Abstract. Tolerance to Zn 2+ by pure cultures of Bacillus, Salmonella and Arthrobacter species isolated from New Calabar River sediment was assessed through dehydrogenase assay. The cultures were exposed to Zn 2+ concentrations of 0.2 to 2.0 mM in a nutrient broth-glucose-TTC medium. The responses of the bacterial strains varied with Zn 2+ concentration. In Salmonella sp. SED2, Zn 2+ stimulated dehydrogenase activity at 0.2 mM. In Bacillus sp. SED1 and Arthrobacter sp. SED4, dehydrogenase activity was progressively inhibited with increasing Zn 2+ concentration. The IC 50 ranges from 0.206 ± 0.030 to 0.807 ± 0.066 mM. Total inhibition of dehydrogenase activity was observed at concentrations ranging from 1.199 ± 0.042 to 1.442 ± 0.062. The order of zinc tolerance is: Salmonella sp. SED2 > Arthrobacter sp. SED4 > Bacillus sp. SED1. The result of the in vitro study indicated that Zinc is potentially toxic to sediment bacteria and could pose serious threat to their metabolism in natural environments.
The dose-response phenomenon characterized by low dose stimulation and high dose toxicity has been reawakened after a long period of marginalization. This phenomenon termed hormesis is induced by biological, physical and chemical agents and occurs in all groups of living things including whole plants and animals, microorganisms, cells and tissues. Hormesis has attracted increased interest among toxicologists from diverse disciplines, resulting to emergence of new scientific tools for its study. Statistical models have been developed and used to characterize hormesis dose-response relationships. Some of these models include the classical Brain-Cousens model, the Cedergreen-Ritz-Streibig model and their reparameterizations. Other hormesis models are the bilogistic models, their modifications or extensions and the hormesis models used in allelopathy such as An-Johnson-Lovett model. These models are used to describe either U-shaped or inverted U-shaped dose-response relationships and to compute hormesis quantities. This review explored the applications of these models in toxicological studies with emphasis to their strengths and weaknesses.
Inhibition of α-glucosidase (EC 3.2.1.20) and β-galactosidase (EC 3.2.1.23) biosynthesis by phenolic compounds (phenol, 2-chlorophenol, 4-chlorophenol, 4-bromophenol and 3,5dimethylphenol) in Escherichia coli, Bacillus and Pseudomonas species isolated from petroleum refinery wastewater was assessed. At sufficient concentrations, phenols inhibited the induction of α-glucosidase and β-galactosidase. The patterns of these toxic effects can be mathematically described with logistic and sigmoid dose-response models. The median inhibitory concentrations (IC 50) varied among the phenols, the bacteria and enzymes. Quantitative structure-activity relationship (QSAR) models based on the logarithm of the octanol-water partition coefficient (log 10 K ow) were developed for each bacterium. The correlation coefficients varied between 0.84and 0.99 for the enzymes. The test results indicated α-glucosidase and β-galactosidase biosynthesis as important microbial indices for evaluation of toxicity of phenolic compounds.
The toxicity of mixtures of formulated glyphosate, phenol, 4-chlorophenol and 2,4-dichlorophenol to river water microbial community was investigated using non specific dehydrogenase activity as endpoint. The microbial community was exposed to individual toxicant and quaternary mixture ratios at concentrations ranging from 50 mg L -1 to 3000 mg L -1 over 24 h. The ecological doses (EC 50 ) as estimated from logistic or hormesis dose-effect models were 1317.946 ± 51.460 mg L -1 , 1046.414 ± 65.534 mg L -1 , 85.080 ± 4.468 mg L -1 and 60.897 ± 5.199 mg L -1 for formulated glyphosate, phenol, 4-chlorophenol and 2,4-dichlorophenol respectively. The toxicity and interaction of the mixtures were evaluated using concentration addition and toxic index models. The model deviation ratios (MDR) ranged from 0.553 ± 0.024 to 1.096 ± 0.021 while the toxic index (TI) varied between 0.912 ± 0.017 and 1.810 ± 0.078. However, the MDR and TI for all mixtures lie between 0.5 and 2.0. Thus, the joint action of the mixtures were considered additive.
The impacts of Hg 2+ , Cd 2+ and Zn 2+ on the activities of periplasmic nitrate reductase (NAP) and dehydrogenase (DHA) enzymes of three organisms isolated from soil and sediment-water interface were analysed in liquid culture studies. NAP and DHA activities were estimated from nitrite and triphenyl formazan produced respectively after 4h incubation at 28 ± 2 o C. Hg 2+ completely inhibited NAP activity in Escherichia and Pseudomonas spp. at all the concentrations (0.2 -1mM) while progressive inhibitions of NAP activity were observed in Escherichia and Pseudomonas spp. with increasing concentrations of Zn 2+ and Cd 2+ . Both metals were stimulatory to NAP of Acinetobacter sp. at 0.2 -1mM. Apart from stimulation of DHA activity by Zn 2+ (0.2 -1mM) in Escherichia sp., Cd 2+ (0.4 -1.0mM) in Acinetobacter sp. and (1.0mM) in Pseudomonas sp., all the metals progressively inhibited DHA activities in the three organisms. In Escherichia sp., the activities of the two enzymes were negatively correlated on exposure to Zn 2+ (r = -0.91) and positively correlated (r = >0.90) on exposure to Cd 2+ and Hg 2+ . Based on IC 50 values of the metals for the DHA and NAP enzymes, the most resistant of the three organisms were Escherichia sp. and Acinetobacter sp. respectively. Quantitatively, NAP with its lower IC 50 values than DHA was a more sensitive toxicity measure for Hg 2+ in all the organisms. The sensitivity of microbial metabolic enzymes to the toxic effects of metals varies with the type of enzyme, metal and the microorganism involved. Keywords: Periplasmic nitrate reductase; Dehydrogenase; Escherichia sp.; Pseudomonas sp.; Acinetobacter sp.; IC 50 ; Hg 2+ ; Cd 2+ and Zn 2+ . Palavras-chave: Reductase do nitrato periplásmico; dehidrogenase; Escherichia sp; Pseudomonas sp; de Acinetobactéria sp; IC 50 ; Hg 2+ ; Cd 2 + e Zn 2+ .
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