Intro:
Glutathione is endogenous within human plasma, erythrocyte lysate and is also bound to the protein within plasma. Glutathione mediates redox chemistry and prevents oxidative damage within and around cellular components via reduction of reactive species (e.g. reactive oxygen, nitrogen, or sulfur species). Polyphenols and antioxidants have been shown to improve NO bioavailability which may reduce long term incidence of endothelial dysfunction. Less is known about whether changes in antioxidant capacity augments the risk of developing hypertension.
Hypothesis:
We hypothesized that acute glutathione supplementation would decrease arterial stiffness and reduce both brachial (bBP) and central blood pressure (cBP) in healthy male and female volunteers.
Methods:
Six males and six females (25 ± 3 and 22 ± 1 years, respectively) participated in a randomized, double blind, placebo controlled, crossover protocol. On two visits separated by 1 week, following a 12-hour fast, participants consumed either a placebo or glutathione (negligible and 200 mg, respectively) supplement via 90 second sublingual absorption which was then swallowed. Concentrations of oxidized (GSSG) and reduced glutathione (GSH) were spectrophotometrically measured in plasma (protein-bound) and erythrocyte lysate using a kinetic, enzymatic assay. Arterial stiffness was measured via pulse wave velocity (PWV) using applanation tonometry, and cBP was determined non-invasively using pulse wave analysis. All data were recorded before supplementation (baseline) and at 10, 30, 60 and 120 minutes post-consumption.
Results:
Linear mixed effect models revealed a significant (p<0.01) increase in total glutathione (GSH+GSSG) in the supplement group compared to placebo across all post-supplementation time points with the greatest increase occurring at 120 minutes (mean 99.0; 95%CI: 7.9,190.1). At 120 minutes post-consumption, no difference was present between glutathione and placebo groups for PWV (5.86 ± 1.19 and 6.08 ± 1.25 m/s, respectively; p=0.43), resting heart rate (52.95 ± 3.55 and 55.83 ± 6.36, respectively; p=0.16), systolic bBP (123.05 ± 12.75 and 123.13 ± 14.52 mmHg; p=0.22), diastolic bBP (71.81 ± 7.87 and 74.21 ± 6.53; p=0.48), systolic cBP (108.05 ± 10.45 and 108.68 ± 11.14 mmHg, respectively; p=0.11) and diastolic cBP (72.03 ± 7.82 and 74.94 ± 6.42 mmHg, respectively; p=0.46).
Conclusion:
Young healthy males and females experienced an increase in circulating humoral antioxidants in response to glutathione supplementation. However, supplementation had minimal effects on resting hemodynamics. Future research should examine glutathione supplementation’s effect in participants with decreased antioxidant capacity and increased oxidative stress including patients with known disease such as hypertension or peripheral artery disease.
Feasibility of non‐invasive measurement of central blood pressure and arterial stiffness in shock
