The Phagocytosis-Associated Respiratory Burst in Human Monocytes Is Associated with Increased Uptake of Glutathione

摘要: During the phagocytic respiratory burst, oxygen is converted to potent cytotoxic oxidants. Monocytes and macrophages are potentially long-lived, we have hypothesized that protective mechanisms against oxidant stress varied fully expressed in these cells. We report here burst monocytes accompanied by an increase uptake of [ 35 S]glutathione ([ S]GSH) after 20–30 min levels up 10-fold greater than those at baseline. By 30 min, 49% cell-associated radioactivity was cytosol, 41% membrane, 10% associated with nuclear fraction. GSH inhibited catalase, which removes hydrogen peroxide (H 2 O ), micromolar H stimulated effectively also lymphocytes. Oxidation glutathione disulfide peroxidase prevented uptake. Acivicin, inhibits breakdown γ-glutamyl transpeptidase (GGT), had no effect on enhanced seen during burst. Uptake cysteine or cystine, possible products GGT activity, stayed same decreased These results suggest a GGT-independent mechanism responsible for describe sodium-independent, methionine-inhibitable transport system K m (8.5 μM) approximating plasma concentration. specific transporter triggered release induces into cell. Such has potential protect phagocyte damage.