Fb. Cooling et al., INHIBITION OF SULFATE RESPIRATION BY 1,8-DIHYDROXYANTHRAQUINONE AND OTHER ANTHRAQUINONE DERIVATIVES, Applied and environmental microbiology, 62(8), 1996, pp. 2999-3004
Derivatives of 9,10-anthracenedione, or anthraquinone, were shown to i
nhibit respiratory sulfate reduction by pure cultures of sulfate-reduc
ing bacteria, as well as by crude enrichment cultures. Structure-activ
ity studies showed that an increasing degree of substitution of the an
thraquinone nucleus resulted in increasing 50% inhibition (I-50) value
s for sulfate respiration. Addition of charged ring substituents also
resulted in an increase in the I-50 concentration. Experiments carried
out with 1,8-dihydroxyanthraquinone demonstrated inhibition of hydrog
en-dependent sulfate respiration but not hydrogen-dependent sulfite or
thiosulfate respiration. Addition of pyruvate resulted in stimulation
of sulfate-dependent hydrogen oxidation in the presence of the anthra
quinone. These observations, together with a direct demonstration of u
ncoupling in French press vesicle preparations, suggest that the under
lying mechanism of inhibition is uncoupling of ATP synthesis from elec
tron transfer reactions. The low I-50 values for inhibition (0.5 to 10
mu M) and the relatively low general toxicity of anthraquinones sugge
st that these compounds may be useful for inhibition of sulfide genera
tion in situations which are incompatible with the use of broadly toxi
c biocides.