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Multiple Choice

What pathway protects RBCs from oxidative damage?

Protecting red blood cells from oxidative damage relies on keeping glutathione in its reduced form, which requires NADPH. The hexose monophosphate shunt (pentose phosphate pathway) is the main source of NADPH in RBCs. This NADPH powers glutathione reductase to recycle oxidized glutathione back to its reduced form, neutralizing reactive oxygen species like hydrogen peroxide. Red blood cells lack mitochondria, so they depend on this pathway rather than mitochondrial NADPH production or other glycolytic shunts. The Embden-Meyerhof pathway mainly makes ATP, not NADPH; the methemoglobin reductase pathway uses NADH to reduce methemoglobin but doesn’t broadly protect against oxidative damage; and the Luebering-Rapoport pathway alters 2,3-BPG and oxygen release without direct redox defense. So, the hexose-monophosphate shunt best protects RBCs from oxidative damage.

Protecting red blood cells from oxidative damage relies on keeping glutathione in its reduced form, which requires NADPH. The hexose monophosphate shunt (pentose phosphate pathway) is the main source of NADPH in RBCs. This NADPH powers glutathione reductase to recycle oxidized glutathione back to its reduced form, neutralizing reactive oxygen species like hydrogen peroxide. Red blood cells lack mitochondria, so they depend on this pathway rather than mitochondrial NADPH production or other glycolytic shunts. The Embden-Meyerhof pathway mainly makes ATP, not NADPH; the methemoglobin reductase pathway uses NADH to reduce methemoglobin but doesn’t broadly protect against oxidative damage; and the Luebering-Rapoport pathway alters 2,3-BPG and oxygen release without direct redox defense. So, the hexose-monophosphate shunt best protects RBCs from oxidative damage.