Effects of selected hydrazines on the early death rates of Enterobacter cloacae.

Abstract

Abstract : 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.