Dihydrostreptomycin sulfate (Dihydrostreptomycin sesquisulfate) inhibits protein synthesis by binding to the 30S ribosomal subunit. Dihydrostreptomycin Sulfate is a semi-synthetic aminoglycoside antibiotic with bactericidal properties. This antibiotic is active against most gram-positive and gram-negative organisms and is used in the treatment of tuberculosis and tularemia.

The primary mechanism of action of the antibiotic dihydrostreptomycin is binding to and modifying the function of the bacterial ribosome, thus leading to decreased and aberrant translation of proteins. It enters bacterial cells by binding to a specific site on MscL(mechanosensitive channel of large conductance) and modifying its conformation, thus allowing the passage of K+ and glutamate out of, and dihydrostreptomycin into, the cell[1].

Dihydrostreptomycin sulfate would cause cochlea damage in mouse model and cell proliferation in the spiral ligament may occur after the dihydrostreptomycin sulfate -induced damage. This process is probably related to the recovery of cochlear function[2].

Briefly, the peptide substrate N-acetyl-Asp-Glu-Val-Asp-ρ-nitroanilide (Ac-DEVD-ρNA) is added to the cell lysates in assay buffer (50 mM HEPES, pH 7.4, 100 mM NaCl, 0.1% CHAPS, 10 mM dithiothreitol, 1 mM EDTA, 10% glycerol) and incubated at 37°C. The cleavage of the substrate is monitored at 405 nm.