Abstract
Staphylococcus aureus possesses a specific mechanism for resistance to salt. We studied the effect of inhibitors specific to the respiratory functions on extracellular nuclease and α-toxin production in S. aureus in relation to the salt-resistance mechanism. The representative respiratory inhibitors, potassium cyanide (KCN) and sodium azide (NaN3), depressed the rates of extracellular production of staphylococcal nuclease and α-toxin, but potassium arsenite (KAsO2) was less effective apparently due to the occurence of by-pass routes on the bacterial respiratory chain. The attenuating effect of oligomycin and 2,4-dinitrophenol (DNP) appeared more severely on the toxin formation than the enzyme formation. The addition of sodium chloride (NaCl), which is known to stimulate the respiratory activity and extracellular enzyme formation in this bacterium, to the cultures treated with the respiratory inhibitors restored the decreased differential rate of nuclease production, but did not overcome the inhibitory effect of DNP, suggesting that the exoprotein formation in S. aureus may closely relate to the activity of bacterial respiration and depend upon the intracellular energy supply. The possible regulatory processes of the respiratory functions on exoprotein formation are discussed.
