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C.GardnerL.Perez-GarciaV.LiQ.et al (2021)

This anti-inflammatory effect helps prevent the transition from acute injury to chronic kidney disease or heart failure, representing a critical therapeutic benefit beyond the immediate protection during the ischemic event itself

(high GSH consumption for regeneration of other redox systems, such as e.g.Ascorbic acid Effects of glutathione Antioxidant effects Non-enzymatic antioxidant Most important hydrophilic antioxidant of the cell (directly binds radicals and nitric oxide (NO) and reduces other antioxidants) It is oxidized to GSSG (and reduced again with the help of the enzyme glutathione reductase) Coenzyme for enzymatic glutathione peroxidases (metalloenzymes) (reduce toxic peroxides such as hydrogen peroxide and lipid hydroperoxides by reacting with glutathione) Enzymes are proteins (they require amino acids, zinc, vitamin B6 and B12) Enzymes require activators (selenium, zinc, manganese) Regeneration of antioxidants Inactivation of activated oxygen Detoxifying effects of GSH Glutathione in detoxification phase I Disposal of radical metabolites (Part of the redox network) Glutathione in detoxification phases II and III Coenzyme for glutathione S-transferases Binding partners of pollutants begins via thiol/sulfhydryl/SH group Toxins, polyvalent heavy metals such as mercury, cadmium, lead and other foreign substances forms Pollutant-glutathione complexes , which are excreted as mercapturic acid derivatives via the kidneys and bile reduces by Complex formation with "good" trace elements pro-oxidative risk of high concentrations of these substances (z.B