Diamide alters membrane Na+ and K+ conductances and increases internal resistance in the isolated rat lens.

The voltage and conductance of the isolated rat lens were measured using a two-internal-microelectrode technique and the potassium permeability was calculated by applying Goldman theory to 86Rb efflux data. The SH oxidizing agent diamide induces a multiphasic response in lens voltage, conductance and potassium permeability. The initial response (less than or equal to 30 min) to 1 mM diamide consists of a small depolarization (approximately 10 mV) of membrane potential accompanied by a significant decrease in conductance. The 86Rb efflux and permeability data also show an initial decrease. As this initial response is abolished by TEA (20 mM) it is probably due to an inactivation of voltage-sensitive potassium channels. After 30 min exposure to 1 mM diamide both the electrical conductance and the rate of depolarization increase. The 86Rb permeability also increases. Since the conductance increase is abolished by replacing Na+ by methyl glucamine and as it is reduced by amiloride (10(-4) M) the second phase is probably due to the activation of nonspecific cation channels. The third phase is only apparent after prolonged (approximately 12 hr) incubation in 1 mM diamide and consists of a marked increase in the bulk resistance component of the lens impedance. It is suggested that this component arises from an increase in the resistance of the fibre cell gap junctions. This cellular uncoupling may be due to calcium entering the lens through the nonspecific cation channels.