Oxygen free-radicals mediate the damaging effect of ultraviolet light on membrane mitochondria.
This paper reports evidence that exposure of mitochondria to near-ultraviolet light inhibits electron transport, collapses the electric gradient, and increases non-specific membrane permeability to matrix solutes such as Ca2+. Membrane energization, as well as superoxide dismutase and catalase avoid membrane leakiness. Increased permeability correlates with a diminution in the titrated thiol groups. Plausibly the pore is formed through the formation of sulfhydryl bridges by the action of UV light-derived oxygen-centered free- radicals on membrane proteins.
Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, México, D.F., México.
E
E
Chávez
C
C
Zazueta
A
A
Cuéllar
H
H
Reyes-Vivas
N
N
García
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004579:Electron Transport; D005609:Free Radicals / Q000378:metabolism*; D007425:Intracellular Membranes / Q000378:metabolism / Q000528:radiation effects*; D017136:Ion Transport / Q000528:radiation effects; D007672:Kidney Cortex; D008928:Mitochondria / Q000378:metabolism / Q000528:radiation effects*; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption / Q000528:radiation effects; D010539:Permeability / Q000528:radiation effects; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D014466:Ultraviolet Rays
D005609:Free Radicals; D002374:Catalase; D013482:Superoxide Dismutase; D010100:Oxygen; D002118:Calcium