Abstract
A neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is known to induce parkinsonism in rodents and human via dopaminergic cell death by a common oxidative mechanism. To find whether a neurotoxin-induced neurotoxicity is prevented by the treatment with an antioxidant, we investigated the effects of ginsenoside Rb1, a major saponin from Panax ginseng, on lipid peroxidaton and neurotoxicity induced by MPTP in mice using chemiluminescense-HPLC. Levels of lipid hydroperoxides in plasma and liver were increased by MPTP treatment, but the increased levels of this were not observed in mice pretreated with ginsenoside Rb1. Activities of protein kinase C and NADPH-cytochrome c reductase in the pretreated group with ginsenoside Rb1 were lower than in MPTP groups. Treatment with ginsenoside Rb1 was, however, less effective in suppressing the influence of MPTP on the levels of dopamine and its metabolite, homovanillic acid in the striatum of mice brain. These results indicate that ginsenoside Rb1 has an antioxidant effect and may not have the ability enough to suppress the neurotoxicity induced by MPTP.
Highlights
Formation of oxygen radicals and lipid peroxidation (LPO) has been suggested to play a key role in various types of tissue degeneration and pathology such as aging, cancer, and retinal degeneration (Marx, 1987; Bulkley, 1983)
Levels of phosphatidylcholine hydroperoxide (PCOOH) of Rb1 + MPTP group in each subcellular fractions were negligible. These results indicate that the LPO was inhibited remarkably by the pretreatment with Ginsenoside Rb1 (G-Rb1)
The activities of protein kinase C (PKC) and NADPH-cytochrome c reductase induced by MPTP PKC, Ca2+/phospholipid-dependent kinase, is known to be involved in the formation of oxygen free radicals by PCOOHa Cytosol Microsome Mitochondria Plasma
Summary
Formation of oxygen radicals and lipid peroxidation (LPO) has been suggested to play a key role in various types of tissue degeneration and pathology such as aging, cancer, and retinal degeneration (Marx, 1987; Bulkley, 1983). The oxidation of membrane phospholipids has been hypothesized to cause an increase in the permeability of cell membranes and/or to inhibit membrane ion pumps and to lead to cell death. These oxdative stress is related with the degeneration of dopaminergic cells. Dopaminergic neurons are destroyed during chronic exposure to amphetamines or after exposure to neurotoxins, such as 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP). MPP+ induces hydroxyl free radical formation when injected into the rat striatum (Wu et al, 1993); the intracerebroventricular administration of MPP+ increases striatal LPO in mice (Rolas et al, 1993). Some evidence from postmortem studies on Parkinson’s disease (Bradbury et al, 1986) suggested that excessive free radicals are involved in toxic effect on the dopaminergic neurons in the zona compacta of the subtantia nigra, and that the loss of protective mechanism against toxic free radicals may induce Parkinson’s disease
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