Effect of Sodium Chloride on Uptake of Substrate by Staphylococcus aureus 196E

Sodium chloride inhibited a number of biochemical parameters in Staphylococcus aureus 196E. Induction of phospho-β-galactosidase, synthesis of staphylococcal enterotoxin A, enzyme activity (phospho-β-galactosidase) and glucose utilization were approximately four times more sensitive to the inhibitory effects of salt than was growth. Uptake of ¹⁴C-2-deoxyglucose and respiratory activity with a number of substrates were inhibited also. The breakdown of o-nitrophenyl-β-galactoside (ONPG) by lactose-grown S. aureus 196E was inhibited by NaCl as well as by other solutes (salts, carbohydrates, amino acids) which suggested that the inhibitory effect is a general one of solutes and not restricted to NaCl. Various ionophores (gramicidin, valinomycin, monensin, lasalocid, m-chlorophenylhydrazone), the H⁺-ATPase inhibitor (N,N′,-dicyclohexylcarbodiimide), and ion channel blockers (quinine, quinidine, chlorpromazinc, tetracaine, verapamil) reversed the inhibitory action of salt on ONPG breakdown by lactose-grown cells; however, these compounds did not reverse NaCl inhibition of glucose utilization. The effects observed here suggest that NaCl (and probably other solutes) exerts an inhibitory effect on transport of substrates into the cells of S. aureus 196E.