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Back to Ritalin Page Back to Adderall Page Ritalin, How to Save Your Body While using It From the National Institute on Drug Abuse, National Institutes of Health : Recent research at Brookhaven National Laboratory may begin to explain how methylphenidate helps people with ADHD. The researchers used positron emission tomography (PET - a noninvasive brain scan) to confirm that administering normal therapeutic doses of methylphenidate to healthy, adult men increased their dopamine levels. The researchers speculate that methylphenidate amplifies the release of dopamine, a neurotransmitter, thereby improving attention and focus in individuals who have dopamine signals that are weak, such as individuals with ADHD. What can increased dopamine levels mean to your health? What can you do to protect yourself? To put this in short, concise laymen terms: Dopamine causes neuronal cell death over time. Glutathione protects the neurons from this. Dopamine depletes glutathione levels. Increasing glutathione levels or reverses the condition. If you are using Ritalin or a similar medication, increase your intracellular glutathione levels while doing so. Someday you will probably want to quit taking the medication, keep your health while doing so. "Dopamine, while an essential neurotransmitter, is also a known neurotoxin that potentially plays a role in several neurodegenerative diseases. Dopamine metabolism and oxidation readily produce reactive oxygen species and dopamine can also be oxidized to a reactive quinone via spontaneous, enzyme-catalyzed or metal-enhanced reactions. These results suggest that dopamine toxicity is tightly linked to intracellular oxidant/antioxidant levels, and that environmental factors, such as excessive Mn exposure, may modulate cellular sensitivity to dopamine."(1) In clinical test "The role of glutathione and other antioxidants in dopamine-induced apoptosis has been analyzed in cultures of the human neuronal cell line NMB. Apoptosis, induced by 0.1-0.3 mM dopamine, was blocked by glutathione in a dose- and time-dependent manner."(2) The dopamine-induced alteration in the cell cycle profile, detected by flow cytometry (FACS), and intranucleosomal DNA fragmentation, were both blocked by glutathione. Treatment of NMB cells with buthionine sulfoximine, an irreversible inhibitor of gamma-glutamylcysteine synthetase, increased the neurotoxic effect of, dopamine, suggesting that endogenous glutathione participates in reducing dopamine neurotoxicity. The relationship between glutathione and dopamine was further investigated by testing the effect of dopamine on the endogenous glutathione level. Dopamine decreased glutathione levels within 16-24 hrs.(2) The results indicate that glutathione has a selective role in protecting human neural cells from the toxic effect of dopamine. This study may contribute, therefore, to a better understanding of the mechanisms underling the excessive loss of dopaminergic neurons in neurodegenerative diseases, such as Parkinson's disease, and in the aging process.(2) "The role of reduced glutathione (GSH) on ascorbate- and dopamine-induced apoptosis in PC12 cells was investigated. Ascorbate is a potent reducing agent and is thus expected to protect against dopamine-induced apoptosis. However, we found that both ascorbate and dopamine killed PC12 cells and ascorbate enhanced dopamine-induced toxicity." (3) "The GSH synthesis inhibitor, DL-buthionine-(S,R)-sulfoximine (BSO), induced cell toxicity and potentiated the toxic effects of ascorbate and dopamine, suggesting that endogenous GSH participates in protecting against basal oxidative stress. We conclude that both ascorbate and dopamine induce apoptosis in PC12 cells and further that GSH protects them from apoptosis. This study indicates that the toxic effects of ascorbate are potentially due to an oxidative mechanism, similar to that induced by dopamine."(3) References (1) Dopamine toxicity in neuroblastoma cells: role of glutathione depletion by L-BSO and apoptosis. (2) Neuropharmacology 1996 May;35(5):571-8 (3) Exp Brain Res 1998 Dec;123(3):263-8
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