IN IONIZATION DISINFECTION
of Escherichia coli injured by Copper
MJ, Robbins JE, Anderson ME, and McFeters GA
Journal of Microbiology 33: 57-62,1987
on evidence that the presence of copper in drinking water, which frequently
occurs naturally, can cause injury to Escherichia coli (E. coli)
and other coliforms, the authors performed experiments to elucidate the
physiologic mechanisms responsible of cellular injury.
coli was isolated from river water and cultured in broth. Washed cells
were placed in an inorganic carbon buffer and the pH adjusted. High concentrations
of copper were introduced to produce injury to the 95% level. The injured
populations were analyzed using a series of tests: oxygen uptake measurements
by oxygraph and differential respirometer, nuclear magnetic resonance
spectroscopy, gas chromatography, and spectrophotometric respiration measurements.
compared to normal cells, short-term oxygen uptake was reduced by 75%
in copper-injured cells. Similarly, long-term respirometry experiments
showed that the rate of oxygen uptake of the injured cells was approximately
47% of the rate in normal cells.
magnetic resonance spectra revealed that the rate of glucose utilization
was 64% compared to normal cells. Similar trends were evident in lactate,
ethanol, acetate, and glutamine accumulation under both aerobic and anaerobic
conditions. The slow utilization of succinate and decreased production of
CO2 under aerobic conditions suggested that copper has major effect on
the aerobic metabolic function of E. coli.
cells reduced six times greater quantities of 2 (p-iodophenyl) -3- (p-nitrophenyl)
-5- phenyltetrazolium chloride (INT) than control cells when NADH was
used as a substrate. A comparison of metabolic end products demonstrated
marked differences in carbon flow in injured cells.
Exposure of E. coli in drinking water to copper produces
a variety of injurious effects. The mechanism include decreased oxygen
utilization of glucose, and lowered accumulation of metabolic products
such as lactate and ethanol. The fact that aerobic succinate was lowered
and less glutamine produced suggest that tricarboxylic acid (TCA) activity
is also inhibited.