Hamster Brown‐Adipose‐Tissue Mitochondria

Hamster brown‐adipose‐tissue mitochondria, swollen in the chloride, bromide or nitrate salts of sodium, or potassium in the presence of nigericin, do not contract on the addition of oxidizable substrate. If albumin is added to the swollen mitochondria a rapid and complete contraction occurs on substrate addition; however no contraction was observed of mitochondria swollen in KCl or potassium phosphate plus valinomycin or in sodium phosphate. Contraction is interpreted as being a consequence of ion expulsion linked to respiration‐dependent proton translocation. GDP inhibits respiration‐independent chloride permeation but does not prevent chloride efflux from the matrix during respiration in the presence of albumin; respiratory control is retained in this condition after completion of contraction. The stoichiometry of chloride extrusion is approximately 2Cl − /O with succinate as substrate in the presence of albumin, and is unchanged if GDP is additionally present. In the presence of albumin the chloride conductance of the inner membrane is approximately 8 nequiv. Cl − × min − × mg − × mV − . The further addition of GDP decreases the conductance, and no chloride efflux is observed if the membrane potential is below 40 mV. The effectiveness of purine nucleotides in inhibiting chloride permeation in non‐respiring systems is attributed to the low membrane potentials generated by diffusion. The possibility that the sites of electrical anion permeation and purine‐nucleotide‐sensitive proton (or hydroxyl ion) permeation are identical is discussed.