPTP-induced Neurotoxicity. Thus, this study provides further evidence that some of the deleterious effects of MPTP may be mediated by O2- radicals. The similarity between the MPTP model and Parkinson9s disease further raises the possibility that oxy-radicals may play a significant role in the etiology of this neurodegenerative disorder.