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Last Updated: 2 years ago

Possible Interaction: Glutathione and 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.
Neurotoxicology  •  2013  |  View Paper
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.
Brain Research Bulletin  •  2008  |  View Paper
In addition, injecting a single high dose of METH caused the reduction of striatal glutathione peroxidase activity at 24 h after the METH injection.
Neurotoxicity Research  •  2020  |  View Paper
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.
Toxicology mechanisms and methods  •  2013  |  View Paper
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.
Neuromolecular medicine  •  2002  |  View Paper
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.
European journal of pharmacology  •  2000  |  View Paper
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.
Neuroscience Letters  •  1998  |  View Paper
Exposure to 2.5 mM METH decreased the cell viability and GSH levels, caused the generation of reactive oxygen species and ultimately induced apoptosis.
Iranian journal of pharmaceutical research : IJPR  •  2021  |  View Paper
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.
Iranian journal of pharmaceutical research : IJPR  •  2019  |  View Paper
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.
Iranian journal of basic medical sciences  •  2019  |  View Paper
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