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PubMed1992

Lack of renal tumour-initiating activity of a single dose of potassium bromate, a genotoxic renal carcinogen in male F344/NCr rats.

The renal tumour-initiating activity of potassium bromate (KBrO3), a known genotoxic rat renal carcinogen, was investigated in male F344/NCr rats. 6-wk-old rats were given KBrO3 intragastrically as a single dose of 300 mg/kg body weight, which was confirmed by our preliminary toxicity study as a maximum tolerated single dose for this strain of rat. Starting 2 wk after KBrO3 treatment, groups of 39 rats received either a basal diet or a diet containing 4000 ppm barbital sodium (BBNa) as a promoting regimen and were killed at 30, 52, or 104 wk. Control rats received either dietary BBNa (4000 ppm) or the basal diet alone from wk 2 to 52 or 104 wk. Nephropathy was observed in all rats treated with KBrO3 followed by BBNa at 30 wk and in rats receiving BBNa alone, but not in rats exposed to KBrO3 alone. Dysplastic renal tubular cell foci (DTF), putative preneoplastic renal tubular cell lesions were found associated with nephropathy in rats exposed to KBrO3 followed by BBNa from 47 wk. The incidences and multiplicities of DTF and renal tubular cell tumours observed from 31 to 104 wk revealed no initiating effect of KBrO3 treatment. These results indicate that the KBrO3 dose of 300 mg/kg did not initiate renal carcinogenesis.

Animals↗
PubMed1994

Oxidative DNA damage induced by potassium bromate in isolated rat renal proximal tubules and renal nuclei.

Oxidative damage caused by potassium bromate (KBrO3), a rat renal carcinogen, was investigated using in vitro preparations of rat renal proximal tubules (RPT) and renal nuclear fractions. Release of lactate dehydrogenase and decrease of SH-group content in RPT (1 mg protein/ml) by KBrO3 (0.5-5 mM) in a concentration- and time-dependent manner were observed. Peroxidized arachidonic acid and 8-hydroxydeoxyguanosine (8-OH-dG) levels in RPT were increased after administration of 2 and 5 mM KBrO3. 8-OH-dG formation was observed after incubation of renal nuclei with a lipid-peroxiding system, autooxidized methyl linolenate, or KBrO3. These findings provide support for involvement of lipid peroxidation in producing oxidized DNA damage by KBrO3 directly to RPT, the target site for renal carcinogenesis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2005

Oxidative DNA damage from potassium bromate exposure in Long-Evans rats is not enhanced by a mixture of drinking water disinfection by-products.

Public drinking water treated with chemical disinfectants contains a complex mixture of disinfection by-products (DBPs) for which the relative toxicity of the mixtures needs to be characterized to accurately assess risk. Potassium bromate (KBrO(3)) is a by-product from ozonation of high-bromide surface water for production of drinking water and is a rodent carcinogen that produces thyroid, mesothelial, and renal tumors. The proposed mechanism of KBrO(3) renal carcinogenesis involves the formation of 8-oxoguanine (8-oxoG), a promutagenic base lesion in DNA typically removed through base excision repair (BER). In this study, male Long-Evans rats were exposed via drinking water to carcinogenic concentrations of KBrO(3) (0.4 g/L), 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (0.07 g/L), chloroform (1.8 g/L), bromodichloromethane (0.7 g/L), or a mixture of all these chemicals at the same concentrations for 3 weeks. Half of one kidney was processed for microscopic examination, and the remaining kidney was frozen for isolation of genomic DNA. Levels of 8-oxoG were measured using HPLC with electrochemical detection in DNA samples incubated with formamidopyrimidine-DNA glycosylase. Aldehydic lesions (e.g. abasic sites) in DNA samples were quantitated using an aldehyde-reactive probe slot-blot assay. Treatment with KBrO(3) produced a measurable increase of 8-oxoG in the kidney, and this effect was greater than that produced by treatment with the DBP mixture. No other single chemical treatment caused measurable increases of 8-oxoG. The mixture effect on the amount of 8-oxoG observed in this study suggests an interaction between chemicals that reduced the generation of oxidative DNA damage. No increases in abasic sites were observed with treatment, but a decrease was apparent in the rats treated with the DBP mixture. These data are consistent with previous studies where chronic exposure to this chemical mixture in drinking water resulted in a less than additive carcinogenic response in Tsc2 mutant Long-Evans rats.

Animals↗
PubMed2006

Ion chromatographic determination of trace iodate, chlorite, chlorate, bromide, bromate and nitrite in drinking water using suppressed conductivity detection and visible detection.

An ion chromatography method for the simultaneous determination of trace iodate, chlorite, chlorate, bromide, bromate and nitrite in drinking water has been developed using an anion-exchange column and the suppressed conductivity detector, followed by post-column addition of reagent to enhance visible absorbance detection of ions. A high capacity anion exchange Ion Pac9-HC column (250 mm x 4 mm I.D.) was used. Eight millimole per liter sodium carbonate was used as eluent, an auto-suppression external water mode was selected, 0.5 g/l o-dianisidine.2HCl (ODA)+4.5 g/l KBr+25% methanel+5.6% nitric acid was used as post-column reagent. The post-column reaction (PCR) temperature was at 60 degrees C, and the visible absorbance detected wavelength at 450 nm. The sample's pH and coexist anions had no influence on determination. The method enjoyed a wide linear range and a good linear correlation coefficient (r>0.999). The method detection limits were between 0.023 and 2.0 microg/l. The average recoveries ranged from 87.5 to 110.0%, and the relative standard deviations (RSD) were in the range of 1.1-4.6%. The analytical results by the method of post-column addition of reagent to enhance visible absorbance detection of anions was compared with that of the suppressed conductivity detection, and the former was proved to be better in sensitivity and selectivity. The results showed that this method was accurate, sensitive and might be good for application and suitable for trace analysis at the level of mug/l.

Anions↗
PubMed2004

Spectrophotometric determination of clozapine based on its oxidation with bromate in a micellar medium.

A simple and sensitive spectrophotometric method was developed for the determination of clozapine in its dosage forms. The method is based on the reaction of the drug with potassium bromate in a perchloric acid medium to produce an intense yellow colored species exhibiting a maximum absorption at 308 nm. Beer's law is obeyed for up to 12.0 microg ml(-1) with a correlation coefficient (n = 6) of 0.9998 and a detection limit (3S(b)) of 0.1 microg ml(-1). The molar absorptivity is 1.986 x 10(4) l mol(-1) cm(-1). The various experimental parameters affecting the development and stability of the colored oxidation product were carefully studied and optimized. The proposed method was successfully applied to the determination of clozapine in its dosage forms. The results obtained were in good agreement with those obtained using the B.P. official method.

Antipsychotic Agents↗
PubMed2006

Catalytic-kinetic determination of trace amount of formaldehyde by the spectrophotometric method with a bromate-Janus green system.

A new simple and rapid catalytic kinetic method for the determination of trace amount of formaldehyde is described. The method is based on the catalytic effect of formaldehyde on the oxidation of Janus green by bromate in the present of sulfuric acid. The reaction monitored spectrophotometrically by measuring the decrease in absorbance of the reaction mixture at 618 nm. The fixed-time method was used for the first 150 s. For initiation of the reaction, under the optimum conditions, in the concentration range of 0.003-2.5 microg ml(-1) formaldehyde can be determined with a limit of detection 0.0015 microg ml(-1). The relative standard deviation of five replicate measurements is 2.3% for 1.0 microg ml(-1) of formaldehyde. The method was used for the determination of formaldehyde in real samples with satisfactory results.

Azo Compounds↗
PubMed2004

Abrogation of potassium bromate-induced renal oxidative stress and subsequent cell proliferation response by soy isoflavones in Wistar rats.

Potassium bromate (KBrO3) is a potent nephrotoxic agent. In this study, we show the modulatory effect of soy isoflavones on KBrO3-mediated renal oxidative stress and subsequent cell proliferation response in Wistar rats. KBrO3 (125 mg/kg body weight, intraperitoneally) caused reduction in renal glutathione content, activities of renal anti-oxidant enzymes, viz., glutathione peroxidase, glutathione reductase, catalase, glucose-6-phosphate dehydrogenase and phase-II metabolising enzymes such as glutathione-S-transferase and quinone reductase with enhancement in xanthine oxidase, lipid peroxidation, gamma-glutamyl transpeptidase and hydrogen peroxide (H2O2). KBrO3 treatment also induced blood urea nitrogen, serum creatinine and tumor promotion markers, viz., ornithine decarboxylase (ODC) activity and thymidine [3H] incorporation into renal DNA. Treatment of rats orally with soy isoflavones (5 mg/kg body weight and 10 mg/kg body weight) resulted in a significant decrease in xanthine oxidase (P < 0.05), lipid peroxidation, gamma-glutamyl transpeptidase, H2O2 generation, blood urea nitrogen, serum creatinine, renal ODC activity and DNA synthesis (P < 0.001). There was also significant recovery of renal glutathione content (P < 0.01), anti-oxidant enzymes and phase-II metabolising enzymes (P < 0.001). Thus, our results show that soy isoflavones acts as potent chemopreventive agent against KBrO3-mediated renal oxidative stress, toxicity and subsequent cell proliferation response in Wistar rats.

Animals↗
PubMed2006

The study using wild-type and Ogg1 knockout mice exposed to potassium bromate shows no tumor induction despite an extensive accumulation of 8-hydroxyguanine in kidney DNA.

In order to assess the effect of potassium bromate (KBrO3) on the induction of tumor formation, a 1-year carcinogenesis study was performed using Ogg1 knockout mice (Ogg1(-/-)) and wild-type mice (Ogg1(+/+)). The mice were chronically exposed to KBrO3 by putting it in the drinking water for 29 weeks, at 2 g/l for the first 18 weeks, and then at 1 g/l for another 11 weeks. After termination of treatment the mice were kept for an additional 23 weeks. The amount of 8-hydroxydeoxyguanosine (8-OH-dG) in kidney DNA after 29 weeks of KBrO3 exposure reached 500 8-OH-dG/10(6) dG, almost 250-fold that of untreated wild-type mice. During the course of study the mice appeared normal, although a decrease of body weight gain in both Ogg1(-/-) and Ogg1(+/+) mice exposed to KBrO3, and some kidney malfunction in KBrO3 treated Ogg1(-/-) mice was observed. Surprisingly, when Ogg1(-/-) and Ogg1(+/+) mice were sacrificed at 52 weeks, no tumor formation could be found in kidney or other organs such as lung, liver, spleen, thymus, stomach and intestine. Microscopic examination also showed the absence of precancerous foci in all tissues of both Ogg1(-/-) and Ogg1(+/+) mice. A possible explanation is presented to reconcile these results with those of others which showed an increased incidence of tumor formation in untreated Ogg1(-/-) mice.

Administration, Oral↗
PubMed2006

Comparative efficacy of oligonol, catechin and (-)-epigallocatechin 3-O-gallate in modulating the potassium bromate-induced renal toxicity in rats.

Potassium bromate (KBrO(3)) is a by-product from ozonation of high-bromide surface water for production of drinking water and is a rodent carcinogen. Oligonol is a product emanating from the oligomerization of polyphenols, typically proanthocyanidin from a variety of fruits (grapes, apples, persimmons, etc.) and contains catechin-type monomers and proanthocyanidin oligomers. In this study, the ability of oligonol derived from grape seeds, grape seeds extracts (Product A, containing biologically active flavonoids and the oligomeric proanthocyanidin) and pine bark extracts (Product B, composed of flavan-3-ol derivatives) to modulate the KBrO(3)-induced renal toxicity was compared with (+) catechin and (-)-epigallocatechin 3-O-gallate (EGCG). In the Trolox equivalent antioxidant capacity (TEAC) assay, the order of the antioxidant activity was EGCG>catechin>oligonol>Product A>Product B. However, oligonol elicits the strongest antioxidant capacity following in vivo supplementation to rats, with the order of efficacy of oligonol>Product A> or =Product B>EGCG>catechin. Blood levels of lipid peroxidation products (LPO), urea nitrogen (BUN) and creatinine were elevated by KBrO(3) treatment. Oligonol significantly restored LPO to the level in the untreated rats and had the strongest potency when compared with the effects of Products A and B. The five materials lowered KBrO(3)-induced BUN level, but this was not statistically significant. Oligonol significantly reduced the increased level of the creatinine, seconded by Product A, Product B and EGCG. Catechin had the lowest effect in both the BUN and creatinine levels. That oligonol was able to modulate KBrO(3)-induced lipid peroxidation and the levels of blood urea nitrogen and creatinine suggests potential chemopreventive function and application in mitigating toxicity due to long-term exposure to KBrO(3) in public drinking water.

Animals↗
PubMed2005

Adsorptive ozonation of 2-methylisoborneol in natural water with preventing bromate formation.

This paper presents an application of our newly developed adsorptive ozonation process using a high silica zeolite adsorbent (USY) for drinking water treatment. First, the adsorption of 2-methylisoborneol (2-MIB) on USY in a river water/pure water mixture was clarified by a batch-type adsorption experiment. The results showed that 2-MIB was adsorbed on USY; however, almost all of the adsorbed 2-MIB was desorbed over time. The desorption rate was increased with the ratio of river water to pure water, indicating that compounds dissolved in the river water, such as natural organic matter (NOM), prevent the adsorption of 2-MIB on USY. Second, the ability of the river water to consume ozone was confirmed in an experiment using a USY-packed column reactor. The ozone consumption was obviously increased by the presence of USY, indicating that USY-adsorbing compounds dissolved in the river water (probably small size NOM) consumed the ozone. However, the rapid ozone consumption was occurred by 6-8 s in the retention times when 3.14-4.38 mgL(-1) of water dissolved ozone was fed, this rapid ozone consumption lasted no more than these times. This result revealed that the rapid consumption of ozone by the adsorptive compounds in our process could be avoided within a certain retention time (6-8 s; especially for the river water used in this study) when enough concentration of ozone (3.14 mgL(-1) or more; same above) was supplied. We therefore performed a trial in which 2-MIB dissolved in river water was continuously decomposed using a USY-packed column with various ozone concentrations. In the process, the adsorptive compound dissolved in the river water adsorbed and reacted with ozone in the parts of the apparatus upstream of the column, while the adsorption and decomposition of 2-MIB took place in the parts of the apparatus downstream of the column. This resulted in a sufficient 2-MIB decomposition with minimizing bromate ion formation.

Adsorption↗
PubMed2002

US Environmental Protection Agency Method 326.0, a new method for monitoring inorganic oxyhalides and optimization of the postcolumn derivatization for the selective determination of trace levels of bromate.

The development of US Environmental Protection Agency (EPA) Method 317.0 provided a more sensitive, acceptable alternative to EPA Method 300.1 to be proposed as one of the recommended compliance monitoring methods for Stage II of the Disinfectants/Disinfection By-Products (DBP) Rule. This work was initiated to evaluate other postcolumn reagents (PCRs) that might be utilized to provide an additional, alternative method in order to augment compliance monitoring flexibility for inorganic oxyhalide DBP anions. Modifications of the method reported by Salhi and von Gunten, which included adjustment and optimization of flow-rates, reaction temperature, and delivery of the PCR, improved the method performance. Method 326.0 incorporates an acidic solution of potassium iodide containing catalytic amounts of molybdenum(VI) as the PCR and provides acceptable precision and accuracy for all analytes and a postcolumn bromate detection limit in reagent water of 0.17 microg/l.

Bromates↗
PubMed1999

Determination of bromide, bromate and other anions with ion chromatography and an inductively coupled plasma mass spectrometer as element-specific detector.

An implementation of the Dionex IonPac AS12A analytical column with an element-specific ICP-MS detection is described for the simultaneous determination of halogen and oxyhalogen anions, sulfate, phosphate, selenite, selenate and arsenate. The chromatographic separation was achieved in less than 4 min with an aqueous 11 mM (NH4)2CO3 (pH 11.2, adjusted with aqueous ammonia) as eluent. Special emphasis was given to optimize the ICP-MS detection conditions for the reliable detection (RSD<5%) of bromate and bromide at a bromine concentration level of 1.0 microg l(-1) with 50 microl sample injection volume. In order to achieve the highest detector response for bromine species an ultrasonic nebulizer equipped with a membrane desolvator had to be employed. The detection limits (S/N=3, sample injection volume 50 microl) obtained with the IC-ICP-MS after the optimization were 0.67 microg l(-1) for BrO3-, 0.47 microg l(-1) for Br-, 69 microg l(-1) for ClO2-, 4 microg l(-1) for Cl-, 47 microg l(-1) for ClO3-, 13 microg l(-1) for SO4(2-), 36 microg l(-1) for PO4(3-), 0.4 microg l(-1) for SeO3(2-), 0.3 microg l(-1) for SeO4(2-), and 0.4 microg l(-1) for AsO4(3-).

Anions↗
PubMed1998

DNA oxidation by potassium bromate; a direct mechanism or linked to lipid peroxidation?

Following incubation of calf thymus DNA with potassium bromate (KBrO3) and glutathione (GSH), a statistically significant increase in the concentration of 8-oxodeoxyguanosine (8-oxodG) relative to deoxyguanosine was measured. This was GSH-dependent and was associated with loss of GSH during incubation. In contrast, 8-oxodG was not found to be elevated significantly in either total tissue DNA or mitochondrial DNA isolated from Sprague-Dawley rat kidney perfused in situ with KBrO3 (5 mM) for 15 min or 1 h. There was also no associated increase in the level of renal lipid peroxidation or reduced or oxidised GSH. Following intraperitoneal administration of KBrO3 to Sprague-Dawley rats, a dose of 100 mg/kg (maximum tolerated) gave evidence for oxidative stress in the kidney at 24 h as indicated by a significant increase in lipid peroxidation (P < 0.05) and oxidised GSH (P < 0.05). This was associated with a greater than 2-fold, significant (P < 0.01) increase in the level of 8-oxodG in kidney total DNA and a 57% (not statistically significant) increase in kidney mitochondrial 8-oxodG. Pretreatment of rats with diethylmaleate (DEM) to deplete GSH, elevated the toxicity of 100 mg/kg KBrO3. However, at a dose of 20 mg/kg, no change in any of the parameters indicative of kidney oxidative stress (including indicators of oxidative DNA damage; 8-oxodG or etheno-DNA adducts, which can be produced by lipid peroxides) was seen either with or without DEM pretreatment with the exception of a small but statistically significant (P < 0.05) increase in mitochondrial 8-oxodG when KBrO3 was given following DEM pretreatment. DNA oxidation in the kidney is therefore not inhibited by GSH depletion (contrasting with in vitro findings) and requires a sustained exposure at a near-toxic concentration of KBrO3 which is associated with lipid peroxidation and GSH oxidation. The results do not support a role, in rat kidney, of a direct, GSH-mediated mechanism for KBrO3-induced DNA oxidation as seen in vitro.

Animals↗
PubMed2002

Mutations in the VHL gene from potassium bromate-induced rat clear cell renal tumors.

Potassium bromate (KBrO(3)) is a rat renal carcinogen and a major drinking water disinfection by-product in water disinfected with ozone. Clear cell renal tumors, the most common form of human renal epithelial neoplasm, are rare in animals but are inducible by KBrO(3) in F344 rats. Detection of cytoplasmic periodic acid-Schiff-positive granules in clear cell tumors, indicative of glycogen accumulation, provides evidence of their biochemical similarity to human counterparts. Mutation in the coding region of the von Hippel-Lindau (VHL) gene is frequently detected in human clear cell renal carcinomas. Detection of VHL mutations in KBrO(3)-induced rat renal tumors could enhance the relevancy of these rat renal tumors for human health risk assessment. Formalin-fixed paraffin-embedded control tissues and renal tumors from male F344 rats exposed to KBrO(3) in the drinking water for 2 years were examined microscopically and were microdissected for DNA extraction. The coding sequence and a promoter region of the VHL gene were examined by polymerase chain reaction-single strand conformation polymorphism and/or DNA sequencing. Two of nine clear cell renal tumors carried the same C to T mutation at the core region of the Sp1 transcription factor binding motif in the VHL promoter and one of four untreated animals had C to T mutation outside the highly conserved core region. Mutation in the VHL coding sequence was only detected in one tumor. No VHL mutations were observed in three chromophilic tumors. KBrO(3)-induced rat renal tumors are morphologically similar to their human counterpart but the genetic basis of tumorigenesis is different.

Adenocarcinoma, Clear Cell↗
PubMed1999

Potassium bromate (KBrO3) induces renal proliferative response and damage by elaborating oxidative stress.

Many chemical compounds which induce oxidative stress in the tissue produce carcinogenesis either alone or act as a tumor promoter in carcinogen-initiated animals after prolonged exposure. Here, we report that potassium bromate (KBrO3) induces renal proliferative response and damage by elaborating oxidative stress. KBrO3 administration dose dependently induced renal ornithine decarboxylase (ODC) activity several fold compared to its activity in saline-treated rats. Similarly renal DNA synthesis which has been measured as [3H]thymidine incorporation in DNA also increases. KBrO3 administration also depleted the level of renal glutathione and glutathione reductase activity in a time dependent manner. The maximum depletion in the levels of renal glutathione and glutathione reductase activity was observed 3 h after KBrO3 treatment which was 60 and 40%, respectively, of saline-treated controls. Parallel to these changes, a sharp increase in the blood urea nitrogen and serum creatinine levels was observed which is indicative of the concurrent renal damage. These results suggest that oxidant generating KBrO3 acts as a potent proliferator of kidney and acts by producing oxidative damage.

Animals↗
PubMed1996

Induction of oh8Gua glycosylase in rat kidneys by potassium bromate (KBrO3), a renal oxidative carcinogen.

It has been suggested that 8-hydroxyguanine (oh8Gua), a DNA adduct formed by active oxygens, impairs the maintenance of genetic integrity, oh8Gua glycosylase removes oh8Gua residues as a free base from DNA strands. In E. coli, it has been demonstrated that oh8Gua glycosylase is induced in response to oxidative stress, but the oxidative inducibility in mammalian tissues has not yet been studied. In the present study, the inducibility of oh8Gua glycosylase was tested by comparing activity changes of this enzyme in the kidney and the liver of rats treated with potassium bromate (KBrO3). KBrO3 is known to cause oxidative damage to the kidney but not to other organs. With a single dose of KBrO3 (80 mg/kg, i.p.), activity in the kidney was found to increase significantly at 3 h compared to that at zero time. At 6 h, activity peaked, showing a 6-fold increase over that at zero time. Thereafter, it decreased and returned to its zero time level at 12 h. With increasing doses of KBrO3 (up to 160 mg/kg, i.p.), activity increased linearly with increased dosage, and over 40 mg/kg, i.p., activity increased to a level significantly higher than that in the control. In contrast to the time- and dose-dependent changes in activity in the kidney, no significant change was observed in the liver under the same conditions as above. These results show that oh8Gua glycosylase is also induced oxidatively in mammalian tissues. The induction in this tissue as well as in E. coli indicates that the adaptive response of this enzyme to oxidative stress is a general phenomenon in aerobic organisms and implies that the repair of oh8Gua residues in DNA is a process important for the survival of organisms in an aerobic environment.

Animals↗
PubMed2000

Intramolecular coupling of BrO stretching vibrations in solid bromates, infrared and Raman spectroscopic studies on M(BrO3)2.6H2O (M = Mg, Co, Ni, Zn) and Ni(ClO3)2.6H2O.

Infrared and Raman spectra of the isostructural cubic halate hexahydrates M(BrO3)2.6H2O (M = Mg, Co, Ni, Zn) and Ni(ClO3)2.6H2O (space group, Pa3; Z = 4) are presented. They are discussed with respect to the strength of the O-H...OXO2 hydrogen bonds (hydrogen bond acceptor capability, synergetic effect) and the order of the BrO stretching modes. In the case of undistorted bromate ions, e.g. at C3 lattice sites, the order of the symmetric (v1) and asymmetric (v3) XO stretching modes is v1 < v3 as for ClO3- but in contrast to IO3- with v1 > v3. The relative order of v1 and v3 of halate ions is mainly governed by the specific masses of the halogen atoms and the angles of the XO3- ions. The latter decrease in the sequence ClO3- (107degrees) > BrO3-> IO3- (< 100 degrees). The Raman scattering intensities of the asymmetric XO stretching modes v3 of the title compounds are unusually low (< 5% those of v1).

Bromates↗
PubMed2002

Vibrational investigation of the stretching region of bromate ion in solution.

The splitting of v1 (794 cm(-1)) and v3 (805 cm(-1)) modes in the stretching region of the bromate (C3v) was observed for the first time in dimethyl sulfoxide (DMSO) using vibrational spectroscopy. Depolarization measurements allowed to assign the asymmetric and symmetric modes in solution. The band at 805 cm(-1) that has been attributed to the symmetric stretching mode (A1) corresponds in fact to the asymmetric stretching mode (E) and the band at 794 cm(-1) corresponds to the symmetric stretching mode (A1).

Biophysical Phenomena↗