ABSTRACT
Adaptation of Mycoplasma gallisepticum to unfavorable growth conditions results in altered morphological and physiological characteristics of the cells. M. gallisepticum populations in a complete nutrient medium contain pear-shaped vegetative cells (d approximately 0.3 microm; l approximately 0.8 microm) with pronounced polar and cytoskeleton-like structures. Such mycoplasma cells are able to induce damage in a bacterial genome, causing an SOS response of the test strain (Escherichia coli PQ37). In a starvation medium, M. gallisepticum produces nanoforms, small coccoid cells (d approximately 0.15-0.2 microm) without either polar or cytoskeleton-like structures. Unlike vegetative cells, nanoforms do not induce genome damage. Alleviation of unfavorable growth conditions results in a reversion of nanoforms to typical vegetative cells.
Subject(s)
Adaptation, Physiological , Mycoplasma gallisepticum/growth & development , Mycoplasma gallisepticum/ultrastructure , SOS Response, Genetics , Biological Products/metabolism , Biological Products/pharmacology , Culture Media , Culture Media, Conditioned/metabolism , Culture Media, Conditioned/pharmacology , DNA Damage , Escherichia coli/drug effects , Escherichia coli/genetics , Escherichia coli/physiology , Mycoplasma gallisepticum/geneticsABSTRACT
It has been shown that the phenotypic dissociation of Bacillus subtilis SK1 and S. typhimurium TA100 is induced by hexylresorcinol, an exogenous non-species-specific autoregulator of pleiotropic action, which is genotoxic for both pro- and eukaryotes. Nongenotoxic homoserine lactone, a chemical analogue of cell-density-responsive species-specific regulators, does not induce bacterial dissociation. The phage resistance of the S- and R-type variants of S. typhimurium TA100 induced by hexylresorcinol has been found to be the same as that of the S- and R-type salmonella variants obtained by the routine subculturing method.
Subject(s)
Bacillus subtilis/drug effects , Hexylresorcinol/pharmacology , Salmonella typhimurium/drug effects , 4-Butyrolactone/analogs & derivatives , 4-Butyrolactone/pharmacology , Bacillus subtilis/genetics , Bacillus subtilis/growth & development , Culture Media , Dose-Response Relationship, Drug , Phenotype , Salmonella typhimurium/genetics , Salmonella typhimurium/growth & developmentABSTRACT
Hexylresorcinol has been demonstrated to induce chromosome aberrations in eukaryotic cells at doses of 0.5, 0.05, and 0.005 mg/g body weight. The metabolic transformation of hexylresorcinol in mice decreases its genotoxic effect. The mutagenic effect is retained for three days only after the administration of the highest dose of hexylresorcinol (0.5 mg/g); during the first two days, lower doses are also genotoxic. Therefore, hexylresorcinol doses lower than 0.5 mg/g body weight are metabolized within two days to the extent precluding the expression of the cytotoxic effect. After a single administration to mice, exogenous hexylresorcinol is transformed at a rate of 0.0025-0.025 mg/day.
Subject(s)
Anti-Infective Agents, Local/toxicity , Blood Cells/pathology , Chromosome Aberrations/chemically induced , Hexylresorcinol/toxicity , Mutagens/toxicity , Animals , Anti-Infective Agents, Local/metabolism , Blood Cells/metabolism , Dose-Response Relationship, Drug , Hexylresorcinol/metabolism , Mice , Mutagens/metabolismABSTRACT
Among examined microbial growth regulators of alkyl hydroxybenzene group (hexylresorcinol, methylresorcinol, and hydroxyethylphenol), only hexylresorcinol induces cellular SOS response, demonstrating a dose-dependent increase of the induction factor in the SOS chromotest with the Escherichia coli PQ37 strain. At the highest of used concentrations (100 micrograms/ml), hydroxyethylphenol and nonalkylated resorcinol were shown to exert a weak toxic effect, reducing the activity of constitutive alkaline phosphatase, but did not induce SOS response. Nontoxic methylresorcinol did not induce genome damage, which can trigger SOS functions. It is concluded that substitutions in phenolic ring affect genotoxic activity of alkylresorcinols.
