Many pathological conditions are associated with decreased GSH levels (Table 1 ). This could be due to several reasons. For instance, oxidative stress could cause GSH loss though oxidation. Another important aspect is nutrition, as it was shown that, even when dietary protein intake is sufficient for maintaining nitrogen balance, it may not be sufficient for maintaining cellular GSH, particularly in conditions of oxidative stress. 9 GSH deficiency could also arise from metabolic problems. For instance, in AIDS patients, a decrease in gamma-cystathionase activity in the liver was reported. 10 The use of stable radioisotopes allowed the characterization of cysteine metabolism and GSH synthesis in septic patients. This study showed that sepsis decreases blood GSH synthesis by 60%. 3 Of note, these patients had an intake of sulfur amino acids below that recommended by the World Health Organization. 3 Studies in animal models have reported an increased requirement for cysteine in sepsis, probably due to an increased turnover of GSH, as GSH synthesis accounts for 40% of the increased cysteine utilization. 11, 12 These and other studies show that even when the dietary intake of cysteine is sufficient for protein synthesis (nitrogen balance), it may not be sufficient to maintain adequate GSH levels. 9 One should also bear in mind that infectious and inflammatory conditions are associated with an increased production of acute-phase proteins by the liver, and it was estimated that they account significantly for the increased utilization of sulfur amino acids, thus competing with GSH. 13, 14 GSH as a regulator of innate immunity Anti-inflammatory role of GSH in lung diseases