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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
supplement:
Glutathione
drug:
Methamphetamine
Research Papers that Mention the Interaction
“ Total glutathione levels were reduced by methamphetamine at lower selenium conditions, while the oxidized fraction of GSH was increased at higher selenium levels.”
Methamphetamine decreases levels of glutathione peroxidases 1 and 4 in SH-SY5Y neuronal cells: protective effects of selenium.“Our present data demonstrate that METH enhances lipid peroxidation and mitochondrial manganese superoxide dismutase (MnSOD) enzyme levels, and decreases the antioxidant-reduced glutathione ( GSH ) together with an inhibition of mitochondrial complex-I activity.”
“In addition, injecting a single high dose of METH caused the reduction of striatal glutathione peroxidase activity at 24 h after the METH injection.”
Epigallocatechin Gallate Mitigates the Methamphetamine-Induced Striatal Dopamine Terminal Toxicity by Preventing Oxidative Stress in the Mouse Brain“ METH decreased glutathione ( GSH ) and glutathione peroxidase (GPx) levels while increased malondialdehyde (MDA), catalase (CAT) and protein carbonyl levels in brain (hypothalamus), liver, and kidney tissues of rats.”
“Intraperitoneal injection of METH at a dose of 10 mg/kg body weight resulted in a significant increase in oxidative stress, as measured by 2,7-dichlorofluorescein (DCF) fluorescence assay, thiobarbituric acid-reactive substances (TBARS), and total glutathione levels.”
“At 2 h, methamphetamine increased GSH and GSSG (32.”
“These findings indicate selectivity of methamphetamine for the glutathione system and a role for methamphetamine in inducing oxidative stress.”
“Binge, but not chronic MA administration was associated with a regionally specific reduction (-17%, P < 0.05) in striatal levels of glutathione 3 h after the last dose of MA , whereas striatal levels of the glutathione-related enzymes were normal.”
“Exposure to 2.5 mM METH decreased the cell viability and GSH levels, caused the generation of reactive oxygen species and ultimately induced apoptosis.”
Protective Effect of Cinnamaldehyde on METH-induced Neurotoxicity in PC12 Cells via Inhibition of Apoptotic Response and Oxidative Stress“In addition, METH treatment increased lipid peroxidation and the levels of oxidized form of glutathione (GSSG), interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and Bax, while reducing reduced form of glutathione (GSH), Bcl-2, P-CREB, and BDNF levels in the hippocampus.”
“Furthermore, METH increased lipid peroxidation and the levels of oxidized form of interleukin 1 beta (IL-1β), glutathione (GSSG), Bax, tumor necrosis factor alpha (TNF-α), and GSK3, while attenuating the extent of glutathione (reduced form (GSH)), P-CREB, Bcl-2, BDNF, and Akt-1 in the hippocampus.”
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