Effects of Selected Hydrazines on the Early Death Rates of Enterobacter cloacae
AIR FORCE AEROSPACE MEDICAL RESEARCH LAB WRIGHT-PATTERSON AFB OH
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The toxicity of hydrazine and several of its methylated derivatives has been studied in a variety of biological systems. London 1979 utilized a soil bacterium to compare the toxicities of these compounds and to suggest the validity of prokaryote and other simple systems as an adjunct to traditional toxicological techniques. Subsequent efforts Mantel and London, 1980 were devoted to elucidating the mechanisms by which the hydrazines exert a toxic effect. The measurements used in these studies were concerned with growth kinetics, i.e., the time and concentration parameters describing the growth cycle. The quantitation of growth was accomplished by turbidimetric determinations of cell mass which is an integrative description of particle size and number. This method provided useful information but was not sufficiently sensitive at the extremes of cell culture density. The insensitivity of low cell densities precluded ascertaining the effects of hydrazine exposure immediately after transfer and during the lag phase of the growth cycle. Since the major indication of intoxication at the test concentrations used 10 ppm hydrazine Hz 20 ppm monomethyl-hydrazine MMH and 50 ppm 1,1-dimethylhydrazine UDMH was an extension of the lag period, a possible mechanism of action is a random or selective killing of inoculum cells, the lengthening of the lag phase being inversely proportional to the fraction of inoculum cells killed or prevented from initiating cell division. Since the experiments based on turbidimetric data could not address this aspect, we studied the early death rate kinetics of hydrazine-exposed cultures using a standard viable cell counting procedure as a more reliable quantitative method to enumerate cell death rate at low culture concentrations.