8-hydroxy-2'-deoxyguanosine (8-OHdG) Can be measured both in blood and urine. Malondialdehyde TBD Whole blood Glutathione TBD Red Blood Cells Glutathione TBD 8-iso-prostaglandin-F2α (8-iso-PGF2α) TBD Other literature Comparative effects of two different forms of selenium on oxidative stress biomarkers in healthy men: a randomized clinical trial, 2014 (PMC)

Restoration of Glutathione (GSH) level should be approached from four angles: Synthesis of new GSH Recycling of oxidized GSH Protecting current GSH from further depletion Finding the cause of GSH depletion Work on GSH synthesis NAC provides Cysteine which is a rate limiting substrate for GSH synthesis. Selenomethionine and Sodium Selenite. Selenomethionine was shown to increase Cystine uptake into the cells, so this can be useful as both a provider of Selenium (not efficient though) and an upregulator of Cystine uptake.

What happens when cells have low level of glutathione or increased level of oxidized glutathione? Lowered GSH Functional Cobalamin deficiency (vitamin B12) / Ref. 1-2 Functional Copper deficiency / Ref. 3 Functional Zinc deficiency / Ref. 4 Cysteine deficiency / Ref. 5 inefficient Iron-Sulfur clusters assembly (impairs energy production) / Ref. 6-7 Inactivation of TPH2 enzyme (in the brain), which leads to reduced Serotonin synthesis (R8) Functional Vitamin D deficiency / (R9, R10) All this can happen despite the normal or high levels of mentioned nutrients in the blood.

Overview The Molybdenum Cofactor (MoCo) is a catalytically active protein which incorporates the element Molybdenum. The biosynthesis of MoCo involves the complex interaction of six proteins and is a process of four steps, which also require iron, ATP, and copper. After its synthesis, Moco is distributed, involving MoCo-binding proteins. Role in Health MoCo deficiency results in a severe inborn error of metabolism causing often early childhood death. Disease-causing symptoms mainly go back to the lack of sulfite oxidase (SO) activity, an enzyme in cysteine catabolism.

Parallel to the alteration of the cell redox status, we observed the accumulation of ceramide, and this increase was inhibited substantially by the exogenous addition of GSH. Therefore, our results suggest that the accumulation of ceramide is an event that lies downstream from ROS generation. The long term accumulation of ceramide might result from increased de novo synthesis via activation of ceramide synthase or from sphingomyelin breakdown by acidic or neutral sphingomyelinases.