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At least 19 recordsLinked to original sources
PubMed2004

Chlorate and nitrate reduction pathways are separately induced in the perchlorate-respiring bacterium Dechlorosoma sp. KJ and the chlorate-respiring bacterium Pseudomonas sp. PDA.

The effect of nitrate on perchlorate and chlorate reduction by perchlorate-respiring bacteria (PRB), and on chlorate reduction by chlorate-respiring bacteria (CRB), is not well understood, particularly with respect to the induction of pathways used to degrade these different chemicals. Based on kinetic data obtained in a series of batch tests, we determined that perchlorate respiratory enzymes were inducible (by chlorate or perchlorate) and separate from those used for denitrification by PRB strain Dechlorosoma sp. KJ. Aerobically grown cultures of KJ had lag times of greater than 0.3-2 days when transferred to a medium containing only perchlorate, chlorate, or nitrate as an electron acceptor. There were no lag times for transfers between identical media. Washed cells reduced very little nitrate (<10%) when grown only on chlorate or perchlorate. When grown on nitrate, they degraded little chlorate or perchlorate. The same lack of activity with these electron acceptors was also observed using cell extracts and methyl viologen as an electron carrier, indicating a lack of reactivity was not due to failure of the chemical to diffuse into the cell. Taken together, these results indicated that enzymes for perchlorate and nitrate reduction are separately expressed in strain KJ. The presence of small amounts of nitrate in contaminated groundwater may actually help to increase rates of perchlorate reduction once the nitrate is completely removed. When strain KJ was pre-grown on nitrate and perchlorate, perchlorate degradation (in the absence of nitrate) was more rapid compared to cells grown only on perchlorate. Pseudomonas sp. PDA was unable to degrade perchlorate or grow using nitrate, and the induction of enzymes necessary for chlorate respiration differed for strains KJ and PDA. While chlorate reductase and chlorite dismutase activity were induced in KJ by chlorate or perchlorate under anaerobic conditions, these two enzymes were constitutively expressed by PDA under anaerobic and aerobic conditions independent of the presence of chlorate. To our knowledge, this is the first report of constitutive expression of both chlorate reductase and chlorite dismutase in a bacterium.

Bacteria, Anaerobic↗
PubMed2006

Effect of sodium [36Cl]chlorate dose on total radioactive residues and residues of parent chlorate in growing swine.

An experimental chlorate-based product has been shown to be efficacious in eliminating economically important, Gram-negative human pathogens in the gastrointestinal tracts of food animals. Prior to the commercial marketing of such a product, the magnitude and chemical nature of residues remaining in edible tissues must be determined. Thus, the objective of this study was to determine the tissue distribution and elimination of sodium [36Cl]chlorate in orally dosed swine. Three sets of pigs, each consisting of a barrow and a gilt, were orally dosed with a total of 20, 40, or 60 mg of sodium [36Cl]chlorate per kg body weight via the drinking water. Urine and feces were collected throughout the 30 h study. Twenty-four hours after the last exposure to [36Cl]chlorate, each pig was harvested and both edible and inedible tissues were collected. Urine and tissue samples were analyzed for total radioactive residues and for chlorate metabolites. Elimination of radioactivity in urine averaged 81.6, 83.7, and 83.9% of the total dose for the low, medium, and high doses, respectively. Fecal elimination of radioactivity averaged 1.1% of the dosed radiochlorine across all doses. Parent chlorate always represented greater than 97.4% of the urinary radiochlorine with the remaining radiochlorine being excreted as chloride ion. Chlorate represented 39-77% of fecal radioactivity, depending upon dose. Chlorate concentrations in edible tissues ranged from 0.01 to 0.49 ppm, with residues in liver and skeletal muscle generally lower than those in kidney and adipose tissue. Chlorate residues were concentrated in thyroid tissues (7.7-25.4 ppm) relative to edible tissues. No evidence for the presence of chlorite was observed in excreta or in tissues. Results of this study suggest that further development of chlorate as a preharvest food safety tool in swine merits consideration.

Animals↗
PubMed2005

Effect of sodium [36Cl]chlorate dose on total radioactive residues and residues of parent chlorate in beef cattle.

The objectives of this study were to determine total radioactive residues and chlorate residues in edible tissues of cattle administered at three levels of sodium [36Cl]chlorate over a 24-h period and slaughtered after a 24-h withdrawal period. Three sets of cattle, each consisting of a heifer and a steer, were intraruminally dosed with a total of 21, 42, or 63 mg of sodium [36Cl]chlorate/kg of body weight. To simulate a 24-h exposure, equal aliquots of the respective doses were administered to each animal at 0, 8, 16, and 24 h. Urine and feces were collected in 12-h increments for the duration of the 48-h study. At 24 h after the last chlorate exposure, cattle were slaughtered and edible tissues were collected. Urine and tissue samples were analyzed for total radioactive residues and for metabolites. Elimination of radioactivity in urine and feces equaled 20, 33, and 48% of the total dose for the low, medium, and high doses, respectively. Chlorate and chloride were the only radioactive chlorine species present in urine; the fraction of chlorate present as a percentage of the total urine radioactivity decreased with time regardless of the dose. Chloride was the major radioactive residue present in edible tissues, comprising over 98% of the tissue radioactivity for all animals. Chlorate concentrations in edible tissues ranged from nondetectable to an average of 0.41 ppm in skeletal muscle of the high-dosed animals. No evidence for the presence of chlorite was observed in any tissue. Results of this study suggest that further development of chlorate as a preharvest food safety tool merits consideration.

Animals↗
PubMed1999

Purification and characterization of (per)chlorate reductase from the chlorate-respiring strain GR-1.

Strain GR-1 is one of several recently isolated bacterial species that are able to respire by using chlorate or perchlorate as the terminal electron acceptor. The organism performs a complete reduction of chlorate or perchlorate to chloride and oxygen, with the intermediate formation of chlorite. This study describes the purification and characterization of the key enzyme of the reductive pathway, the chlorate and perchlorate reductase. A single enzyme was found to catalyze both the chlorate- and perchlorate-reducing activity. The oxygen-sensitive enzyme was located in the periplasm and had an apparent molecular mass of 420 kDa, with subunits of 95 and 40 kDa in an alpha(3)beta(3) composition. Metal analysis showed the presence of 11 mol of iron, 1 mol of molybdenum, and 1 mol of selenium per mol of heterodimer. In accordance, quantitative electron paramagnetic resonance spectroscopy showed the presence of one [3Fe-4S] cluster and two [4Fe-4S] clusters. Furthermore, two different signals were ascribed to Mo(V). The K(m) values for perchlorate and chlorate were 27 and <5 microM, respectively. Besides perchlorate and chlorate, nitrate, iodate, and bromate were also reduced at considerable rates. The resemblance of the enzyme to nitrate reductases, formate dehydrogenases, and selenate reductase is discussed.

Amino Acid Sequence↗
PubMed1976

Chlorate toxicity in Aspergillus nidulans. Studies of mutants altered in nitrate assimilation.

It had previously been held that chlorate is not itself toxic, but is rendered toxic as a result of nitrate reductase-catalysed conversion to chlorite. This however cannot be the explanation of chlorate toxicity in Aspergillus nidulans, even though nitrate reductase is known to have chlorate reductase activity. Among other evidence against the classical theory for the mechanism of chlorate toxicity, is the finding that not all mutants lacking nitrate reductase are clorate resistant. Both chlorate-sensitive and resistant mutants lacking nitrate reductase, also lack chlorate reductase. Data is presented which implicates not only nitrate reductase but also the product of the nirA gene, a positive regulator gene for nitrate assimilation, in the mediation of chlorate toxicity. Alternative mechanisms for chlorate toxicity are considered. It is unlikely that chlorate toxicity results from the involvement of nitrate reductase and the nirA gene product in the regulation either of nitrite reductase, or of the pentose phosphate pathway. Although low pH has an effect similar to chlorate, chorate is not likely to be toxic because it lowers the pH; low pH and chlorate may instead have similar effects. A possible explanation for chlorate toxicity is that it mimics nitrate in mediating, via nitrate reductase and the nirA gene product, a shut-down of nitrogen catabolism. As chlorate cannot act as a nitrogen source, nitrogen starvation ensues.

Aspergillus nidulans↗
PubMed1993

Toxicity of and mutagenesis by chlorate are independent of nitrate reductase activity in Chlamydomonas reinhardtii.

Spontaneous chlorate-resistant (CR) mutants have been isolated from Chlamydomonas reinhardtii wild-type strains. Most of them, 244, were able to grow on nitrate minimal medium, but 23 were not. Genetic and in vivo complementation analyses of this latter group of mutants indicated that they were defective either at the regulatory locus nit-2, or at the nitrate reductase (NR) locus nit-1, or at very closely linked loci. Some of these nit-1 or nit-2 mutants were also defective in pathways not directly related to nitrate assimilation, such as those of amino acids and purines. Chlorate treatment of wild-type cells resulted in both a decrease in cell survival and an increase in mutant cells resistant to a number of different chemicals (chlorate, methylammonium, sulphanilamide, arsenate, and streptomycin). The toxic and mutagenic effects of chlorate in minimal medium were not found when cells were grown either in darkness or in the presence of ammonium, conditions under which nitrate uptake is drastically inhibited. Chlorate was also able to induce reversion of nit- mutants of C. reinhardtii, but failed to produce His+ revertants or Arar mutants in the BA-13 strain of Salmonella typhimurium. In contrast, chlorate treatment induced mutagenesis in strain E1F1 of the phototrophic bacterium Rhodobacter capsulatus. Genetic analyses of nitrate reductase-deficient CR mutants of C. reinhardtii revealed two types of CR, to low (1.5 mM) and high (15 mM) chlorate concentrations. These two traits were recessive in heterozygous diploids and segregated in genetic crosses independently of each other and of the nit-1 and nit-2 loci. Three hcr loci and four lcr loci mediating resistance to high (HC) and low (LC) concentrations of chlorate were identified. Mutations at the nit-2 locus, and deletions of a putative locus for nitrate transport were always epistatic to mutations responsible for resistance to either LC or HC. In both nit+ and nit- chlorate-sensitive (CS) strains, nitrate and nitrite gave protection from the toxic effect of chlorate. Our data indicate that in C. reinhardtii chlorate toxicity is primarily dependent on the nitrate transport system and independent of the existence of an active NR enzyme. At least seven loci unrelated to the nitrate assimilation pathway and mediating CR are thought to control indirectly the efficiency of the nitrate transporter for chlorate transport. In addition, chlorate appears to be a mutagen capable of inducing a wide range of mutations unrelated to the nitrate assimilation pathway.

Animals↗
PubMed1998

Effect of long-term treatment of 3T3-L1 adipocytes with chlorate on the synthesis, glycosylation, intracellular transport and secretion of lipoprotein lipase.

Lipoprotein lipase (LPL) is synthesized and glycosylated in the endoplasmic reticulum (ER), transported through the Golgi to the cell surface, and finally secreted. To examine the role of heparan sulphate proteoglycans (HSPG) in the synthesis, activity, intracellular transport and secretion of LPL, 3T3-L1 adipocytes were cultured for 7 days in the presence of 20 mM chlorate, an inhibitor of sulphation of HSPG. Treatment of cells with 20 mM chlorate for 7 days caused a 55% decrease in LPL activity in the intracellular compartment and a 79% decrease in the cell-surface compartment. The synthetic rate of LPL in chlorate-treated cells was identical with that in control cells as determined by biosynthetic labelling. The study with endoglycosidase H (endo H) showed that the treatment with chlorate increased the proportion of LPL subunits which were totally endo H-sensitive. The study with a heparin-Sepharose column showed that 3T3-L1 adipocytes contained three forms of LPL. The first form, accounting for 35% of the LPL, did not bind to the heparin-Sepharose column and had little or no activity; the second form, accounting for 32%, bound to the column and was eluted with 0.4-0.75 M NaCl but had no activity; the third form, accounting for 33%, bound to the column and was eluted with 0.8-1.2 M NaCl and had activity. In chlorate-treated cells, the first form accounted for 66% of the LPL, the second form 15% and the third form 19%. When cells were incubated for 1 h with brefeldin A, which translocates Golgi proteins to the ER [J. Lippincott-Schwartz, L.C. Yuan, J.S. Banifacino and R.D. Klausner (1989) Cell 56, 801-813; J. Lippincott-Schwartz, J. Glickman, J.E. Donaldson, J. Robbins, T.E. Kreis, K.B. Seamon, M.P. Sheetz and R.D. Klausner (1991) J. Cell Biol. 112, 567-577], the chlorate-induced decrease in cellular LPL activity was restored. These findings indicate that LPL synthesized in chlorate-treated cells can be processed to be fully active, but chlorate-treated cells are unable to transport LPL to the Golgi and accumulate inactive LPL with a lower affinity for heparin in the ER. The treatment with chlorate decreased the proportion of LPL subunits that were endo H-resistant, indicating that the processing of oligosaccharide chains of LPL in the trans-Golgi was impaired in chlorate-treated cells. The amount of 35S-labelled LPL secreted by chlorate-treated cells was identical with that secreted by control cells, whereas the level of LPL activity in the medium of chlorate-treated cells was 25% of that in the medium of control cells, indicating that most of the LPL secreted by chlorate-treated cells was inactive.

3T3 Cells↗
PubMed2001

Escherichia coli O157:H7 becomes resistant to sodium chlorate in pure culture, but not in mixed culture or in vivo.

AIMS: Chlorate kills Escherichia coli O157:H7 and may be an effective feed additive for use in food animals. This study was designed to determine if development of chlorate-resistant E. coli O157:H7 strains was likely. METHODS AND RESULTS: Escherichia coli O157:H7 was chlorate-sensitive, but became chlorate-resistant in pure batch culture and in sterilized faecal fluid; it was killed in mixed culture and did not become resistant. Addition of chlorate to continuous pure cultures caused chlorate resistance, but chlorate addition to mixed continuous culture eliminated E. coli O157:H7 and no resistance occurred. Piglets challenged with E. coli O157:H7 were treated with chlorate; populations were reduced and colonies were always chlorate-sensitive. CONCLUSION: Chlorate-resistant E. coli O157:H7 can be selected in pure, but not mixed culture, and results suggest that terminal chlorate feeding will not select for chlorate-resistance in vivo. SIGNIFICANCE AND IMPACT OF THE STUDY: Chlorate can reduce food-borne pathogens prior to harvest, but development of resistance does not appear likely in vivo.

Animals↗
PubMed1999

Chlorate as an inorganic disinfection by product in swimming pools.

Chlorate and chlorite concentrations were determined in water samples taken from 33 swimming pools. In the pools under investigation, disinfection of the water is carried out either by gaseous chlorine (n = 14) or hypochlorite solution in conjunction with flocculation and sand filtration. A number of the pools also use ozone treatment to augment the disinfection process. Chlorite was not detectable in any of the samples (detection limit 1 mg/l). High concentrations of chlorate were detected in samples from a number of the pools; in one case as high as 40 mg/l. Higher chlorate concentrations were found to be associated with those pools using hypochlorite solution as a disinfecting agent. In contrast, relatively low chlorate concentrations were found in pools treated with gaseous chlorine. In order to elucidate any relationship between the chlorate content of pool water and that of the respective hypochlorite stock solution, chlorate and bromate concentrations were determined in the hypochlorite stock solutions of nine pools. Bromate concentration in the stock solutions were not found to exceed 1.2 g/l, chlorate was measured in concentrations of up to 44.5 g/l. The additional use of ozone as part of the water purification process appears to have no significant influence on chlorate concentration. Chlorate has no bactericidal properties and does not interfere with the measurement of certain parameters relevant to hygiene in swimming pools such as free and combined chlorine, pH or redox potential. At present, the effects of high chlorate concentrations in swimming pool water are unclear. Our initial investigations indicate that chlorate has no cytotoxic (Neutral-Red assay) or irritating properties (HET-CAM assay). However, both chlorate and chlorite are known to interfere with the haematopoetic system. In Germany, the MCL for chlorite in drinking water is 0.2 mg/l. It is therefore strongly recommended that measures should be taken to reduce chlorate concentrations in swimming pool water.

Animals↗
PubMed1991

Effect of Chlorate Treatment on Nitrate Reductase and Nitrite Reductase Gene Expression in Arabidopsis thaliana.

The herbicide chlorate has been used extensively to isolate mutants that are defective in nitrate reduction. Chlorate is a substrate for the enzyme nitrate reductase (NR), which reduces chlorate to the toxic chlorite. Because NR is a substrate (NO(3) (-))-inducible enzyme, we investigated the possibility that chlorate may also act as an inducer. Irrigation of ammonia-grown Arabidopsis plants with chlorate leads to an increase in NR mRNA in the leaves. No such increase was observed for nitrite reductase mRNA following chlorate treatment; thus, the effect seems to be specific to NR. The increase in NR mRNA did not depend on the presence of wild-type levels of NR activity or molybdenum-cofactor, as a molybdenum-cofactor mutant with low levels of NR activity displayed the same increase in NR mRNA following chlorate treatment. Even though NR mRNA levels were found to increase after chlorate treatment, no increase in NR protein was detected and the level of NR activity dropped. The lack of increase in NR protein was not due to inactivation of the cells' translational machinery, as pulse labeling experiments demonstrated that total protein synthesis was unaffected by the chlorate treatment during the time course of the experiment. Chlorate-treated plants still retain the capacity to make functional NR because NR activity could be restored by irrigating the chlorate-treated plants with nitrate. The low levels of NR protein and activity may be due to inactivation of NR by chlorite, leading to rapid degradation of the enzyme. Thus, chlorate treatment stimulates NR gene expression in Arabidopsis that is manifested only at the mRNA level and not at the protein or activity level.

Journal Article↗
PubMed1995

The ecotoxicity of chlorate to aquatic organisms: a critical review.

In order to assess the risk posed by chlorate in aquatic ecosystems, data on the effects of chlorate on aquatic organisms (microorganisms, algae, invertebrates, and fish) and mesocosm studies have been collated and critically reviewed. The geometric mean E(L)C50 values for both freshwater and marine species were (as ClO3-): microorganisms, 38,583 mg.liter-1; microalgae, 563 mg.liter-1; invertebrates, 2442 mg.liter-1; fish, 3815 mg.liter-1. Marine macro red algae were insensitive to chlorate, whereas marine macro brown algae (e.g., Fucus sp.) appeared to be exceptionally sensitive to chlorate, adverse long-term effects having been reported at concentrations as low as 0.015 mg ClO3-.liter-1. Evidence for the mechanism by which chlorate is thought to be particularly toxic to these species is also reviewed. It is concluded that, based on the species reported, chlorate is nontoxic (acute toxicity > 100 mg.liter-1) to most of the freshwater and marine species examined. However, chlorate is highly toxic (acute toxicity < 0.1 mg.liter-1) to certain macro brown algal species. For macro brown algae, the NOEC after 6 months was reported to be approximately 0.005 mg ClO3-.liter-1. It is also concluded that an improved understanding of the actual mode of action of chlorate in sensitive species is desirable. Together with further information on the environmental fate of chlorate, this will improve the risk assessment for chlorate in the aquatic environment.

Animals↗
PubMed2004

Effect of dietary mannanoligosaccharide and sodium chlorate on the growth performance, acute-phase response, and bacterial shedding of weaned pigs challenged with Salmonella enterica serotype Typhimurium.

A 28-d experiment evaluated the growth, acute-phase response, and bacterial shedding patterns in pigs (n = 96; initially 6.8 +/- 1.3 kg) fed mannanoligosaccharides (MANNAN) and sodium chlorate (CHLORATE) before and after oral challenge with Salmonella enterica serotype Typhimurium (ST). The negative control diet contained no antimicrobial (CON), and the positive control contained carbadox (CARB; 55 ppm). Test diets contained (as-fed basis) MANNAN (1,500 ppm) or CHLORATE (800 ppm). Pigs were fed diets for 14 d and then given ST orally. Pigs fed CARB had greater ADG over the entire study than pigs from other treatments (P < 0.05). During wk 1 to 2, before ST challenge, feed intake (as-fed basis) was lower for pigs fed MANNAN and CHLORATE than pigs fed CARB (P < 0.05). During the final 2 wk, pigs fed CARB had greater feed intake than pigs on other treatments (P < 0.05). Gain/feed was greater for pigs fed CARB in the 2 wk before ST (P < 0.05); however, in wk 3 to 4 after ST, gain/feed was reduced for CON pigs compared to pigs on other treatments (P < 0.05). Serum IGF-I was decreased at 2 and 4 d after ST (P < 0.001), and, overall, IGF-I was greater in pigs fed CARB than CON or CHLORATE (P < 0.05). Serum haptoglobin concentrations were greater (P < 0.001) for all treatments at d 6 compared with d 13 after ST. Overall, haptoglobin was greater for MANNAN than for CARB and CHLORATE (P < 0.05) and tended to be increased (P < 0.06) relative to CON. Interleukin-6 was not affected by treatment or day post-ST challenge. Fecal shedding of salmonellae organisms was less for CHLORATE (P < 0.05) than all other treatments at 7 d after ST. Shedding scores decreased from d 7 to 14 after ST (P < 0.05) for the CON, CARB, and MANNAN treatments. We conclude that feeding MANNAN and CHLORATE before acute enteric disease challenge may support improved gut function as evidenced by improved gain/feed, and that CHLORATE may decrease bacterial shedding. But neither MANNAN nor CHLORATE enhanced growth relative to the absence of dietary antimicrobials, nor was either treatment as effective as CARB following ST challenge.

Acute-Phase Reaction↗
PubMed1991

Effect of chlorate on the sulfation of lipoprotein lipase and heparan sulfate proteoglycans. Sulfation of heparan sulfate proteoglycans affects lipoprotein lipase degradation.

In avian-cultured adipocytes 76% of the newly synthesized lipoprotein lipase is degraded before release into the medium (Cupp, M., Bensadoun, A., and Melford, K. (1987) J. Biol. Chem. 262, 6383-6388). The same group (Cisar, L. A., Hoogewerf, A. J., Cupp, M., Rapport, C. A., and Bensadoun, A. (1989) J. Biol. Chem. 264, 1767-1774) has proposed that the interaction of lipoprotein lipase with a class of cell surface heparan sulfate proteoglycans is necessary for degradation to occur. To test further this hypothesis, the binding capacity of the plasma membrane for the lipase was decreased by inhibiting the sulfation of glycosaminoglycans with sodium chlorate, an inhibitor of sulfate adenyltransferase. Chlorate decreased sulfate incorporation into trypsin-releasable heparan sulfate proteoglycans to 20% of control levels. The amount of uronic acid in the trypsin-releasable heparan sulfate proteoglycans remained constant. Therefore, chlorate decreased sulfation density on heparan sulfate chains by approximately 5-fold. In the same fractions, chlorate increased the median heparan sulfate Mr measured on Sephacryl S-300. Chlorate decreased the maximum binding of 125I-lipoprotein lipase to adipocytes by 4-fold, but no significant effects on the affinity constants were observed. Chlorate increased lipoprotein lipase secretion in a dose-dependent relationship up to 30 mM. Utilizing a pulse-chase protocol, it was shown that lipase synthesis in control and chlorate-treated cells was not significantly different and that the increased secretion could be accounted for by a decreased lipoprotein lipase degradation rate. In control cells 77 +/- 11% of the synthesized enzyme was degraded whereas in chlorate-treated cells degradation was reduced to 42 +/- 9% of the synthesized amount. The present study shows that decreased sulfation of heparan sulfate proteoglycans decreases the maximum binding of the lipase for the adipocyte cell surface. Consistent with the model that binding of lipoprotein lipase to cell surface heparan sulfate is required for lipase degradation, degradation is reduced in chlorate-treated cultures. In this report it is also shown that chlorate inhibits lipoprotein lipase sulfation and that desulfation of the enzyme has no effect on its catalytic efficiency or on its binding to cultured adipocytes.

Adipose Tissue↗
PubMed1981

Induction and Characterization of Chlorate-resistant Strains of Rosa damascena Cultured Cells.

The sensitivity of Rosa damascena cultured cells to chlorate was measured by plating samples of suspensions in agar containing NaClO(3). This sensitivity depended on the age of the cultures that were plated. Chlorate-resistant colonies isolated from 5- to 7-day cultures retained their resistance through many generations of growth in medium lacking NaClO(3); they also retained resistance when mixed with sensitive cells. Treating cell aggregates with ultraviolet (UV) light (254 nanometers), or UV light (360 nanometers) in the presence of 4'-methoxymethyltrioxsalen, increased the proportion that was resistant to NaClO(3). However, the amount of increase was low (three times) and required very specific doses of UV light. The UV treatments did not select for chlorate-resistant cells over chlorate-sensitive cells. The data suggested that UV had induced mutations leading to chlorate resistance. Approximately 15% of the resistant strains did not grow on medium containing nitrate as the sole nitrogen source. These strains lacked ability to reduce chlorate to chlorite. This observation supports the current idea that chlorate toxicity depends on the activity of nitrate reductase. Approximately 85% of the resistant strains grew on medium containing nitrate as the sole nitrogen source. These strains lost catalase activity following chlorate treatment, indicating that they took up and reduced chlorate. These strains have a mechanism for tolerating chlorate and its reduction products, rather than avoiding them.

Journal Article↗
PubMed2006

Benzene degradation coupled with chlorate reduction in a soil column study.

Perchlorate and chlorate are electron acceptors that during reduction result in the formation of molecular oxygen. The produced oxygen can be used for activation of anaerobic persistent pollutants, like benzene. In this study chlorate was tested as potential electron acceptor to stimulate benzene degradation in anoxic polluted soil column. A chlorate amended benzene polluted soil column was operated over a period of 500 days. Benzene was immediately degraded in the column after start up, and benzene removal recovered completely after omission of chlorate or a too high influent chlorate concentration (22 mM). Mass balance calculations showed that per mole of benzene five mole of chlorate were reduced. At the end of the experiment higher loading rates were applied to measure the maximal benzene degradation rate in this system; a breakthrough of benzene was not observed. The average benzene degradation rate over this period was 31 micromol l(-1) h(-1) with a maximal of 78 micromol l(-1) h(-1). The high degradation rate and the necessity of chlorate indicate that oxygen produced during chlorate reduction indeed is used for the activation of benzene. This is the first column study where benzene biodegradation at a high rate coupled with anaerobic chlorate reduction is observed.

Anaerobiosis↗
PubMed2002

Sodium chlorate supplementation reduces E. coli O157:H7 populations in cattle.

Cattle are a natural reservoir of the food-borne pathogen Escherichia coli O157:H7. Therefore, strategies that reduce E. coli O157:H7 prior to slaughter will reduce human exposures to this virulent pathogen. When bacteria that can anaerobically respire on nitrate (e.g., E. coli) are exposed to chlorate, they die because the intracellular enzyme nitrate reductase converts nitrate to nitrite, but also co-metabolically reduces chlorate to cytotoxic chlorite. Because chlorate is bactericidal only against nitrate reductase-positive bacteria, it has been suggested that chlorate supplementation be used as a strategy to reduce E. coli O157:H7 populations in cattle prior to harvest. Cattle (n = 8) were fed a feedlot-style high-grain diet experimentally infected with three strains of E. coli O157:H7. Cattle were given access to drinking water supplemented with 2.5 mM KNO3 and 100 mM NaCl (controls; n = 4) or 2.5 mM KNO3 and 100 mM NaClO3 (chlorate-treated; n = 4). Sodium chlorate treatment for 24 h reduced the population of all E. coli O157:H7 strains approximately two logs (10(4) to 10(2)) in the rumen and three logs (10(6) to 10(3)) in the feces. Chlorate treatment reduced total coliforms and generic E. coli from 106 to 10(4) in the rumen and by two logs throughout the rest of the gastrointestinal tract (ileum, cecum, colon, and rectum). Chlorate treatment reduced E. coli O157:H7 counts throughout the intestinal tract but did not alter total culturable anaerobic bacterial counts or the ruminal fermentation pattern. Therefore, it appears that chlorate supplementation is a viable potential strategy to reduce E. coli O157:H7 populations in cattle prior to harvest.

Animals↗